11 Principles of Anesthesia in Skull Base Surgery Normal values of intracranial pressure (ICP) range from 3 to 15 mmHg (~ 5–20 cmH2O). Two physiological mechanisms tend to limit the increase in ICP as the tumor increases in size: • Displacement of intracranial blood volume by increasing venous outflow or reducing cerebral blood flow (CBF) • Displacement of cerebrospinal fluid (CSF) from cranium to spinal subarachnoid space or by increasing CSF reabsorption However, beyond a certain threshold, if intracranial contents continue to increase in volume, the ability to compensate is impaired and ICP increases steeply.1–3 Raised ICP is a common feature in skull base tumors that are: • Large or cause significant edema and therefore create a large mass effect • Obstruct CSF pathways and lead to obstructive hydrocephalus Understanding this dynamic is critical for a safe anesthetic approach in skull base surgery. Symptoms and signs of raised ICP should be always identified during the preoperative patient evaluation (Table 11.1). Carbon dioxide (CO2) is the most potent cerebral vasodilator, and the manipulation of arterial carbon dioxide tension (partial pressure of carbon dioxide in arterial gas, Paco2) results in modification of the CBF and the cerebral blood volume (CBV). Table 11.1 Symptoms of Raised Intracranial Pressure (ICP) in Skull Base Tumors
Basic Pathophysiological Consideration
Intracranial Pressure
Importance
Carbon Dioxide
Raised ICP related • Headache (usually worse in the morning) • Nausea and vomiting • Papilledema • Drowsiness/impairment of consciousness/somnolence • Abnormal breathing pattern • Hypertension + bradycardia • Cushing’s ulcer (esophageal, gastric, duodenal) |
Other • First-time seizure • Difficulty with balance and coordination • Dizziness • Change in personality • Weakness or loss of sensation in an arm or leg • Facial pain, twitching, or paralysis • Hearing loss • Tinnitus (ringing in the ears) • Double vision or vision loss • Difficult in swallowing • Speech difficulties • Hoarseness |
Importance
Hyperventilation induces hypocapnia, which decreases CBF, CBV, and ICP. The goal of a short-term temporary and therapeutic hyperventilation is generally to maintain partial pressure of carbon dioxide (Pco2) in the range of 25 to 35 mmHg.4,5 Hyperventilation is often used intraoperatively to produce brain relaxation, reduce ICP, and facilitate surgical exposure.
• There is no evidence that an aggressive hyperventilation (Paco2 < 25 mmHg) offers an advantage over a more moderate hypocapnia, and it should be avoided because it has been shown to produce cerebral ischemia.6
• Following removal of the tumor, generally normocarbia (Pco2 35–40 mmHg) is used to enable a return of normal cerebral circulation, to identify areas of poor hemostasis, and to enable normal brain to gradually reexpand into the surgical cavity.
Autoregulation
Autoregulation is the ability of the cerebral circulation to maintain a constant CBF by altering cerebrovascular resistance (CVR) despite variation in cerebral perfusion pressure (CPP). CBF is directly related to CPP and is remarkably stable over a wide range of mean arterial pressure (MAP). CPP is usually > 70 mmHg. However, autoregulation has limits that are usually cited as 60 and 150 mmHg.7,8 Above and below these limits, CBF is passively dependent on MAP.
Table 11.2 Other Factors Affecting Cerebral Blood Flow (CBF)
• Hematocrit |
• Sympathetic tone • β1 stimulation: vasodilation • α2 stimulation: vasoconstriction |
• Elevated central venous pressure |
• Temperature |
• Increased local metabolic activity (e.g., nitric oxide) |
• High blood pressure |
Importance
Both intracranial pathology (e.g., brain tumor, trauma, hypoxia, hypercapnia) and anesthetic agent (e.g., volatile agent in a dose-dependent way) may impair autoregulation and compromise CPP through effects on MAP or ICP. Other factors affecting CBF are presented in Table 11.2.
Hemodynamic Stability
Based on the physiological cerebral dynamics, an optimal blood pressure and heart rate management plays an important role in preventing major intraoperative and postoperative complications.
Importance
• The key goal is always to avoid severe variations in blood pressure, either high or low, during induction of anesthesia, at the time of intubation, during head-holder pins fixation, throughout the procedure, and at the time of extubation. Hypotension can lead to ischemia in areas of impaired autoregulation, whereas hypertension increases the risk for vasogenic edema and hemorrhage. The management of hypertension perioperatively always requires consideration of the effect of such treatment on intracranial dynamics and cardiovascular function. For example, in a patient with hypertension due to raised ICP for a tumor pressing on the brainstem, an acute normalization of blood pressure might cause worsening of a neurologic deficit.
• Of particular note is the trigeminocardiac reflex (TCR) that can occur during procedures at the anterior, middle, and posterior skull base.9 The TCR has been defined as a drop in MAP and heart rate of more than 20% compared with the baseline values before the stimulus and coinciding with the manipulation around the trigeminal nerve or the distribution of the trigeminal nerve branches.10 Although TCR is rare (it has been reported to be in the range of 1.6 to 2.1%),11 transient bradycardia, hypotension, or asystole can occur regardless of whether there is pressure on the brainstem during posterior fossa meningioma surgery.12 Clear communication between the surgery and anesthesia teams is crucial if any of these signs occurs; tumor manipulation should be temporary stopped, and blood pressure or dysrhythmia treated if required, although they usually subside with interruption of the stimulus.
Preoperative Assessment
Given the complexity of most skull base surgeries, accurate and detailed preoperative assessment is crucial for effective and safe neuroanesthesia care. The clinical evaluation of patients with skull base tumors should be used to identify patients at greater risk of perioperative complications. Clear communication within the whole team in the operating room (e.g., surgeons, anesthetist, and nurses) and those outside the operating room (e.g., preoperative endocrinologists and the intensive care unit) is critical.
Symptoms Evaluation
Symptoms may vary according to the tumor location (e.g., meningioma, vestibular schwannoma, pituitary adenoma, chordoma), size, tumor growth rate, and involvement of adjacent structures, such as the brainstem, cranial nerves and arteries. Focal or global neurologic deficits should be clearly documented preoperatively and symptoms of raised ICP or seizures noted and accounted for by the anesthesia technique (Table 11.1).
Table 11.3 Skull Base Tumor: Symptoms Related to Pituitary’s Hormones Level Changes
• Round face |
• Disproportionate face, hands, and feet |
• Tall stature |
• Obesity |
• Thin skin |
• Joint pains |
• Excess sweating |
• Easy bruising |
• Stretch marks |
• Hypertension |
• Hypokalemia, hypernatremia |
• Diabetes mellitus |
Hormones Secretion Assessment
Pituitary Tumors
Failure to recognize hypocortisolism, Cushing’s disease, or acromegaly preoperatively can have serious consequences.
• Acromegaly can be associated with systemic hypertension, left ventricular hypertrophy, and diastolic dysfunction.13 Growth hormone hypersecretion can cause potentially difficult airway management: enlarged and thickened tongue (macroglossia), hypertrophy of the laryngeal soft tissue, and epiglottis and prognathism with malocclusion. These patients also have marked bony and soft tissue hypertrophy, which can lead to excessive bleeding during surgery.
• Cushing’s disease can be associated with hypertension, fluid retention, hyperglycemia, osteopenia, and obesity.14 Pituitary adenomas in Cushing’s disease may be quite small, and the surgical approach, particularly in the case of unoccluded intercavernous sinuses, may be associated with excessive bleeding15 (Table 11.3).
• All patients undergoing pituitary surgery are at risk of developing diabetes insipidus due to a perioperative antidiuretic hormone deficiency (see Chapter 9, page 239), but this is not usually encountered in the operating room.
Neurologic Assessment
A careful neurologic examination is of crucial importance, in particular to evaluate:
• The level of consciousness (i.e., is the patient alert and oriented, or somnolent and drowsy?)
• The presence or absence of baseline increased ICP (Table 11.1)
• Limb strength and movement
• Extent of neurologic deficits
In patients with clinically elevated ICP it may be necessary to prescribe an aggressive preoperative therapy with steroids and hyperosmolar agents to reduce edema; this therapy typically is started by the neurosurgeon.
Airway and Cardiorespiratory Assessment
Assessment of the airway and cardiorespiratory system is important in planning a smooth anesthesia induction and emergence, avoiding any maneuver that raises ICP or causes airway irritability, bronchospasm, laryngospasm, or cardiovascular instability.
Critical for airway management is the prospective assessment of whether or not the patient’s airway potentially poses difficulties.16 In particular, the anesthesiologist needs to be experienced with alternative methods of intubation (e.g., tracheotomy, submental orotracheal intubation) that have been described in the literature for transfacial or transmaxillary approaches to the cranial base (e.g., chondrosarcomas), when neither nasal nor orotracheal intubation is indicated for limiting the exposure of the cranial base.17,18
Blood Work
Preoperative blood work should include an assessment of preoperative hemoglobin, international normalized ratio (INR), glucose, CO2, and, if necessary, hormonal values such as 8 AM cortisol, free thyroxine (T4), growth hormone, and insulin-like growth factor-1 (IGF-1: somatomedin C).
Diagnostic Imaging
Diagnostic brain imaging should be assessed to identify the type of tumor; its location and vascularity; the evidence of mass effect, midline shift, hydrocephalus, or edema; and the amount of space around the basal cisterns and posterior fossa.
Intraoperative Management
General Problems
Intracranial Pressure Management
In the operating room, raised ICP may be controlled by the use of any of the following19,20:
• Free venous drainage
• Hyperventilation
• Anesthesia agent (e.g., reduce volatile anesthetic, change to intravenous anesthetic)
• Hyperosmolar agents (e.g., mannitol/hypertonic saline)
• Drainage of CSF
• Avoidance of the development of ischemic or hemorrhagic brain by continuous retraction or vascular injury
Fluid Management
Fluid optimization is crucial in neuroanesthesia. Patients undergoing skull base surgery frequently present with coexisting endocrine and electrolytes disorders (e.g., diabetes insipidus, Cushing’s disease, fluid retention), and in these patients the choice of fluid is determined by the nature of the disorder involved.
• There is no specific evidence to support the optimal use of crystalloids over colloids in terms of patient outcome.21
• Maintenance of normal osmolarity or mild hyperosmolarity of plasma is desirable, avoiding hypo-osmolar and dextrose-containing solution. Normal saline (0.9% NaCl) commonly is the fluid of choice because it is slightly hyperosmolar (308 mOsm) and is thought to attenuate formation of brain edema.22
• Fluid management strategies need to be individualized and directed by an understanding of the underlying pathophysiological mechanisms. These patients often experience rapid changes in intravascular volume caused by positioning, administration of diuretics, bleeding, or marked cerebral edema. For many years, a restrictive fluid management in neuroanesthesia has been the treatment of choice.23 Recent evidence has changed this approach completely.24
• The goals for a rational fluid administration should be to maintain an adequate cardiac output and electrolytes balance; to replace urinary output, blood loss, and insensible loss; and to avoid excessive fluid resuscitation.25
Seizure Prevention
Patients with skull base tumors often present first with headache and seizure, primarily due to increased ICP by the growing tumor. Seizure activity is associated with increased neuronal activity, increased CBF and CBV, and consequently increased ICP.26
• Seizure prophylaxis is not typically considered as part of the anesthesia plan; the anesthesiologist needs to be aware of whether the patient has received (or needs to receive prophylactically) antiseizure medications perioperatively to prevent potential cerebral injuries.
• Anticonvulsant agents such as phenytoin may decrease the duration of action of non-depolarizing muscle relaxant.27,28
Steroid Supplementation
Steroids can be used to replace physiological levels lost due to interruption of the hypothalamic-pituitary axis (e.g., craniopharyngioma or pituitary macroadenoma) or as a means of reducing cerebral edema.
• For replacement, hydrocortisone 25 or 50 mg IV is often used peri-operatively (see also Chapter 9).
• For peritumoral edema, to reduce swelling (not the size of the tumor in itself), to decrease ICP, and to improve associated neurologic deficit, dexamethasone 2 to 10 mg IV is considered most often.29,30
Hyperosmolar Agents
Osmotic agents are commonly used intraoperatively to reduce ICP, improve cerebral perfusion, and facilitate surgical exposure before opening of the dura or as needed.
• There is little evidence to support the use of one specific agent (e.g., mannitol vs hypertonic saline).31
• When using mannitol (0.25 to 1 g/kg, 15 to 20 minutes before opening of the dura mater), the anesthesiologist needs to consider the osmotic-mediated diuresis that can result in important intravascular volume-depletion, hypotension, and imbalance of electrolytes such as sodium and potassium.
• The use of hypertonic saline (3 mL/kg; the optimal dose is not known32) is effective in reducing ICP without the disadvantage of subsequent osmotic diuresis. However, plasma osmolarity, sodium concentration, and renal function need to be carefully monitored during administration.33
• Both mannitol and hypertonic saline should be used carefully in a patient with a history of congestive heart failure because they induce a transient increase in intravascular volume.
• The use of furosemide (0.2 to 0.5 mg/kg) is not supported by the evidence and is at the discretion of the anesthetist.34
Glucose Control
Both hyperglycemia and hypoglycemia should be avoided because they have been demonstrated to have adverse metabolic and cerebral ischemic effects.35
• There is no definitive evidence to support a very “tight” glucose control in critically ill patients,36 and whether it improves outcome in elective craniotomy is yet to be proven.
• A perioperative continuous insulin infusion protocol might be justifiable only in selected cases assessed by an endocrinologist preoperatively in those skull base tumors (e.g., some pituitary tumors) that are associated with diabetes, or in patients with insulin-dependent diabetes.
Pain Control
Pain control postcraniotomy remains challenging and controversial, as there are no large-scale trials determining effective treatments and side effects.37 In transsphenoidal approaches, postoperative pain is usually moderate, and it can be controlled with modest doses of opioids and acetaminophen.
• A multimodal analgesia approach has been proposed in order to reduce opioids’ side effects and achieve an effective pain control.38
• Measures to decrease postoperative pain include scalp nerves block, and incision line and pin-site infiltration with bupivacaine or ropivacaine.39,40
• Typically modest intravenous doses of morphine (10–15 mg) or hydromorphone (1–2 mg) are safe without a significant increase of their adverse effects or delayed emergence from anesthesia.
• Acetaminophen can be used safely in addition to opioids.
• The use of nonsteroidal anti-inflammatory drugs remains controversial because they may contribute to bleeding or postoperative renal failure.41
Nausea and Emesis Prevention

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