The lateral position can be an alternative to the sitting or prone position. A vacuum mattress conforms to the patient’s anatomy. The patient must not move after head fixation. This can cause strain in the cervical area.⁶ The lateral position is used particularly for approaches to the cerebellopontine angle, and for skull base approaches to the foramen magnum, petrous bone, and petroclival junction. It is the most complex positioning and requires great attention to detail to prevent axillary compression, brachial plexus stretch injuries, vascular compromise, and adequacy of monitoring placement.

The term sitting is a misnomer. The patient is in a modified recumbent position, as shown in Figure 20-1A and B. The legs are high to promote venous return and to elevate central venous pressure (CVP). This enhances circulatory stability and may reduce the chance for air embolism. Modifications to the sitting position permit lowering of the head without taking the patient out of the head holder. This is important if venous air embolus (VAE) is suspected because it allows rapid lowering of the head in a critical situation.

FIGURE 20-1 A–D, Variations of sitting position.

(From Miller RD, ed [2004]. Anesthesia, 4th ed, chapter 56, p. 1900, figure 56-1. Philadelphia: Churchill Livingstone, reproduced with permission.)

Head flexion is required to improve access to posterior structures. A two-fingerbreadth distance between the chin and the chest must be maintained to prevent compression ischemia. The bite block or oral airway must be positioned to prevent pressure on the base of the tongue. Large increases in ICP can occur with extreme head flexion and rotation or the addition of the positive end-expiratory pressure (PEEP).⁷ Head flexion may also result in downward migration of the endotracheal tube down the right mainstream bronchus. The positions shown in Figure 20-1C and D permit surgery to continue with the head to heart venous pressure gradient dimensions. Only the position shown in Figure 20-1D is compatible with closed-chest cardiac massage.

The sitting position for neurosurgery remains controversial. Its use has been diminishing because of potential serious complications, although many surgeons believe it is highly advantageous. The sitting position may be used because it provides better access to midline lesions, improved cerebral venous decompression, lower ICP, and gravity drainage of blood and CSF. The latter minimizes the need for exhaustive cautery with improved preservation of arachnoid plains. The sitting position also facilitates direct observation of facial musculature as a means of determining irritation of the facial nerve. Intraoperative facial electromyography improves direct observation by providing a continuous and more sensitive monitor of facial nerve functions.^1,⁸

Complications related to the use of the sitting position include venous air embolism (VAE), paradoxical VAE, circulatory instability, pneumocephalus, subdural hematoma, compressive peripheral neuropathy, quadriplegia, and skin compressive lesions.⁹ The severity of these complications have made most neurosurgeons in the United States abandon the position, while it is still used extensively in other parts of the world, particularly in Europe. Mild transient postural hypotension (–20 to –30 mm Hg) occurs in about one third of anesthetized patients placed in the sitting position. Marked hypotension (–50% of supine values) occurs in 2% to 5% of cases.^10,¹¹ Patients with heart failure or severe coronary/or cerebral occlusive vascular disease are a relative contraindication to the sitting position.

Intraoperative hydration and wrapping the legs with elastic bandages counteracts gravitational shifts of intravascular blood. The major hemodynamic change associated with sitting posture relates to poor venous return. They include a decrease in left ventricular function, cardiac index, and arterial pressure. One can help avoid hypotension by selecting an anesthetic technique that promotes high sympathetic tone but it will also increase myocardial demands by increasing systemic vascular resistance. Maintaining arterial blood pressure with slow positional change is recommended. A small amount of vasopressors may be useful.

Retrospective reviews of surgeons who performed procedures in the sitting and various horizontal positions concluded that each position has its own benefits and risks. They found no support of increased morbidity or mortality with either position.^12,¹³ In one series, although VAE occurred more than three times as often in seated patients as in the horizontally positioned patients, no increased clinical complication rate was found. Seated patients lost less blood and required fewer blood transfusions when compared with supine, prone, and lateral patients.¹³

Venous Air Embolism

Venous air entrainment (VAE) results from both an open vein and negative intravenous pressure relative to atmospheric pressure. It occurs when the head is positioned above the heart to encourage cerebral venous drainage. One study found VAE incidence rates of 25%, 18%, 15%, and 10% associated with sitting, lateral, supine, and prone positions, respectively. Low CVP and poor surgical techniques increase VAE incidence. With the use of a precordial Doppler monitor, the VAE incidence ranges form 25% to 50% during suboccipital craniotomy.¹⁴^–¹⁶

The highest risk portion of the operation for VAE is during skin–muscle incisions and when bone venous sinusoids are exposed during the dissection.⁹ Highly vascular lesions also predispose to VAE. VAE is most severe when a dural sinus is open, and therefore skull-base approaches, with their exposure of multiple venous sinuses, are particularly prone to VAE. It may also occur from headholder pins, burr holder, and connections in venous catheter systems.⁹

The clinical significance of VAE is influenced by several factors, including the volume of intravascular gas, its rate of entrainment, the presence of a patent foramen ovale, elevated right heart pressure, the presence of nitrous oxide, anesthetic depression of cardiovascular function, and the patient’s cardiopulmonary compensatory capacity. Small bubbles of air entrained slowly are of little physiologic significance. The venous gas bubbles are removed by the lungs at a rate that depends mainly on a compensatory rise in pulmonary artery pressure (PAP).^17,¹⁸ The PAP plateaus as the rate of venous entrainment of the gas equals the rate of its pulmonary excretion. At this point equilibrium occurs. If this excretion capacity overloads it leads to further PAP increases, pulmonary shunting, and reduced cardiac output and circulatory collapse. VAE-reduced cardiac output and/or increased dead space leads to a decrease in end-expired carbon dioxide, making end-tidal carbon dioxide monitoring extremely useful in this setting. A fall in end-tidal CO₂ is the first sign of a VAE. Mild carbon dioxide retention occurs as dead space increases in embolized regions. The diagnosis of VAE may be confirmed by a blood gas measurement. A large end-tidal carbon dioxide to PaCO₂ gradient in the absence of a recent change in controlled ventilation results. A late occurrence during an air embolism is hypoxemia, which occurs as a result of the shunting of pulmonary blood flow.¹⁸

Chronic postoperative perfusion deficits associated with increased pulmonary vascular permeability have been seen with small amounts of air over a prolonged period.^19,²⁰ Acute respiratory distress syndrome may result.

Paradoxical air embolism is another serious complication of VAE. With a patent foramen ovale, intravenous gas may pose to the left side of the heart and lodge in the brain, heart, or other vital organs. A patent foramen ovale and elevated right heart pressure occurs in about 5% to 10% of adult neurosurgical patients.²¹ A transesophageal echocardiogram (TEE) can be used to detect the presence of left-sided aerated saline.²² The operative TEE, however, is of limited value and can only provide guidance of a positive test result. In the presence of a known patent foramen ovale, a position other than seated should be used. PAP monitoring can detect a right-to-left arterial pressure gradient. It may reveal a paradoxical VAE.²³ Volume loading to elevate left atrial pressure or lowering the table can be helpful. PEEP elevates cerebral venous pressure and may reduce the potential for VAE, but its use remains controversial. Its ability to reverse the normal PAP to left atrial pressure gradient remains unclear.²⁴

When nitrous oxide is used as part of the anesthetic technique, the volume of entrained intravascular gas is increased.²² Nitrous oxide is 34 times more soluble in blood than nitrogen. It rapidly diffuses into an intravascular air bubble. It has been suggested that reducing the inspired concentration of nitrous oxide enhances safety.²⁵ A clinical study comparing 50% nitrous oxide with nitrogen showed that the use of 50% nitrous oxide has no effect on clinical outcome in the presence of minor episodes of VAE.¹⁶

The risks versus the benefits of nitrous oxide administration should be weighted according to the individual having neurosurgery. Certain guidelines have been suggested. Sensitive gas emboli detection techniques should be used. One hundred percent oxygen should be immediately instituted if suspicion of an embolus occurs.

The surgeon should be informed and the prevention of additional air entry should be prevented. The wound should be packed, and cerebral venous pressure should be increased by applying jugular venous compression or by lowering the patient’s head. Pharmacologic cardiovascular support should be used if deterioration occurs and the patient should be placed supine and resuscitation should proceed. The left lateral decubitus position may remove air from the pulmonary artery back into the right ventricle.^5,²⁶

The sitting position promotes CSF drainage form the intracranial space with resultant air entry and consequent pneumocephalus. Some degrees of pneumocephalus can occur in any craniotomy, but is accentuated in procedures performed in the sitting position.²⁷ Air entry is further facilitated by surgical decompression, diuretics, and hyperventilation. Air can remain trapped inside the skull when the dura is closed and can produce a mass effect. This mass effect may be asymptomatic or may be associated with headache, confusion, impaired memory, and lethargy. The symptoms usually resolve over 4 days.⁹ Breathing 100% oxygen will hasten reabsorption of the pneumocephalus.

Tension pneumocephalus, although rare, does occur and can result if high pressure develops in the air cavity. Occasionally it will require urgent decompression. Pressurization occurs with brain reexpansion, brain rehydration, and possibly brain edema. After the dura is closed, nitrous oxide removal occurs at a much faster rate than air reabsorption and should counter the ICP rise anticipated with brain expansion. Therefore, nitrous oxide can be used safely when the surgery is complete. However, if air is already within a closed cranium, as it is after a pneumoencephalogram or a prior craniotomy, nitrous oxide should not be used.

Cervical spinal cord ischemia due to neck flexion can result in quadriplegia.²⁸ Hypotension in the sitting position could potentiate this injury. Patient should be questioned perioperatively about upper extremity paresthesia related to neck position. Vigilance should he exerted to avoid extreme neck flexion, which in addition to cord ischemia can obstruct venous return resulting in marked swellings of the head and tongue. Small oral airway and late blocks should be used to ensure jugular venous patency.⁹ One should consider evoked potential monitoring to detect intraoperative cervical spinal cord ischemia.

Padding should be used in dependent areas and anatomically correct positioning should be maintained. Stretching the sciatic nerve and compression ischemia of the nerves and skin should be avoided.⁹

Monitoring

The margin of safety during neurosurgical anesthesia can be improved by using specialized monitoring that provides information on brain function and circulation. Early detection of threats to brain function and circulation is important. Changes in anesthetic and/or surgical approach may alter the neurologic outcome of the patient.

Neurophysiologic monitoring such as electroencephalography (EEG) and evoked potentials (somatosensory evoked potentials [SSEPs], brain stem auditory evoked response [BAER]) are valuable tools for detecting threat to the brain and spinal cord. These clinical applications are discussed in another chapter. Computed tomography (CT) and magnetic resonance imaging (MRI) are discussed in the neuroradiologic section of this book.

Specific monitoring techniques are available that will improve the safety of patients who are placed in positions at increased risk for venous air embolism. Transesophageal echocardiography is the most sensitive device for detecting air in the heart (0.02 mL/kg), and it is the only monitor that can detect air bilaterally. Its disadvantages include the risk of recurrent laryngeal nerve damage from the TEE probe that can occur in the flexed neck of a neurosurgical patient. One also needs a trained observer to interpret the TEE data.

The precordial Doppler ultrasound transducer is a very sensitive device for the detection of air in the right atrium. Small amounts of air (0.2 mL/kg) are detected easily because air is a good acoustic reflector. It is recommended that this device be used in conjunction with a capnogram for the detection of venous air embolism. The arterial-to-end tidal CO₂ gradient is increased with an air embolism. Low cardiac output and hypothermia may also alter this relationship.

Premedication

Administration of preoperative medication should be individualized based on the patient’s physical status, the presence of elevated ICP, and the level of patient anxiety. Chronic antihypertensive medication is continued. Corticosteroids and antibiotics are administered. Specifically, data show that preoperative antibiotics must be infused within 30 to 60 minutes of skin incision if infection rates are to be affected. Narcotic premedication is often avoided because CO₂ retention may increase ICP. Benzodiazepines are effective in reducing anxiety but may also cause carbon dioxide retention.

Induction of Anesthesia

Direct arterial blood pressure monitoring allows for tighter control of blood pressure and cerebral perfusion pressure during induction and intubation. Two large-bore intravenous catheters are recommended for meningioma surgery because these surgical procedures tend to be bloody. Intravenous thiopental, propofol, and etomidate are used as induction agents. A low-dose (3–5 µg/kg fentanyl), narcotic based N₂O/O₂ relaxant technique with supplemental volatile inhalation anesthetic can be used. Another technique that is growing in popularity for neurosurgical patients is total intravenous anesthesia (TIVA). Propofol or dexmedetomidine infusions in combination with a synthetic opioid infusion may be used.

Both techniques offer adequate analgesia and amnesia, preserve the autonomic nervous system activity, and allow rapid awakening at the end of the surgical procedure.

Beta-adrenergic blockage drugs and direct-acting vasodilators may be used to treat hypertension. Vasopressor administration may be needed after induction or during position. Short-acting drugs, such as ephedrine or Neo-Synephrine are usually effective.

The position of the endotracheal tube must be verified after positioning and before surgical incision. Access to the airway is limited due to the proximity of the operative site. Neck flexion or extension can produce displacement of the endotracheal tube, caudal or cephalad, by as much as 2 cm. Palpation of the endotracheal cuff in the sternal notch is helpful.

Maintenance of Anesthesia

Controlled positive pressure ventilation with paralysis is used as it facilitates the maintenance of lighter levels of anesthesia; it allows for hyperventilation, which decreases PaCO₂, producing a decreased sympathetic stimulation and decreased blood pressure at any depth of anesthesia. In addition, hyperventilation causes cerebral vasoconstriction with decreased ICP, reduced bleeding, and less cardiovascular depression.

Pinaud and colleagues ²⁹ found only minor and clinically insignificant differences among propofol-fentanyl, isoflurane nitrous oxide, and fentanyl-nitrous oxide anesthetics. They concluded that overemphasis on minor ICP effects of anesthetic drugs do not warrant such caution.

ICP alterations constitute one factor to be considered within specific intracranial pathology. In the presence of intracranial hypertension, cerebral vasodilating drugs increase cerebral blood volume (CBV) and thereby raise ICP, and are not good choices.

Most intravenous anesthetic drugs either reduce ICP or have little effect on it, provided ventilation is controlled to prevent PaCO₂ elevation. These drugs elicit a coupled reduction in cerebral metabolism and cerebral blood flow (CBF) and thereby ICP. Use of barbiturates, propofol, and etomidate are followed by a relative fall in ICP. Benzodiazepines create a moderate fall and narcotics have little to no direct ICP reducing action.²⁹^–³³ Under clinical conditions, all volatile anesthetic agents have the potential to elevate CBF, CBV, and ICP. Relative potency differences with regard to ICP elevation exist: halothane >> enflurane > sevoflurane, isoflurane, desflurane.^20,³⁴

The addition of nitrous oxide to an established volatile anesthetic under normocapnic conditions result in a dose-dependent elevation in CBV and CBF. With hypocapnia, the CBF-elevating action of the addition of nitrous oxide to an established volatile anesthetic is blocked with isoflurane.^35,³⁶

Nondepolarizing muscle relaxants have no direct cranial effects and are selected on the basis of minimizing cardiovascular and intracranial side effects.

Severe intraoperative hypothermia (<32°C) should be avoided, unless a specific hypothermic cardiac arrest is planned for management of complex vascular lesions. This is a very rare circumstance that we do not address in this chapter. Under routine circumstances, a 2° to 3°C intraoperative fall in patient temperature may provide a measure of cerebral protection, although this remains controversial.

A small dose of furosemide (5–10 mg) will promote diuresis of excess fluids reabsorbed from the extravascular space. Glucose-containing solutions are avoided owing to the possible detrimental effect of hyperglycemia on areas of the brain at risk for cerebral ischemia.³⁷ Normal saline is the preferred intravenous fluid. Lactated Ringer’s may be used if the patient does not have elevated ICP and its use is limited. Approximately 180 mL of free water is produced with each liter of lactated Ringer’s. It should be remembered that the osmolarity of normal plasma is about 285 mOsmol. Lactated Ringer’s is 275 mOsmol and saline is 305 mOsmol. The use of osmotic and loop diuretics may predispose patients to electrolyte disturbance and hypotension. Intravenous colloid can be used to maintain cerebral perfusion pressure. It has minimal effect on the cerebral dehydrating effect of the diuretic.

Emergence from Anesthesia

The anesthetic goals are to prevent abrupt rises in blood pressure, effect rapid awakening and return of motor strength, and minimize coughing and straining on the endotracheal tube.

A patient should demonstrate that he or she is awake, following commands, and demonstrate return of the protective airway reflexes.^38,³⁹

CRITICAL CARE CONSIDERATIONS

Intracranial Venous Congestion

One of the most difficult intraoperative aspects of meningioma removal is the network of cerebral veins and venous sinuses with which the tumor is often intimately related, especially in the parasagittal location. The neurosurgical goal of complete tumor resection, especially in benign lesions such as meningiomas, often is compromised by the association of these tumors with venous channels. On occasion, either by design or through unexpected thrombosis, venous channels are compromised. If collateral drainage exists, this may transpire without consequence. If this is not the case, however, venous congestion will result with consequent parenchymal swelling,⁴⁰ which at is extremes can be joined by intraparenchymal hemorrhage typical of venous infarction. Edematous cerebral parenchyma can lose function, generate seizures,⁴¹ and, if a large enough territory is involved, lead to intracranial hypertension or herniation.

Cerebral edema can also be caused directly by the meningioma itself, especially if the tumor is high grade with penetration through the pial membrane into the parenchyma. One study found a 2.9% incidence of postoperative edema caused directly by the tumor among patients who underwent surgery for a supratentorial meningioma.⁴²

Proximity to or direct involvement of a venous sinus is an especially challenging problem, as venous congestion caused by sinus compromise is frequently severe and can have fatal consequences, especially in the region of the superior sagittal sinus. Whereas complete ligation of the anterior third of the superior sagittal sinus is acceptable, compromise of the posterior third or even the middle third is not. There is less risk if the sinus is reconstructed, but it is often best not to resect the portion of the meningioma adherent to or invading the sinus.⁴³^–⁴⁶ Recent advances in radiosurgery have made it possible to treat tumor remnants in the sinus effectively. In the posterior fossa, unilateral transverse or sigmoid sinus ligation is possible if the contralateral sinus is present and test occlusion is tolerated (even if the contralateral sinus is nondominant).⁴⁷

Surgery to resect a nearby meningioma can also lead to venous sinus thrombosis. The possible prothrombotic combination of flow alteration, endothelial injury, and postoperative state (i.e., Virchow’s triad) places the patient at risk for the same venous congestion complications as direct surgical compromise of a sinus or vein. Unlike direct surgical compromise, however, sinus thrombosis is potentially treatable albeit not without risk. The treatment is full anticoagulation, which is obviously relatively contraindicated in the postoperative setting. If the benefits of anticoagulation in a particular case outweigh the risks, then it should be achieved with unfractionated heparin without bolus dose. Contrary to anticoagulation with low molecular weight heparin, unfractionated heparin can be easily titrated and, more importantly, rapidly reversed with protamine. Mechanical endovenous thrombectomy has been described but these patients also received full anticoagulation.⁴⁸

Seizure

Another frequent complication of meningioma surgery is seizure. Among patients undergoing resection of a supratentorial meningioma, studies have found that 36.5% to 37.3% who had preoperative seizures and 8.4% to 20.0% of those who did not, suffered postoperative seizures.^49,⁵⁰ Risk of postoperative seizure has been shown to be higher in patients with preoperative seizures,^50,⁵¹ parietal tumor location,⁵⁰ subtotal tumor resection,⁵⁰ and peritumoral edema.⁵¹ As described earlier, one cause of peritumoral edema is venous compromise. Seizures are a classic symptom of a venous infarct. Overall, intraoperative manipulation and irritation of an adherent cortex is also thought to contribute to the generation of seizures after the resection of some meningiomas. Seizure prophylaxis with antiepileptic medication(s) is a common practice for high-risk or, frequently, all postoperative meningioma patients.

Systemic Venous Thromboembolism

Among complications of meningioma surgery, deep venous thrombosis (DVT) and pulmonary embolism (PE) are not uncommon. A meta-analysis found an incidence of 4.3% for DVT and 1.4% for PE without prophylaxis.⁵² Risk factors include older age (one study defined this as greater than 65 years old),^42,⁵³ male gender,⁵³ and postoperative nonambulatory status.⁵³ As the mortality of a postcraniotomy PE has been shown to be 51%,⁵⁴ prophylaxis against PE and its precursor DVT is now standard of care in postoperative patients. Multiple methods of prophylaxis exist in singular or in combination and can be grouped into mechanical, low-dose unfractionated heparin, and low molecular weight heparin.

Mechanical methods of DVT/PE prophylaxis include graded compression stockings, intermittent pneumatic compression devices, early ambulation, and early physical and occupational therapy. These methods are usually well tolerated, and unlike other methods, do not carry a risk of harm to the patient. A meta-analysis of postcraniotomy patients found an incidence of 1.42% for DVT and 0.68% for PE with mechanical prophylaxis alone, rates lower than in patients without any prophylaxis.⁵²

Low-dose unfractionated heparin (LDUH) is usually given subcutaneously at a dose of 5000 units twice daily. Most studies have shown it to effectively reduce the incidence of DVT/PE when combined with mechanical prophylaxis versus mechanical prophylaxis alone in craniotomy for tumor patients (to a symptomatic DVT/PE incidence of 0% in one randomized controlled trial [RCT]).⁵⁵ Although a recent meta-analysis did not agree,⁵⁴ most believe that it is effective. The use of postoperative anticoagulation in any form has in the past provoked trepidation in neurosurgeons owing to the fear of intracranial hemorrhage (ICH). The mortality of postcraniotomy ICH has been estimated to be 27.5% with a severe morbidity, defined as a permanent, serious neurologic deficit, of 36.7%.⁵⁴ Numerous studies including at least one RCT, however, have found no increased risk of ICH with LDUH, leading most to accept it as a safe means of DVT/PE prophylaxis in neurosurgery.^56,⁵⁷

Low molecular weight heparin (LMWH), including enoxaparin and dalteparin, are given subcutaneously once daily. LMWH is favored over LDUH (both combined with mechanical prophylaxis) in other surgical subspecialties owing to its greater efficacy in preventing DVT and lower risk of causing heparin-induced thrombocytopenia.^58,⁵⁹ Patients appreciate the once daily dosing, but the monetary cost is higher than for LDUH. The use of LMWH versus LDUH (both combined with mechanical prophylaxis) in neurosurgery remains controversial, however, because of the results of conflicting studies regarding its safety and efficacy. One RCT of mechanical and LMWH versus mechanical alone in postoperative neurosurgical patients found a statistically significant decrease in rates of DVT with the addition of LMWH and no difference in rates of ICH.⁶⁰ Two RCTs of LMWH versus LDUH (both combined with mechanical prophylaxis) showed no statistically significant difference in DVT/PE rates between the two groups.^55,⁶¹ One of these two RCTs also examined ICH rates and found no statistically significant difference.⁶¹ A large meta-analysis of LMWH versus LDUH (both combined with mechanical prophylaxis), however, showed a decrease in DVT rates from 1.83% to 0.50% and a decrease in PE rates from 0.34% to 0.15% but an increase in ICH rates from 1.87% to 3.16% in the LMWH group.⁵⁴ To complicate matters further, a decision analysis model taking into account the deleterious effects of potential anticoagulant side effects (i.e., ICH) concluded that overall outcomes were best with mechanical prophylaxis alone. Differences between the treatment groups, however, were modest and reached statistical significance only when comparing the LMWH group to the other groups. In addition, assumptions used in this type of analysis limit its power and generalizability.⁵⁴

Overall, it is safe to conclude that prophylaxis against DVT and PE in neurosurgical patients is essential with at least mechanical methods. The addition of LDUH appears to be safe, and most studies conclude that it is effective as well. The evidence for LMWH is more heterogeneous and, anecdotally, neurosurgeons are more divided on the merits of its use.

Hydrocephalus

The incidence of hydrocephalus after meningioma surgery is estimated to be 3.4% to 8.2%.^42,⁶² It is more common after resections of skull base or intraventricular meningiomas and, as such, some advocate the use of a preemptive ventriculostomy for these procedures. Intraoperatively, this strategy would allow CSF drainage to create more working room during skull base meningioma resections⁶³ and would allow the drainage of any intraventricular hemorrhage or debris after resection of an intraventricular meningioma.⁶⁴ Postoperatively, this group of patients can potentially demonstrate a prolonged emergence from anesthesia commensurate with an often prolonged operative duration. A ventriculostomy in these patients would allow intracranial pressure measurement during a prolonged emergence period to rule out hydrocephalus as the cause. It would also allow rapid treatment of hydrocephalus should it occur in this group of patients who are prone to its development.

Hydrocephalus can also lead to wound complications. In a patient who develops a pseudomeningocele, one must consider the possibility of underlying hydrocephalus. Moreover, the incidence of pseudomeningocele has been shown to be increased among patients with preoperative hydrocephalus.⁶³ Postoperative hydrocephalus can also increase the risk for CSF leak.

CSF Leak

CSF leak can occur via multiple routes. CSF can enter the frontal, ethmoid, sphenoid, or less frequently maxillary sinuses, drain into the nasal cavity (or enter the nasal cavity directly), and escape as CSF rhinorrhea. It can enter the mastoid air cells or middle ear and drain through a perforated tympanic membrane as CSF otorrhea. CSF otorrhea from a laceration of the external ear canal is also possible but rare. CSF in the air cells or middle ear can also travel down the eustachian tube and exit as CSF rhinorrhea or, more commonly, drain into the pharynx where it is swallowed. Entry of CSF into these usually secluded spaces can occur due to trauma or tumor erosion, but in the postoperative setting the cause is almost certainly surgical entry that went unrecognized or was inadequately repaired. CSF leak can also occur via the surgical incision in cases of inadequate wound closure with or without hydrocephalus.

CSF leak after meningioma surgery is, not surprisingly, most common after resection of a skull-base lesion. The reported incidence varies, but one study found that 17% of 257 skull-base tumor resections (mostly meningiomas) were complicated by a CSF leak.⁶² The diagnosis is often obvious but in cases of uncertainty one can assay for beta-2-transferrin in the leaking fluid, as this protein is found only in CSF.⁶⁵

CSF leak is an emergency due the risk of ascending meningitis ^66,⁶⁷ and tension pneumocephalus.⁶⁸ If the leak is from an incision, that incision should be oversewn but that alone is not sufficient. All patients with a postoperative CSF leak should undergo a computed tomography (CT) scan to assess for the source. Fine image cuts and/or the instillation of radiopaque dye into the subarachnoid space can aid in its location. Reports of leak sources distant from the operative site must be kept in mind.⁶⁹

If the CT scan reveals a repairable source or if the surgeon is not completely confident of meticulous air sinus obliteration and wound closure, the patient should return to the operating room expeditiously for an exploration and repair of potential leak sources. If appropriate to the leak source or original surgery, an endonasal endoscopic repair may be considered.⁷⁰ If the CT scan does not reveal a leak source and the surgeon is completely confident of meticulous air sinus obliteration and wound closure, a trial of external lumbar drainage may be attempted to divert CSF flow away from the leak source and allow it to heal. During the trial, a 10 mL/hr drainage rate is advised as higher rates risk overdrainage (normal CSF production is approximately 20 mL/hr). We strongly recommend that the hourly 10 mL be drained using an “open/close” method rather than a continuous drip. The latter is prone to accidental catastrophic overdrainage, which can lead to devastating complications such as pneumocephalus with or without tension,^71,⁷² extra-axial hemorrhage from sagging parenchyma and stretched blood vessels, herniation,⁷² and reports of temporary blindness.⁷² We also recommend that the duration of drainage be approximately 5 days to give the leak source an adequate chance to heal. Frequent, premature “clamping trials” or “leak challenges” should be avoided as they may cause fluid to break through sites of weak preliminary healing. It should be noted that external lumbar drainage is unlikely to heal a leak in cases where the leak was unexpected and no primary repair was attempted. In these cases, the leak will be through bony openings with no chance of secondary scarring and it is often wise to return immediately to the operating room. In cases where a leak was considered a potential problem and a primary skull base repair was attempted, then the likelihood of success with lumbar spinal drainage trail is reasonable.

If a CSF leak is accompanied by persistent hydrocephalus, a shunt should be considered. One should keep in mind the possibility of pneumocephalus (with a risk of tension) from flow reversal through an unhealed leak source after shunting. Among postoperative skull-base tumor (mostly meningioma) patients with a CSF leak, 23% ultimately required shunting in one retrospective study.⁶²

The use of prophylactic antibiotics to prevent meningitis when a CSF leak is present is debated; however, the literature regarding posttraumatic CSF leaks seems to suggest that their use does decrease meningitis rates, especially if the leak is present for greater than 7 days.^73,⁷⁴

In an attempt to decrease rates of CSF leak after skull-base tumor resection, some neurosurgeons begin CSF diversion preoperatively. One retrospective review of skull-base tumor resections found a statistically significant decrease in postoperative CSF leak rate when a lumbar drain was placed preoperatively.⁷⁵ A review of cerebellopontine angle tumors revealed a trend toward increased rates of CSF otorrhea or rhinorrhea if hydrocephalus was present preoperatively. The authors suggested that the preoperative placement of a ventriculostomy may aid in leak prevention in these patients.⁶³

Pneumocephalus

Pneumocephalus following craniotomy for meningioma can be troublesome to the patient, as it can cause headache, nausea, and vomiting, as we mentioned earlier in this chapter. It can also be troublesome to the surgeon because there is the risk of progressive mass effect from tension development (the accumulation of intracranial air under pressure through an entry site acting as a one-way valve). Most postoperative pneumocephalus is caused by ambient air entering the craniotomy at the time of surgery and is usually not under tension. In an attempt to reduce the volume of postoperative pneumocephalus, the subarachnoid space is routinely filled with saline just before final dural closure. One group has attempted to augment this technique using carbon dioxide, which is heavier and more readily absorbed than air. Their technique consisted of a sterile cannula that delivered carbon dioxide gas to the surgical field at a rate of 2 L/min during the intradural portion of the operation. The subarachnoid space was filled with saline just before final dural closure per routine. In their randomized population of 40 patients with intraventricular or paraventricular tumors (20 experimental, 20 controls) they found the technique to be safe. They also concluded that the technique was associated with statistically significant decreases in postoperative intraventricular gas volume, time to complete resolution of gas, incidence of postoperative emesis, and duration of postoperative emesis.⁷⁶ This type of routine postoperative pneumocephalus can be treated with normobaric 100% oxygen via a non-rebreather facemask (or endotracheal tube if already intubated) to increase the nitrogen gradient that facilitates air absorption.⁷⁷

More worrisome causes of postoperative pneumocephalus are a CSF leak or overdrainage of an external lumbar drain because they can both lead to tension development. This is especially true for perinasal CSF leak sources that are susceptible to maneuvers that increase airway pressure (e.g., coughing, sneezing, nose blowing, Valsalva).⁷⁸

Hematoma

In a population operated on for a supratentorial meningioma, the incidence of postoperative hematoma has been estimated to be 2.5% among 19- to 64-year-old patients and 7.4% among 65- to 84-year-old patients.⁴² Another study reported 21 postoperative hematomas requiring surgical evacuation in a population of 296 intracranial meningioma patients (7.1%). There was an increased risk among older patients in this study as well.⁷⁹ Intra-axial hematomas are likely caused by intraoperative brain manipulation, inadequate hemostasis, delayed vessel rupture, and of great significance in the meningioma population, venous infarction with secondary hemorrhage. In the case of intra-axial hematomas associated with venous infarction, all attempts should be made to treat the problem medically, as the tissue involved with the hematoma has significant capacity for recovery once the swelling and hematoma subside.

Extra-axial hematomas are likely the result of a sagging brain and associated stretch on bridging blood vessels. This can be accentuated by therapeutic maneuvers to reduce ICP such as the too liberal use of osmotic diuretics, hyperventilation, or CSF drainage. We have recently seen a number of cases of extra-axial hemorrhage caused by aggressive drainage from sub-galeal drains in the setting of an incompletely closed dural layer. This pathophysiology may be more pronounced in older patients due to baseline cerebral atrophy. These extra-axial hematomas should be surgically evacuated if they are at all large and/or symptomatic.

Rare Conditions

A few conditions at the case report level merit mentioning because they can be diagnostically challenging. There has been a case report of adrenal apoplexy following craniotomy for meningioma resection.⁸⁰ This is extremely rare, but can cause significant complications and be both easily treated and easily misdiagnosed. Risk factors include sepsis, hypotension, use of anticoagulants, administration of adrenocorticotropic hormone (ACTH), and long-term corticosteroid use. Treatment is with steroid replacement, but some patients will require adrenalectomy. There has also been a case series reporting that psychogenic pseudoseizure may develop after craniotomy for a nonepilepsy indication.⁸¹ This may be considered as a diagnosis of exclusion in a patient whose extensive seizure workup is negative.

Specific Skull Base Sites

Certain skull-base operative sites are associated with a specific but nonexclusive cluster of potential complications. A primary risk of anterior fossa meningioma resection (e.g., anterior falcine, olfactory groove, tuberculum sella) is involvement of the nearby air sinuses without adequate postoperative obliteration and seal. This can lead to CSF rhinorrhea, ascending meningitis, or tension pneumocephalus. As maneuvers that increase airway pressure (e.g., coughing, sneezing, nose blowing, Valsalva) can contribute to tension development, some recommend prophylactic tracheostomy for those with significant bony defects between the sinonasal cavity and anterior fossa.⁷⁸ Others, however, believe that prophylactic tracheostomy is unnecessary.⁸²

Resection of middle fossa meningiomas (e.g., sphenoid ridge, anterior clinoid, cavernous sinus, and anterior petrosal) can lead to the same air sinus complications described in the preceding text, especially in the case of an unrecognized pneumatized anterior clinoid or petrous apex. Exposure of the cavernous or petrous carotid artery can be accompanied by injury to the artery with extensive intraoperative bleeding. If intraoperative carotid injury is not definitely repaired, postoperative pseudo-aneurysms can form with devastating postoperative bleeding. In cases of anterior approaches to extensive skull base meningiomas, this can present as delayed arterial epistaxis. This is obviously an emergency, which requires urgent angiography and which on occasion can be amenable to management with endovascular techniques.

Cavernous sinus compromise can cause orbital venous stasis with cavernous sinus syndromes and ophthalmoplegia. In the case of a meningioma with cavernous sinus involvement, most now recommend not resecting the intracavernous portion because of the high risk of complications and little benefit to tumor control.⁸³ This can be followed by radiosurgery to the region of residual tumor. In our opinion, a strategic approach to these lesions should be carried out preoperatively where a clear surgical plan for complete resection of all tumor outside the cavernous sinus, and specifically in the superior portion of the sinus should be performed. This surgical resection should clear the inferior portion of the optic apparatus from tumor by at least 1 cm so that postoperative radiation can be given with a high enough dose for tumor control, while still allowing the optic system to receive minimal radiation, ideally less than 9 Gy.

Posterior fossa meningiomas (e.g., cerebellopontine angle, petroclival, foramen magnum, jugular foramen) can be particularly hazardous due to their proximity to the cranial nerves and brainstem. Lower cranial nerve involvement (IX, X, XI) can lead to airway compromise. The patient should be extubated cautiously and the surgeon should have a low threshold for obtaining a rapid evaluation by an otolaryngologist, which should include assessment of vocal cord mobility and posterior laryngeal sensation. If prolonged intubation seems likely, early tracheostomy should be considered. This option can decrease airway and oropharyngeal trauma, does not require sedation which would otherwise mask the all-important neurologic exam, often results in a more rapid ventilator wean, and is reversible. If a tracheostomy is not performed, but the patient shows evidence of unilateral aspiration from vocal chord paralysis, a chord medialization procedure should be considered. The type of procedure (gel foam injection vs. thyroplasty) will be selected based on the expected course of the palsy.

A peripheral facial nerve lesion can cause inability to close the eye, leading to dangerous desiccation. If this is combined with a deficit in the ophthalmic branch of the trigeminal, it can lead to a devastating corneal injury. In such a case, an early tarsorrhaphy is recommended. In the case of lesser deficits, saline eye drops should be instilled during the day and lubricating ointment at night. As there is a risk of corneal abrasion from eyelid taping, a rigid protective orbit cover is preferred.

Lower cranial nerve involvement, including XII, can also lead to swallow compromise. As this complication can lead to devastating aspiration events, postoperative swallow function should be thoroughly assessed if there is the slightest concern. The head of the patient’s bed should always be kept in a position at least 30 degrees from the horizontal for aspiration prophylaxis. A formal swallow evaluation by a speech therapist should be performed and should include a test of the gag reflex (IX, X). If both swallow and otolaryngology evaluations are indicated, the swallow evaluation should be secondary. In patients with swallowing compromise, consider early gastrostomy rather than prolonged presence of a nasogastric tube.