Preoperative Evaluation and Preparation

We present the elements of neurosurgical anesthesia practice, including preoperative assessment, premedication, drug selection, induction, maintenance, and recovery room care.

When intracranial procedures are planned, the preoperative evaluation must address various physiologic aspects of the patient’s condition. Neurologically there must be documentation of the patient’s level of consciousness, cranial nerve function, neurologic deficits, and the presence or absence of elevated intracranial pressure (ICP). Patients with a history of hypertension, cardiovascular disease, cerebral vascular insufficiency, or previous carotid endarterectomy may have altered levels of cerebral autoregulation, impaired cerebral perfusion, or abnormal baroreceptor function.^1–3 Intravascular volume depletion may be a result of diminished oral intake from nausea and vomiting, preoperative osmotic diuresis, and even the use of intravenous contrast administration for diagnostic studies.

Application of thigh-high pressure stockings to the legs is a routine practice to limit venous pooling in the lower extremities. Assessment of vascular access is helpful. Patients with poor vascular access or patients with short, thick necks should be identified early so the necessary time can be allotted for them.

Choice of Patient Position

Preoperative knowledge of positioning requirements is necessary in planning for monitoring. One must determine the patients’ risk and their ability to safely tolerate a surgical procedure or a specific position. The supine, prone, lateral, and sitting positions are commonly encountered with modifications unique to a specific procedure or surgeon.

Complications related to maintaining abnormal positions may occur. Extreme care is required regarding prophylactic padding. Hyperflexion–extension of the head is to be avoided. Head flexion can result in oropharyngeal complications. Compression by artificial airways and endotracheal tubes can occur.⁴ Leg pneumatic venous compression devices are used to relieve the incidence of deep venous thrombosis (DVT) from prolonged immobilization. This is true for all neurosurgical interventions, but is particularly important in patients with meningiomas, as these patients often present with a hypercoagulable state and are prone to the development of DVT.

Sitting

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.