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Anesthesia for Posterior Fossa Surgery

Operations in the posterior fossa are often demanding, delicate, and long. Anesthesia for these cases can also be challenging. In addition to the anesthetic management issues that apply to supratentorial surgery, posterior fossa surgery presents special problems related to positioning, cranial nerve dysfunction, and prevention of and monitoring for (VAE).

I. Preoperative considerations

The reticular activating system, cranial nerves, and structures vital for control of the airway and cardiovascular and respiratory systems are contained within a very small space in the posterior fossa. Accordingly, patients may present with dysphagia, laryngeal dysfunction, respiratory irregularities, or altered states of consciousness. In some cases, chronic aspiration owing to loss of airway reflexes can further compromise respiratory function.
Hydrocephalus caused by obstruction of ventricular outflow is a common cause of increased intracranial pressure (ICP) with posterior fossa lesions. This is evident on the preoperative computed tomographic scan or magnetic resonance imaging scan and can be treated by ventricular drainage, endoscopic third ventriculostomy, or hypertonic osmotherapy with mannitol and furosemide administered either pre- or intraoperatively.

II. Positioning

General issues
Posterior fossa surgery often requires unusual patient positioning. The prone, lateral, park bench, and sitting positions are commonly used. Regardless of the position chosen, care in positioning is of utmost importance because most problems are presumably avoidable with careful positioning and padding of vulnerable areas.
In the prone position, facial skin ulcerations can occur from uneven pressure distribution when the horseshoe headrest is used, and blindness can result from pressure on the globe of the eye.
In the lateral and park bench positions, there is a risk of brachial plexus injury if the up arm is pulled caudally to gain access to the retromastoid area.
Excessive neck rotation can also stretch and damage the brachial plexus, and extreme neck flexion is associated with the risk of quadriplegia.
Injury to the ulnar nerve at the elbow and peroneal nerve at the knee is also possible.
The sitting position
Advantages of the sitting position include good surgical exposure, improved ventilation, better access to the airway, greater comfort for the surgeon, and possibly reduced blood loss.
Disadvantages include the risk of VAE and pneumocephalus and the potential for hemodynamic instability. Additional complications include sciatic nerve injury from extreme flexion of the hip, massive swelling of the face and tongue from extreme neck flexion and/or rotation, and midcervical quadriplegia (ostensibly caused by a combination of stretch or compression of the cord by extreme neck flexion and hypotension).
The main contraindication to the use of the sitting position, however, is the presence of a documented right-to-left intracardiac or pulmonary shunt, which would facilitate systemic embolization of air.
VAE
VAE can occur whenever pressure within an open vessel is subatmospheric. Clinically significant VAE is unusual unless the surgical site is >20 cm above the level of the heart. Hence, VAE is a particular problem during surgery in the seated position, but it also occurs, albeit less frequently, in patients operated on in the lateral or prone position.
When open vessels cannot collapse, which is the case with major venous sinuses as well as bridging and epidural veins, the risk of VAE increases substantially. Most studies indicate that the incidence of VAE during posterior fossa procedures in the sitting position is 40% to 45%. For seated cervical laminectomy or surgery in the prone or lateral positions, VAE occurs in approximately 10% to 15% of cases.
Massive air embolism produces abrupt and catastrophic hemodynamic changes. Fortunately, this type of VAE is rare.
More commonly, air entrainment occurs slowly over a longer period of time and may produce little or no respiratory or hemodynamic compromise.
a. As air is cleared to the pulmonary circulation, pulmonary vascular resistance and pulmonary artery (PA) and right atrial pressures increase.
b. This vascular obstruction increases dead-space ventilation, resulting in the decrease in end-tidal carbon dioxide (ETco2) and increase in partial pressure of arterial carbon dioxide (Paco2) that are characteristic of VAE. In addition, nitrogen appears in the exhaled gas.
c. Hypoxemia develops owing to the partially occluded pulmonary vasculature and the local release of vasoactive substances.
d. If unchecked, cardiac output decreases as a result of right heart failure and/or reduced left ventricular filling.
Despite firmly held opinions and anecdotes, there is little evidence that the sitting position at least when used in large centers doing large numbers of sitting cases is less safe than alternative surgical positions. It is therefore difficult to argue that the sitting position should be abandoned purely because of the risk of VAE.
  Paradoxic air embolism (PAE)
When air enters the venous circulation, there is a risk that the air could pass via the pulmonary vascular bed or a patent foramen ovale (PFO) to the arterial side and embolize to coronary or cerebral vessels. The incidence of clinically significant PAE is unknown, and only a handful of cases have been reported (most without complications).
Approximately 25% of the population have a probe-PFO, and the incidence of VAE is approximately 45%. Therefore, approximately 10% to 15% of patients operated in the sitting position are at potential risk for PAE.
Precordial echocardiography has been used preoperatively to identify patients at risk because of a PFO. While detection of a PFO indicates that a patient is at risk for PAE, failure to identify a PFO is not reassuring because precordial echo has a high false-negative rate. Hence, echocardiography is not presently recommended as a routine part of the preoperative evaluation of such patients.

III. Anesthetic management

Premedication
There is no contraindication to premedication of patients who have small cranial nerve or cerebellar lesions. If the patient has either elevated ICP or symptomatic hydrocephalus, heavy premedication should be avoided.
General monitoring issues
For most posterior fossa cases, routine operative monitoring, usually with the addition of an intraarterial catheter for blood pressure monitoring, suffices.
For sitting cases, two additional issues arise. First, blood pressure should be measured at the level of the head because blood pressure measured at the level of the heart will underestimate that perfusing the brain. Second, monitoring for and prevention of VAE are major considerations.
 Monitoring for VAE
Hemodynamic changes. Monitoring of hemodynamics may not provide sufficient advanced warning in the case of massive air embolism because the hemodynamic changes are abrupt and catastrophic.
Doppler and ETco2 monitoring. Clinically, several monitoring options are available. In general, Doppler and ETco2 monitoring are considered the acceptable minimum.
Precordial Doppler
1. This device can detect 1 mL of air or less, which makes it more sensitive than any other monitor except transesophageal echocardiography (TEE). The Doppler is not quantitative, however, and it requires experience to recognize which of the various sounds it emits is indicative of air.
2. The Doppler probe should be placed after the patient is in the operative position. The probe is usually positioned at the middle third of the sternum on the right side but, because the position of the right atrium varies with the patient's position, proper placement must be confirmed. Hearing heart tones is not enough.
3. To test for proper placement of the probe, agitated saline is injected through a right atrial catheter or peripheral intravenous line; alternatively, the injection of 0.5 to 1 mL of air, carbon dioxide (CO2), or circuit gas is acceptable. The probe is properly placed if this maneuver produces characteristic Doppler sounds signaling air embolism.
4. Because of its sensitivity, a properly positioned Doppler, combined with end-tidal gas monitoring, is essential for all posterior fossa procedures in the seated position.
End-tidal gas monitoring
1. For reasons already stated, VAE is associated with a decreasing ETco2 and the presence of end-tidal nitrogen (ETn2).
2. While theoretically quantitative, ETn2 monitoring is less useful in practice because the ETn2 concentration produced by even a large air embolus is small and just reaches the threshold of the sensitivity of clinically available end-tidal gas monitors.
3. ETco2 monitoring is of intermediate sensitivity but provides a qualitative estimate of the size of a VAE. In general, the larger the embolus, the greater the decrease in ETco2. A decrease in ETco2 is not specific for VAE, however, because a decrease in cardiac output from any cause has the same effect.
4. The ETco2 monitoring is particularly useful for corroborating evidence of VAE from the Doppler and judging the clinical and physiologic significance of the embolus.
Central venous catheter (CVP)
1. As a monitor for VAE, the CVP is insensitive and easily superseded by other devices. It has another utility, however.
2. The CVP can help in positioning the Doppler. Also, the aspiration of air both confirms the diagnosis of VAE and serves as a treatment.
3. To facilitate rapid aspiration of air, a multiorificed catheter is recommended. Because air tends to localize at the junction between the superior vena cava and the right atrium, greatest air retrieval occurs when the catheter orifices traverse this region.
4. Catheter position can be confirmed in a number of ways. The catheter can be advanced until a right ventricular pressure trace is obtained and then withdrawn several centimeters. Alternatively, a chest x-ray can be obtained to confirm position. One simple method involves using the electrocardiogram, but its use has a risk of microshock. The right arm lead is connected to the catheter by a fluid column of sodium bicarbonate or via the J wire used to place the catheter. The tip is advanced until a biphasic P wave appears, at which point the catheter is withdrawn a few centimeters.
5. One should always attempt to insert a CVP catheter in posterior fossa cases requiring the sitting position, but whether the inability to do so should result in cancellation of the case is controversial.
PA pressure
1. Because PA pressures rise with significant VAE, the PA catheter can be useful for both diagnosis and therapy.
2. However, it is difficult to aspirate air from the distal port of a PA catheter, and the middle port may not be an optimal location. Aspiration is more effective with a CVP catheter.
3. In addition, as a diagnostic tool, the PA catheter offers no advantage over ETco2 monitoring.
Transesophageal echocardiography (TEE)
1. TEE is more sensitive than Doppler ultrasound and is specific because the air bubbles are visualized directly. It is the only monitor that can detect PAE.
2. TEE is expensive, requires special expertise, and demands near constant attention. For these reasons, in most centers, it is not a routine monitor for VAE.
Prevention of VAE
Positive end-expiratory pressure (PEEP)
1. The use of PEEP to prevent VAE in the sitting position is controversial. High levels of PEEP (>10 cm H2O) are needed to increase venous pressure at the head, and studies are inconsistent as to whether PEEP decreases the incidence of VAE. PEEP can, however, reduce venous return, cardiac output, and mean arterial blood pressure, which may be detrimental.
2. Experimental data also indicate that the discontinuation of PEEP is associated with the entrainment of venous air and promotes right-to-left shunting of air. Overall, PEEP is not recommended.
Volume loading
Although hypovolemia has been proposed as a predisposing factor for VAE, evidence for a prophylactic effect of volume loading on the incidence of VAE and PAE is not strong enough to warrant its routine use. Adequate hydration is the goal.
Deliberate hypoventilation
1. While some studies suggest that moderate hypoventilation may reduce the risk of VAE, hypoventilation also increases cerebral blood flow and cerebral blood volume, which may impair surgical exposure.
2. Until the benefits of hypoventilation are confirmed, mild hyperventilation is the more common practice.
Anesthetic technique
There is no evidence that any one anesthetic drug or technique is superior to another for posterior fossa surgery. Moreover, hemodynamic changes associated with the assumption of the sitting position are minor regardless of the anesthetic technique.
The use of nitrous oxide (N2O) is controversial. Because of the risk of VAE and the ability of N2O to expand air bubbles, some practitioners argue that N2O should be avoided in sitting position cases. This is a debatable position, however, because (a) N2O has not been shown to increase the risk of VAE in sitting cases and (b) morbidity has not been shown to increase if N2O is used provided it is discontinued the moment VAE is suspected. We subscribe to the latter reasoning; N2O is used but discontinued if VAE occurs. Sensitivity of the embolism-detection device does not change.
The airway requires special attention. Often with posterior fossa cases, substantial neck flexion is required for optimal surgical exposure. Such flexion can advance the tip of the endotracheal tube into a mainstem bronchus or cause kinking of the endotracheal tube in the posterior pharynx.
1. Some clinicians use a wire-reinforced tube while others prefer nasotracheal intubation. We use neither routinely but emphasize that careful assessment of tube patency and position is of utmost importance because access to the airway is quite limited.
2. This assessment should be conducted after positioning the patient but before making the skin incision. Palpation of the cuff above the sternal notch is useful in confirming the position of the tube.
3. If evidence of partial obstruction of the tube (e.g., high airway pressures, slow upstroke of the ETco2 tracing) exists, demonstrate that a suction catheter passes freely through the endotracheal tube, and insist on repositioning of the head and neck if it does not.
In most cases, controlled mild hyperventilation is desirable to improve surgical exposure and reduce retraction pressure on the brain. However, changes in respiration may be more sensitive to brain stem manipulation than hemodynamic changes. As such, the use of spontaneous ventilation may be appropriate in rare circumstances, when manipulation or ischemia of respiratory centers is likely. This should only be undertaken after discussion with the surgeon since hypoventilation that occurs with spontaneous ventilation during general anesthesia may cause brain engorgement and make surgical exposure more difficult.
Intraoperative considerations
Cardiovascular reflexes
1. Operations on or near the brain stem (e.g., during acoustic schwannoma surgery) can produce abrupt, often profound, cardiovascular responses that may signal potential damage to the brain stem.
2. Stimulation of the floor of the fourth ventricle, medullary reticular formation, or trigeminal nerve results in hypertension, usually in association with bradycardia. Bradycardia also results from stimulation of the vagus nerve.
3. If such changes occur, the surgeon should be alerted immediately so that he or she can avoid the manipulation that provokes the response.
4. Masking such changes with pharmacologic treatment is undesirable unless the changes are recurrent and severe. Hypertensive responses are typically so abrupt and transient that by the time a drug is administered, the stimulus is gone and treatment becomes unnecessary.
5. Bradycardia can be both treated and prevented with glycopyrrolate or atropine, but the tachycardia produced by the former is less marked.
Brain stem monitoring
1. Cranial nerve injury is a significant risk of operations in the area of the cerebellopontine angle and lower brain stem. Therefore, intraoperative stimulation and recording from cranial nerves V, VII, VIII, XI, and XII are often utilized.
2. Monitoring techniques include somatosensory evoked potentials (SSEPs), brain stem auditory evoked potentials (BAEPs), and the spontaneous and evoked electromyogram (EMG).
3. This monitoring can be a challenge for the anesthesiologist because muscle relaxants complicate interpretation of the EMG, and N2O and high-dose inhalation anesthesia may interfere with SSEPs. The BAEPs are robust and minimally influenced by anesthetics.
4. Although direct intracranial stimulation of the facial nerve produces facial movement even in well-paralyzed patients, "spontaneous" (i.e., surgical manipulation-induced) EMG discharges are subtle. Hence, some electrophysiologists request that, with the exception of succinylcholine for intubation, no muscle relaxants be given. The clinical necessity for this "pure" state has not been documented, however, and some centers are satisfied with a continuous infusion of relaxant to maintain a constant level of modest twitch suppression.
Treatment of VAE
1. Except in rare cases of severe hemodynamic instability, changing the patient's position is seldom required and often inconvenient. (The surgeon cannot identify a source of air entrainment if the wound faces the floor!) Other measures should be used first.
2. Alert the surgeons; they should irrigate the field with saline.
3. If N2O is being used, discontinue it immediately.
4. Aspirate the right atrial catheter.
5. Provide cardiovascular support as needed.
6. Modify the anesthetic technique as needed.
7. Ask an assistant to compress both jugular veins lightly to minimize air entrainment.
8. Change patient position if the preceding measures fail to prevent ongoing VAE.
Emergence from anesthesia
General objectives
1. As with other types of intracranial neurosurgery, prompt, smooth emergence and avoidance of coughing, straining, and abrupt increases in blood pressure are desirable.
2. The feasibility of extubation depends on the usual factors plus preexisting neurologic impairments, the nature and extent of the surgery, and the likelihood of brain stem edema or injury. Even if extubation is not planned, one should attempt to awaken the patient for postoperative neurologic evaluation.
Ventilation/airway abnormalities
1. Because of disease- or surgery-induced dysfunction of cranial sensory or motor nerves, patients may have difficulty swallowing, vocalizing, or protecting the airway. In addition, damage to or edema of the respiratory centers from intraoperative manipulation can result in hypoventilation or erratic respiratory patterns. Therefore, longer-term ventilation and airway protection might be required in some patients.
2. Severe tongue and facial edema can occur owing to position-induced venous or lymphatic obstruction. The endotracheal tube should be left in place until the edema resolves.
3. Pulmonary edema may result from large VAE. Although pulmonary edema is usually responsive to conservative measures such as supplemental oxygen (O2) and diuretics, continued postoperative ventilation may be appropriate until evaluation is completed.
Cardiovascular issues
Hypertension is common after posterior fossa surgery and may contribute to edema formation and intracranial hemorrhage. Hence, one should be prepared to control postoperative hypertension.
Neurologic complications
1. A variety of untoward neurologic complications can occur after posterior fossa operations. These include altered levels of consciousness, varying degrees of paresis, and specific cranial nerve deficits (e.g., visual disturbances, facial nerve paresis, impaired swallowing or phonation).
2. Treatment is supportive, but evaluation of delayed emergence should proceed lest a treatable nonanesthetic cause go unrecognized. If cerebral paradoxical air embolism is suspected, hyperbaric oxygen therapy may be warranted.
Pneumocephalus
1. Air is retained in the cranial cavity after all craniotomies regardless of position. When the patient is in the sitting position, cerebrospinal fluid drains easily, and a larger amount of air may be trapped when the wound is closed. In most cases, the air is reabsorbed uneventfully over several days and no treatment is necessary. There is little evidence that anesthetic technique influences either the incidence or the volume of pneumocephalus.
2. Tension pneumocephalus can occur when the brain re-expands and compresses the air. This situation is difficult to diagnose but should be suspected if emergence is delayed after an otherwise uneventful operation or if either cardiovascular collapse or neurologic deterioration occurs postoperatively.
3. In such rare circumstances, surgical evacuation may be indicated.

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