Ebook Morgan & mikhail’s clinical anesthesiology (6/E): Part 2

(BQ) Part 2 book Morgan & mikhail’s clinical anesthesiology has contents: Kidney physiology & anesthesia, anesthesia for genitourinary surgery, anesthesia for orthopedic surgery, obstetric anesthesia, pediatric anesthesia, geriatric anesthesia, peripheral nerve blocks,... and other contents.

Optimal recovery of air following venous air embolism is provided by amultiorificed catheter positioned at the junction between the right

atrium and the superior vena cava Confirmation of correct catheterpositioning can be accomplished by intravascular electrocardiography,radiography, or transesophageal echocardiography

In a patient with head trauma, correction of hypotension and control ofany bleeding take precedence over radiographic studies and definitiveneurosurgical treatment because systolic arterial blood pressures of lessthan 80 mm Hg predict a poor outcome

Sudden, massive blood loss from injury to the great vessels can occurintraoperatively with adjacent thoracic or lumbar spine procedures

hypertension and marginal cerebral perfusion In addition, many neurosurgicalprocedures require patient positions (eg, sitting, prone) that further complicatemanagement This chapter applies the principles developed in Chapter 26 to theanesthetic care of neurosurgical patients

Intracranial Hypertension

Intracranial hypertension is defined as a sustained increase in intracranial

pressure (ICP) above 15 mm Hg Intracranial hypertension may result from anexpanding tissue or fluid mass, a depressed skull fracture if it compresses a

venous sinus, inadequate absorption of cerebrospinal fluid (CSF), excessivecerebral blood volume (CBV), or systemic disturbances promoting brain edema(see next section) Multiple factors may be present For example, tumors in theposterior fossa usually not only are associated with some degree of brain edemaand mass effect, but also readily obstruct CSF outflow by compressing the fourthventricle (obstructive hydrocephalus)

Although many patients with increased ICP are initially asymptomatic, theytypically develop characteristic symptoms and signs, including headache,

nausea, vomiting, papilledema, focal neurological deficits, and altered

consciousness When ICP exceeds 30 mm Hg, cerebral blood flow (CBF)

progressively decreases, and a vicious circle is established: ischemia causesbrain edema, which in turn, increases ICP, resulting in more ischemia If leftunchecked, this cycle continues until the patient dies of progressive neurological

damage or catastrophic herniation Periodic increases in arterial blood

pressure with reflex slowing of the heart rate (Cushing response) can be correlated with abrupt increases in ICP (plateau waves) lasting 1 to 15 min.

This phenomenon is the result of autoregulatory mechanisms periodically

decreasing cerebral vascular resistance and increasing arterial blood pressure inresponse to cerebral ischemia Eventually, severe ischemia and acidosis

completely abolish autoregulation (vasomotor paralysis)

CEREBRAL EDEMA

An increase in brain water content can be produced by several mechanisms.Disruption of the blood–brain barrier (vasogenic edema) is most common andallows the entry of plasma-like fluid into the brain Increases in blood pressureenhance the formation of this type of edema Common causes of vasogenic

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insults (cytotoxic edema), such as hypoxemia or ischemia, results from failure ofbrain cells to actively extrude sodium, causing progressive cellular swelling.Interstitial cerebral edema is the result of obstructive hydrocephalus and entry ofCSF into brain interstitium Cerebral edema can also be the result of intracellularmovement of water secondary to acute decreases in serum osmolality (waterintoxication)

TREATMENT

Treatment of intracranial hypertension, cerebral edema, or both, is ideally

directed at the underlying cause Metabolic disturbances are corrected, and

operative intervention is undertaken whenever appropriate Vasogenic edema—particularly that associated with tumors—often responds to corticosteroids

(dexamethasone) Vasogenic edema from trauma typically does not respond tocorticosteroids Blood glucose should be monitored frequently and controlledwith insulin infusions (if indicated) when steroids are used Osmotic agents areusually effective in temporarily decreasing brain edema and ICP until moredefinitive measures can be undertaken Diuresis lowers ICP chiefly by removingintracellular water from normal brain tissue Moderate hyperventilation (PaCO2

of 30–33 mm Hg) is often very helpful in reducing CBF, CBV, and ICP acutely,but may aggravate ischemia in patients with focal ischemia

Mannitol, in doses of 0.25 to 1 g/kg, is particularly effective in rapidly

decreasing intracranial fluid volume and ICP Its efficacy is primarily related toits effect on serum osmolality A serum osmolality of 300 to 315 mOsm/L isgenerally considered desirable Mannitol can transiently decrease blood pressure

by virtue of its weak vasodilating properties, but its principal disadvantage is atransient increase in intravascular volume, which can precipitate pulmonaryedema in patients with borderline cardiac or renal function Mannitol shouldgenerally not be used in patients with intracranial aneurysms, arteriovenousmalformations (AVMs), or intracranial hemorrhage until the cranium is opened.Osmotic diuresis in such instances can expand a hematoma as the volume of thenormal brain tissue around it decreases Rapid osmotic diuresis in elderly

patients can also occasionally cause a subdural hematoma due to rupture offragile bridging veins entering the sagittal sinus Rebound cerebral edema mayfollow the use of osmotic agents

Hypertonic saline (3% NaCl) is sometimes used to reduce cerebral edema and

Chapter 49) Serum sodium concentration and osmolality should be frequentlymonitored In patients with traumatic brain injury, interventions in addition tomannitol to lower intracranial pressure include head elevation, CSF drainage viaventriculostomy, moderate hypocapnia, and metabolic suppression with

barbiturates Decompressive craniectomy has been shown to decrease mortality

in patients with sustained increases in ICP (> 25 mm Hg) following traumaticbrain injury

or glioblastoma), ependymal cells (ependymoma), or supporting tissues

(meningioma, schwannoma, or choroidal papilloma) Childhood tumors includemedulloblastoma, neuroblastoma, and astrocytoma

Regardless of the cause, intracranial masses present symptoms and signsaccording to growth rate, location, and ICP Slowly growing masses are

frequently asymptomatic for long periods (despite relatively large size), whereasrapidly growing ones may present when the mass remains relatively small

Common presentations include headache, seizures, a general decline in cognitive

or specific neurological functions, and focal neurological deficits Symptomstypical to supratentorial masses include seizures, hemiplegia, or aphasia,

reviewed for evidence of brain edema, midline shift greater than 0.5 cm, or

ventricular displacement or compression Imaging studies typically will be

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Laboratory evaluation should rule out corticosteroid-induced hyperglycemia,electrolyte disturbances due to diuretics, or abnormal secretion of antidiuretichormone Anticonvulsant blood concentrations may be measured, particularlywhen seizures are not well controlled

Premedication

Sedative or opioid premedication is best avoided, particularly when intracranialhypertension is suspected Hypercapnia secondary to respiratory depressionincreases ICP Corticosteroids and anticonvulsant therapy should be continueduntil the time of surgery

INTRAOPERATIVE MANAGEMENT

Monitoring

In addition to standard monitors, direct intraarterial pressure monitoring andbladder catheterization are used for most patients undergoing craniotomy Rapidchanges in blood pressure during anesthetic procedures, positioning, and surgicalmanipulation are best managed with guidance from continuous invasive

monitoring of blood pressure Moreover, arterial blood gas analyses are

necessary to closely regulate PaCO2 We zero the arterial pressure transducer atthe level of the head (external auditory meatus)—instead of the right atrium—tofacilitate calculation of cerebral perfusion pressure (CPP), and we document thispractice in the anesthetic record End-tidal CO2 measurements alone cannot berelied upon for precise regulation of ventilation; the arterial to end-tidal CO2gradient must be determined Central venous access and pressure monitoringmay be considered for patients requiring vasoactive drugs Use of the internaljugular vein for access is theoretically problematic because of concern that thecatheter might interfere with venous drainage from the brain The external

jugular, subclavian, or other peripheral veins may be suitable insertion sites forcentral venous catheters A bladder catheter is necessary because of the use ofdiuretics, the long duration of most neurosurgical procedures, and the utility of

temperature Neuromuscular function should be monitored on the unaffectedside in patients with hemiparesis because the twitch response is often abnormallyresistant on the affected side Monitoring visual evoked potentials may be useful

in preventing optic nerve damage during resections of large pituitary tumors.Additional monitors for surgery in the posterior fossa are described later in thisdiscussion

Management of patients with intracranial hypertension may be guided bymonitoring ICP perioperatively Various ventricular, intraparenchymal, and

subdural devices can be placed by neurosurgeons to provide measurements ofICP The transducer should be zeroed to the same reference level as the arterialpressure transducer (usually the external auditory meatus, as previously noted)

A ventriculostomy catheter provides the added advantage of allowing removal ofCSF to decrease ICP

Induction

Induction of anesthesia and tracheal intubation are critical periods for patientswith compromised intracranial pressure to volume relationships, particularly ifthere is an elevated ICP Intracranial elastance can be improved by osmotic

diuresis or removal of small volumes of CSF via a ventriculostomy drain Thegoal of any technique should be to induce anesthesia and intubate the tracheawithout increasing ICP or compromising CBF Arterial hypertension duringinduction increases CBV and promotes cerebral edema Sustained hypertensioncan lead to marked increases in ICP, decreasing CPP and risking herniation.Excessive decreases in arterial blood pressure can be equally detrimental bycompromising CPP

The most common induction technique employs propofol together with

modest hyperventilation to reduce ICP and blunt the noxious effects of

laryngoscopy and intubation All patients receive controlled ventilation once thepropofol has been injected A neuromuscular blocker (NMB) is given to

facilitate ventilation and prevent straining or coughing, both of which can

abruptly increase ICP An intravenous opioid given with propofol blunts thesympathetic response, particularly in young patients Esmolol (0.5–1.0 mcg/kg)

is effective in preventing tachycardia associated with intubation in lightly

anesthetized patients

The actual induction technique can be varied according to individual patientresponses and coexisting diseases Succinylcholine may theoretically increase

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induction or when there are concerns about a potentially difficult airway, ashypoxemia and hypercarbia are much more detrimental than any effect of

succinylcholine to the patient with intracranial hypertension

Hypertension during induction can be treated with β1-blockers or by

deepening the anesthetic with additional propofol Modest concentrations ofvolatile agents (eg, sevoflurane) may also be used, provided that

hyperventilation is also used Sevoflurane best preserves autoregulation of CBFand produces limited vasodilation; it may be the preferred volatile agent in

patients with elevated ICP Because of their potentially deleterious effect onCBV and ICP, vasodilators (eg, nicardipine, nitroprusside, nitroglycerin, andhydralazine) are avoided until the dura is opened Hypotension is generallytreated with incremental doses of vasopressors (eg, phenylephrine)

Positioning

Frontal, temporal, and parietooccipital craniotomies are performed in the supineposition The head is elevated 15° to 30° to facilitate venous and CSF drainage.The head may also be turned to the side to facilitate exposure Excessive flexion

or rotation of the neck impedes jugular venous drainage and can increase ICP.Before and after positioning, the tracheal tube should be secured and positionverified, and all breathing circuit connections checked The risk of unrecognizeddisconnections is increased because the patient’s airway cannot be easily

assessed after surgical draping; moreover, the operating table is usually turned90° or 180° away from the anesthesia provider

Maintenance of Anesthesia

Anesthesia can be maintained with inhalation anesthesia, total intravenous

anesthesia techniques (TIVA), or a combination of an opioid and intravenoushypnotic (most often propofol) with a low-dose inhalation agent Even thoughperiods of stimulation are few, neuromuscular blockade is recommended—unless neurophysiological monitoring contradicts its use—to prevent straining,bucking, or other movement Increased anesthetic requirements can be expectedduring the most stimulating periods: laryngoscopy–intubation, skin incision,dural opening, periosteal manipulations, including Mayfield pin placement andclosure TIVA with remifentanil and propofol facilitates rapid emergence and

(PEEP) and increased mean airway pressure; in such patients, the effect of PEEP

on ICP is variable

Intravenous fluid replacement should be limited to glucose-free isotoniccrystalloid Hyperglycemia is common in neurosurgical patients and has beenimplicated in increasing ischemic brain injury Hyperglycemia should be

corrected preoperatively Neurosurgical procedures are often associated withoccult blood loss (underneath surgical drapes or on the floor) Hypotension andhypertension should both be expeditiously corrected

Emergence

Most patients undergoing elective craniotomy can be extubated at the end of theprocedure Patients who will remain intubated should be sedated to preventagitation Extubation in the operating room requires special handling duringemergence Straining or “bucking” on the tracheal tube may precipitate

intracranial hemorrhage or worsen cerebral edema As the skin is being closed,the patient may resume breathing spontaneously Should the patient’s head besecured in a Mayfield pin apparatus, care must be taken to avoid any patientmotions (eg, bucking on the tube), which could promote neck or cranial injuries.After the head dressing is applied and full access to the patient is regained (thetable is turned back to its original position as at induction), any anesthetic agentsare discontinued and the neuromuscular blockade is reversed Rapid awakeningfacilitates immediate neurological assessment and is generally expected

Delayed awakening may be seen following opioid or sedative overdose, whenthe end-tidal concentration of the volatile agent remains greater than 0.2

minimum alveolar concentration (MAC), or when there is a metabolic

derangement or a perioperative neurological injury Patients may need to betransported to the CT scanner directly from the operating room for evaluationwhen they do not respond as predicted Immediate reexploration may be

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Anesthesia for Surgery in the Posterior Fossa

Craniotomy for a mass in the posterior fossa presents a unique set of potentialproblems: obstructive hydrocephalus, possible injury to vital brainstem centers,pneumocephalus, and, when these procedures are performed with the patient in

the sitting position, an increased risk of postural hypotension and venous air embolism.

Obstructive Hydrocephalus

Infratentorial masses can obstruct CSF flow through the fourth ventricle or thecerebral aqueduct of Sylvius Small but critically located lesions can markedlyincrease ICP In such cases, a ventriculostomy is often performed under localanesthesia to decrease ICP prior to induction of general anesthesia

Brainstem Injury

Operations in the posterior fossa can injure vital circulatory and respiratorybrainstem centers, as well as cranial nerves or their nuclei Such injuries mayoccur as a result of direct surgical trauma or ischemia from retraction or otherinterruptions of the blood supply Damage to respiratory centers is said to nearlyalways produce circulatory changes; therefore, abrupt changes in blood pressure,heart rate, or cardiac rhythm should alert the anesthesia provider to the

possibility of such an injury Such changes should be communicated to the

surgeon Isolated damage to respiratory centers may rarely occur without

premonitory circulatory signs during operations in the floor of the fourth

ventricle Historically, some clinicians have employed spontaneous ventilationduring these procedures as an additional monitor of brain function At

completion of the surgery, brainstem injuries may present as an abnormal

respiratory pattern or an inability to maintain a patent airway following

extubation Monitoring brainstem auditory evoked potentials may be useful inpreventing eighth nerve damage during resections of acoustic neuromas

Electromyography is also used to avoid injury to the facial nerve but requiresincomplete neuromuscular blockade intraoperatively

Although most explorations of the posterior fossa can be performed with thepatient in either a modified lateral or prone position, the sitting position may bepreferred by some surgeons

The patient is actually semirecumbent in the standard sitting position (Figure 27–1); the back is elevated to 60°, and the legs are elevated with the knees

flexed The head is fixed in a three-point holder with the neck flexed; the armsremain at the sides with the hands resting on the lap

Figure 27–1 The sitting position for craniotomy.

Careful positioning and padding help avoid injuries Pressure points, such asthe elbows, ischial spines, heels, and forehead, must be protected Excessiveneck flexion has been associated with swelling of the upper airway (due to

venous obstruction), and, rarely, quadriplegia (due to compression of the cervicalspinal cord) Preexisting cervical spinal stenosis probably predisposes patients tothe latter injury

Pneumocephalus

The sitting position increases the likelihood of pneumocephalus In this position,

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patients with cerebral atrophy, drainage of CSF is marked; air can replace CSF

on the surface of the brain and in the lateral ventricles Expansion of a

pneumocephalus following dural closure can compress the brain Postoperativepneumocephalus can cause delayed awakening and continued impairment ofneurological function Because of these and other concerns, nitrous oxide israrely used for sitting craniotomies (see further discussion that follows)

Venous Air Embolism

Venous air embolism can occur when the pressure within an open vein issubatmospheric These conditions may exist in any position and during anyprocedure whenever the wound is above the level of the heart The incidence ofvenous air embolism is greater during sitting craniotomies (20–40%) than incraniotomies in any other position Entry into large cerebral venous sinusesincreases the risk

The physiological consequences of venous air embolism depend on the

volume and the rate of air entry and whether the patient has a right-to-left

intracardiac shunt (eg, patent foramen ovale [10–25% incidence]) The latter areimportant because they can facilitate passage of air into the arterial circulation

(paradoxical air embolism) Modest quantities of air bubbles entering the

venous system ordinarily lodge in the pulmonary circulation, where they areeventually absorbed Small quantities of embolized air are well tolerated by mostpatients When the amount entrained exceeds the rate of pulmonary clearance,pulmonary artery pressure rises progressively Eventually, cardiac output

decreases in response to increases in right ventricular afterload Preexistingcardiac or pulmonary disease enhances the adverse effects of venous air

embolism; relatively small amounts of air may produce marked hemodynamicchanges Nitrous oxide, by diffusing into air bubbles and increasing their

volume, can markedly accentuate the effects of even small amounts of entrainedair The lethal volume of venous air in experimental animals receiving nitrousoxide anesthesia is reduced to one-third to one-half that of control animals notreceiving nitrous oxide

In the absence of echocardiography, definitive signs of venous air embolismare often not apparent until large volumes of air have been entrained A decrease

in end-tidal CO2 or arterial oxygen saturation may be noticed prior to

hemodynamic changes Arterial blood gas values may show only slight increases

in PaCO2 as a result of increased dead space ventilation (areas with normal

manifestations, such as sudden hypotension, can occur well before hypoxemia isnoted Moreover, large amounts of intracardiac air impair tricuspid and pulmonicvalve function and can produce sudden circulatory arrest by obstructing rightventricular outflow

Paradoxic air embolism can result in a stroke or coronary occlusion, whichmay be apparent only postoperatively Paradoxic air emboli are more likely tooccur in patients with right-to-left intracardiac shunts, particularly when thenormal transatrial (left > right) pressure gradient is consistently reversed

A Central Venous Catheterization

A properly positioned central venous catheter can be used to aspirate entrainedair, but there is only limited evidence that this influences outcomes after venousair embolism Some clinicians have considered right atrial catheterization

mandatory for sitting craniotomies, but this is a minority viewpoint Optimalrecovery of air following venous air embolism is provided by a multiorificedcatheter positioned at the junction between the right atrium and the superior venacava Confirmation of correct catheter positioning can be accomplished by

intravascular electrocardiography, radiography, or transesophageal

echocardiography (TEE), with the latter being simplest and easiest Intravascularelectrocardiography is accomplished by using the saline-filled catheter as a “V”lead Correct positioning near the cavoatrial junction is indicated by the

appearance of a maximally biphasic P wave If the catheter is advanced fartherinto the heart, the P wave changes from a biphasic to a undirectional deflection

A right ventricular or pulmonary artery waveform may also be observed whenthe catheter is connected to a pressure transducer and advanced too far, but

pressure waveforms do not identify the cavoatrial junction

B Monitoring for Venous Air Embolism

The most sensitive detectors available should be used Detecting even smallamounts of venous air emboli is important because it allows surgical control ofthe entry site before additional air is entrained Currently, the devices capable ofdetecting the smallest volumes of air are TEE and precordial Doppler

sonography These monitors can detect air bubbles as small as 0.25 mL TEE hasthe added benefit of detecting the volume of the bubbles and any transatrialpassage through a patent foramen ovale, as well as evaluating any effect venousair embolism may have on cardiac function Doppler methods employ a probeover the right atrium (usually to the right of the sternum and between the third

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Venous air embolism causes a sudden decrease in end-tidal CO2 tension in

proportion to the increase in pulmonary dead space; however, decreases can also

be seen with hemodynamic changes unrelated to venous air embolism, such asdecreased cardiac output A reappearance (or increase) of nitrogen in expiredgases may also be seen with venous air embolism Changes in blood pressureand heart sounds (“mill wheel” murmur) are late manifestations of venous airembolism

C Treatment of Venous Air Embolism

1 The surgeon should be notified so that he or she can flood the surgical field

with saline or pack it with wet gauzes and apply bone wax to the skull edgesuntil the entry site is identified and occluded

7 Some clinicians advocate PEEP to increase cerebral venous pressure;

however, reversal of the normal transatrial pressure gradient may promoteparadoxical embolism in a patient with incomplete closure of the foramenovale

8 If the previously listed measures fail, the patient should be placed in a head-down position, and the wound should be closed quickly

9 Persistent circulatory arrest necessitates the supine position and institution of

resuscitation efforts using advanced cardiac life support algorithms

Stereotaxis can be employed in treating involuntary movement disorders,

intractable pain, and epilepsy and can also be used when diagnosing and treatingtumors that are located deep within the brain

These procedures are often performed under local anesthesia to allow

evaluation of the patient Propofol or dexmedetomidine infusions are often usedfor sedation and amnesia Sedation should be omitted, however, if the patientalready has increased ICP The ability to rapidly provide controlled ventilationand general anesthesia for emergency craniotomy is mandatory but is

complicated by the platform and localizing frame that is attached to the patient’shead for the procedure Although mask ventilation or ventilation through a

laryngeal mask airway (LMA) or orotracheal intubation might be readily

accomplished in an emergency, awake intubation with a fiberoptic bronchoscope

or videolaryngoscope prior to positioning and surgery may be the safest

approach when intubation is necessary for a patient whose head is already in astereotactic head frame

Functional neurosurgery is increasingly performed for removal of lesionsadjacent to speech and other vital brain centers Sometimes patients are managedwith an asleep–awake–asleep technique, with or without instrumentation of theairway Such operations require the patient to be awake to participate in corticalmapping to identify key speech centers, such as Broca’s area Patients sleepduring the painful periods of surgery (ie, during opening and closure) LMAs areoften employed to assist airway management during the asleep portions of thesesurgeries Local anesthetic infiltration of the scalp facilitates awake craniotomy.Patients undergo deep brain stimulator insertion for control of movement andother disorders A stimulator electrode is placed via a burr hole using

radiological guidance to establish coordinates for electrode placement A

microelectrode recording (MER) is obtained to determine the correct placement

of the stimulator in brain structures The effect of stimulation upon the patient isnoted Sedative medications can adversely affect MER potentials, complicatingthe location of the correct depth of stimulator placement Dexmedetomidine hasbeen used to provide sedation to these patients; however, during MER and

stimulation testing, sedative infusions should be discontinued to facilitate patientparticipation in determining correct electrode placement (Table 27–1)

TABLE 27–1 Advantages and disadvantages of drugs used for conscious sedation 1,2

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Head injuries are a contributory factor in up to 50% of deaths due to trauma.Most patients with head trauma are young, and many (10–40%) have associatedintraabdominal or intrathoracic injuries, long bone fractures, or spinal injuries.The outcome from a head injury is dependent not only on the extent of the

neuronal damage at the time of injury, but also on the occurrence of any

secondary insults or sequelae from other injuries or complications (see Chapter

39) These secondary insults include (1) systemic factors such as hypoxemia,hypercapnia, or hypotension; (2) formation and expansion of an epidural,

subdural, or intracerebral hematoma; and (3) sustained intracranial hypertension.Head-injured patients may have a wide variety of other injuries, may arrive athospital in an intoxicated state, and are subject to the usual range of

complications encountered in critical care (sepsis, acute respiratory distresssyndrome [ARDS], etc) Surgical and anesthetic management of these patients isdirected at immediate treatment of the primary injuries and avoiding these

secondary insults The Glasgow Coma Scale (GCS) score ( Table 27–2)

generally correlates well with the severity of injury and outcome A GCS score

of 8 or less on admission is associated with approximately 35% mortality

Evidence of greater than a 5-mm midline shift (on imaging) and ventricularcompression on imaging are associated with substantially worse outcomes

TABLE 27–2 Glasgow coma scale.

Specific lesions include skull fractures, subdural and epidural hematomas,brain contusions (including intracerebral hemorrhages), penetrating head

injuries, and traumatic vascular occlusions and dissections The presence of askull fracture greatly increases the likelihood of an intracranial lesion Linearskull fractures are commonly associated with subdural or epidural hematomas.Basilar skull fractures may be associated with CSF rhinorrhea, pneumocephalus,cranial nerve palsies, or even a cavernous sinus–carotid artery fistula Depressedskull fractures often present with an underlying brain contusion Contusions may

be limited to the surface of the brain or may involve hemorrhage in deeper

hemispheric structures or the brainstem Rapid deceleration injuries often

produce both coup (frontal) and contrecoup (occipital) lesions Epidural andsubdural hematomas can occur as isolated lesions, as well as in association withcerebral contusions (more commonly with subdural than epidural lesions)

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evacuation of epidural, subdural, and some intracerebral hematomas; and

debridement of penetrating injuries Decompressive craniectomy is used to

provide room for cerebral swelling The cranium is subsequently reconstructedfollowing resolution of cerebral edema

ICP monitoring is usually indicated in patients with lesions associated withintracranial hypertension: large contusions, mass lesions, intracerebral

hemorrhage, or evidence of edema on imaging studies ICP monitoring shouldalso be considered in patients with signs of intracranial hypertension who areundergoing nonneurological procedures Acute intracranial hypertension leading

to herniation should be treated with hyperventilation, osmolar therapy, and

barbiturates Immediate neurosurgical intervention is mandated Multiple studieshave found that sustained increases in ICP of greater than 60 mm Hg result insevere disability or death Randomized trials have failed to detect the efficacy ofearly use of large doses of glucocorticoids in patients with head trauma

Hypothermia has likewise failed to improve survival following traumatic braininjury

PREOPERATIVE MANAGEMENT

Anesthetic care of patients with severe head trauma begins in the emergencydepartment Measures to ensure patency of the airway, adequacy of ventilationand oxygenation, stabilization of the cervical spine, and correction of systemichypotension should proceed simultaneously with neurological and trauma

surgical evaluation Airway obstruction and hypoventilation are common Up to70% of such patients have hypoxemia, which may be complicated by pulmonarycontusion, fat emboli, or neurogenic pulmonary edema The latter is attributed tomarked systemic and pulmonary hypertension secondary to intense sympatheticnervous system activity Supplemental oxygen should be given to all patientswhile the airway and ventilation are evaluated Many patients will have

substance intoxication All patients must be assumed to have a cervical spineinjury (up to 10% incidence) until the contrary is proven radiographically

Patients with obvious hypoventilation, an absent gag reflex, or a persistent scorebelow 8 on the GCS (Table 27–2) require tracheal intubation All other patientsshould be carefully observed for deterioration

Intubation

All patients should be regarded as having a full stomach and should have cricoid

questionable In-line stabilization should be used during airway manipulation tomaintain the head in a neutral position, unless radiographs confirm that there is

no cervical spine injury Following preoxygenation, the adverse effects of

intubation on ICP are blunted by prior administration of propofol, 1.5 to 3.0mg/kg, and a rapid-onset NMB Succinylcholine may produce mild and transientincreases in ICP in patients with closed head injury; however, the necessity forexpeditious airway management trumps these theoretical concerns Rocuronium

is often used to facilitate intubation The presence of a hard collar for cervicalspine stabilization will increase intubation difficulty Video laryngoscopy

performed with in-line stabilization generally permits neutral position intubation

of the trauma patient An intubating bougie should be available to facilitate tubeplacement If a difficult intubation is encountered with video laryngoscopy,

fiberoptic or other techniques (eg, intubating LMA) can be attempted If airwayattempts are unsuccessful, a surgical airway should be obtained Blind nasalintubation or blind passage of a nasogastric tube should be avoided in the

presence of a basilar skull fracture due to the possibility of passing tubes directlythrough the fracture into the brain The diagnosis of basilar skull fracture is

suggested by CSF rhinorrhea or otorrhea, hemotympanum, or ecchymosis intoperiorbital tissues (raccoon sign) or behind the ear (Battle sign)

mm Hg predict a poor outcome Glucose-containing or hypotonic solutions

should not be used (see earlier discussion) Otherwise, crystalloids and bloodproducts can be administered as necessary Massive blood loss in the patient withmultiple injuries should result in activation of a massive transfusion protocol toprovide a steady supply of platelets, fresh frozen plasma, and packed red bloodcells Invasive monitoring of arterial pressure, central venous pressure, and ICPare valuable, but should not delay diagnosis and treatment Arrhythmias andelectrocardiographic abnormalities in the T wave, U wave, ST segment, and QT

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Diagnostic Studies

The choice between operative and medical management of head trauma is based

on radiographic and clinical findings Patients should be stabilized prior to any

CT or other imaging studies Critically ill patients must be closely monitoredduring such studies Restless or uncooperative patients may require generalanesthesia for imaging Sedation in such cases without control of the airwayshould be avoided because of the risk of further increases in ICP from

elevated ICP and bradycardia is termed the Cushing reflex

Hypertension can be treated with additional doses of the induction agent, withincreased concentrations of an inhalation anesthetic (provided modest

hyperventilation has been established) or with antihypertensives β-Adrenergicblockers are usually effective in controlling hypertension associated with

tachycardia CPP should be maintained between 70 and 110 mm Hg

Vasodilators should be avoided until the dura is opened Excessive

hyperventilation (PaCO2 <35 mm Hg) should be avoided in trauma patients

(unless the patient manifests signs of impending herniation) to prevent excessivedecreases in oxygen delivery

Disseminated intravascular coagulation occasionally may be seen with severehead injuries Such injuries cause the release of large amounts of brain

thromboplastin and may also be associated with ARDS Pulmonary aspiration

adequate CPP Diabetes insipidus, characterized by inappropriately dilute

polyuria, is frequently seen following brain trauma, especially with injuries tothe pituitary Other likely causes of polyuria should be excluded and the

diagnosis confirmed by measurement of urine and serum osmolality prior totreatment with fluid restriction and vasopressin (see Chapter 49)

Gastrointestinal bleeding from stress ulceration is common in patients not

receiving prophylaxis

The decision whether to extubate the trachea at the conclusion of the surgicalprocedure depends on the severity of the injury, the presence of concomitantabdominal or thoracic injuries, preexisting illnesses, and the preoperative level

of consciousness Young patients who were conscious preoperatively may beextubated following the removal of a localized lesion, whereas patients withdiffuse brain injury should remain intubated Moreover, persistent intracranialhypertension requires continued paralysis, sedation, CSF drainage, and elevatedhead position Protracted hyperventilation may be employed should other

usually treated medically

CEREBRAL ANEURYSMS

Preoperative Considerations

Cerebral aneurysms typically occur at the bifurcation of the large arteries at thebase of the brain; most are located in the anterior circle of Willis Approximately10% to 30% of patients have more than one aneurysm The general incidence of

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of those with aneurysms will have complications Rupture of a saccular

aneurysm is the most common cause of subarachnoid hemorrhage (SAH) Theacute mortality following rupture is approximately 10% Of those who survivethe initial hemorrhage, about 25% die within 3 months from delayed

complications Moreover, up to 50% of survivors are left with neurological

deficits As a result, the emphasis in management is on prevention of rupture.Unfortunately, most patients present only after rupture has already occurred

Unruptured Aneurysms

Patients may present with prodromal symptoms and signs suggesting progressiveenlargement The most common symptom is headache, and the most commonphysical sign is a third-nerve palsy Other manifestations could include

brainstem dysfunction, visual field defects, trigeminal nerve dysfunction,

cavernous sinus syndrome, seizures, and hypothalamic–pituitary dysfunction.The most commonly used techniques to diagnose an aneurysm are MRI,

angiography, and helical CT angiography Following diagnosis, patients arebrought to the operating room, or more likely the “hybrid” suite, for coiling orclipping of the aneurysm Most patients are in the 40- to 60-year-old age groupand in otherwise good health

Ruptured Aneurysms

Ruptured aneurysms usually present acutely as SAH Patients typically complain

of a sudden severe headache without focal neurological deficits, but often

associated with nausea and vomiting Transient loss of consciousness may occurand may result from a sudden rise in ICP and precipitous drop in CPP If ICPdoes not decrease rapidly after the initial sudden increase, death usually follows.Large blood clots can cause focal neurological signs in some patients Minorbleeding may cause only a mild headache, vomiting, and nuchal rigidity Theseverity of SAH is graded according to the Hunt and Hess scale (Table 27–3), aswell as the World Federation of Neurological Surgeons grading scale of SAH(Table 27–4) The Fisher grading scale, which uses CT to assess the amount ofblood detected, gives the best indication of the likelihood of the development ofcerebral vasospasm and patient outcome (Table 27–5)

TABLE 27–3 Hunt and Hess grading scale for SAH 1

TABLE 27–4 World Federation of Neurological Surgeons grading scale for aneurismal SAH 1

TABLE 27–5 Fisher grading scale of cranial computerized tomography (CCT) 1

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is a major cause of morbidity and mortality Previously, cerebral arterial

vasospasm was considered the primary cause of DCI following SAH Whilecerebral artery vasospasm does occur it often does not correlate with areas ofcerebral infarction Consequently, other mechanisms are considered as also

contributing to DCI These include cortical spreading depolarizations and

microthrombosis Cortical spreading depolarizations (CSDs) are progressiveneuronal depolarizations of grey matter following brain injury such as SAH.CSDs can both increase and decrease cerebral blood flow Cerebral ischemia

results secondary to inadequate perfusion following CSDs in injured brains N-methyl-D-aspartate (NMDA) receptor antagonists such as ketamine may

modulate CSDs SAH is also thought to contribute to platelet activation andformation of microthrombi, which likewise produce cerebral ischemia

Manifestations of DCI are due to cerebral ischemia and infarction and depend onthe severity and distribution of the involved vessels The Ca2+ channel

antagonist nimodipine is used following SAH to mitigate the effects of DCI.Both transcranial Doppler and brain tissue oxygen monitoring can be used toguide vasospasm therapy Increased velocity of flow greater than 200 cm/s isindicative of severe spasm The Lindegaard ratio compares the blood velocity ofthe cervical carotid artery with that of the middle cerebral artery A ratio greaterthan 3 is likewise indicative of severe spasm Brain tissue oxygen tension less

than 20 mm Hg is also worrisome In patients with symptomatic vasospasm with an inadequate response to nimodipine, intravascular volume expansion and induced hypertension (“triple H” therapy: hypervolemia, hemodilution, and hypertension) are added as part of the therapeutic regimen Recent

of euvolemia while acknowledging that hypertension may be most beneficial inthe management of DCI Refractory vasospasm may be treated with catheter-delivered vasodilators, angioplasty, or both However, radiological improvement

in the vessel diameter does not necessarily correlate with an improvement inclinical status

PREOPERATIVE MANAGEMENT

In addition to assessing and documenting neurological findings, the preoperativeevaluation should include a search for coexisting diseases, such as hypertensionand renal, cardiac, or ischemic cerebrovascular disease Electrocardiographicabnormalities are commonly seen in patients with SAH, but do not necessarilyreflect underlying heart disease However, increases of cardiac troponin duringSAH are associated with myocardial injury and may herald a poor outcome.Stress-induced cardiomyopathy may also be present Most conscious patientswith normal ICP are sedated following rupture to prevent rebleeding; such

sedation should be continued until induction of anesthesia Patients with

persistent elevation in ICP should receive little or no premedication to avoidhypercapnia

INTRAOPERATIVE MANAGEMENT

Aneurysm surgery can result in exsanguinating hemorrhage as a consequence ofrupture or rebleeding Blood should be available prior to the start of these

operations

Regardless of the anesthetic technique employed, anesthetic managementshould focus on preventing rupture (or rebleeding) and avoiding factors thatpromote cerebral ischemia or vasospasm Intraarterial pressure monitoring isuseful Sudden increases in blood pressure with tracheal intubation or surgicalstimulation should be avoided Judicious intravascular volume loading permitssurgical levels of anesthesia without excessive decreases in blood pressure.Because calcium channel blockers, angiotensin receptor blockers, and

angiotensin-converting enzyme inhibitors cause systemic vasodilation and

reduce systemic vascular resistance, patients receiving these agents

preoperatively may be particularly prone to hypotension

The great majority of cerebral aneurysms are addressed via an endovascularapproach The anesthetic concerns of patients taken for coiling in the

neurointerventional suite are similar to those of patients undergoing craniotomy

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neurointerventionalist as to the desired activated clotting time and need for

protamine reversal is essential Moreover, anesthesia staff in the neuroradiologysuite must be prepared to manipulate and monitor the blood pressure, as with anopen surgical procedure

For the less common situation in which open craniotomy is required, once thedura is opened, mannitol is often given to facilitate surgical exposure and reducethe need for surgical retraction Rapid decreases in ICP prior to dural opening areavoided as they may promote rebleeding by removing a tamponading effect onthe aneurysm

Elective (controlled) hypotension has been used in aneurysm surgery

Decreasing mean arterial blood pressure reduces the transmural tension acrossthe aneurysm, making rupture (or rebleeding) less likely and facilitating surgicalclipping Controlled hypotension can also decrease blood loss and improve

surgical visualization in the event of bleeding The combination of a slightlyhead-up position with a volatile anesthetic enhances the effects of any of thecommonly used hypotensive agents Should accidental rupture of the aneurysmoccur, the surgeon may request transient hypotension to facilitate control of thebleeding Neurophysiological monitoring may be employed during aneurysmsurgery to identify potential ischemia during clip application Rarely,

hypothermic circulatory arrest is used for large basilar artery aneurysms

Depending on neurological condition, most patients should be extubated atthe end of surgery Extubation should be handled similarly to other craniotomies(see earlier discussion) A rapid awakening allows neurological evaluation in theoperating room, prior to transfer to the intensive care unit

ARTERIOVENOUS MALFORMATIONS

AVMs cause intracerebral hemorrhage more often than SAH These lesions aredevelopmental abnormalities that result in arteriovenous fistulas; they typicallygrow in size with time AVMs may present at any age, but bleeding is most

common between 10 and 30 years of age Other common presentations includeheadache and seizures The combination of high blood flow with low vascularresistance can rarely result in high-output cardiac failure In most cases an

endovascular approach to occlude the vessels feeding the AVM will be attempted

in the “hybrid” operating room or neurointerventional suite This may providedefinitive therapy or may render the AVM more amenable to surgical excision

Anesthetic management of patients undergoing resection of AVMs may becomplicated by extensive blood loss Venous access with multiple large-borecannulas is necessary Hyperventilation and mannitol may be used to facilitatesurgical access Hyperemia and swelling can develop following resection,

possibly because of altered autoregulation in the remaining normal brain

Emergence hypertension is typically controlled with agents that do not induceincreases in CBF, such as β-blockers and clevidipine

Acute Ischemic Stroke

Acute ischemic strokes are treated with thrombolysis (with tissue plasminogenactivator [tPA]), or endovascular clot removal and stenting, or both Multiplewell-performed randomized clinical trials reported in 2015 have confirmed thatimmediate endovascular intervention greatly improves outcomes relative to tPAalone in patients with occlusions of proximal large cerebral arteries The mantra

in neurology and neurosurgery is “time is brain.” The goal is to have the patientrevascularized as soon as possible Endovascular treatment should not be

delayed for placement of arterial lines, etc These patients are at immediate risk

of death and disability without treatment and certainly meet the criteria for anAmerican Society of Anesthesiologists physical status of 5E! The benefit fromendovascular treatment of acute ischemic stroke is even greater (a smaller

number of patients need to be treated to have a patient with outcome benefit)than that for immediate revascularization for myocardial infarctions with

elevated ST segments (STEMIs) However, the only patients who will benefitfrom endovascular treatment will have a significant amount of the ischemicbrain tissue that remains “recoverable” as assessed in imaging studies by

measures of CBF, CBV, and tissue transit time In infarcted brain, all are

abnormal In recoverable brain tissue, at a minimum the CBV may be

maintained or even increased

Several post hoc analyses of the original clinical trials have suggested anassociation between the use of general anesthesia (versus sedation and

monitoring) and worse outcomes in patients undergoing endovascular

embolectomy Nevertheless, general anesthesia remains the preference in manycenters and will be required for many patients We have observed that patientswith acute left middle cerebral artery occlusion and aphasia may not hold still nomatter how loudly they are asked!

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Anesthesia for Surgery on the Spine

Spinal surgery is most often performed for symptomatic nerve root or cord

compression secondary to trauma or degenerative disorders Compression mayoccur from protrusion of an intervertebral disk or osteophytic bone (spondylosis)into the spinal canal or an intervertebral foramen Prolapse of an intervertebraldisk often occurs at either the fourth or fifth lumbar or the fifth or sixth cervicallevels in adults Spondylosis tends to affect the lower cervical spine more thanthe lumbar spine and typically afflicts older patients Operations on the spinalcolumn can help correct deformities (eg, scoliosis), decompress the cord, andfuse the spine if disrupted by trauma or degenerative conditions Spinal surgerymay also be performed to resect a tumor or vascular malformation or to drain anabscess or hematoma

PREOPERATIVE MANAGEMENT

Preoperative evaluation should focus on any anatomic abnormalities and limitedneck movements (from disease, traction, “collars,” or other devices) that mightcomplicate airway management Neurological deficits should be documented.Neck mobility should be assessed Patients with unstable cervical spines can bemanaged with either awake fiberoptic intubation or intubation after inductionwith in-line stabilization

INTRAOPERATIVE MANAGEMENT

Spinal operations involving multiple levels, fusion, and instrumentation are alsocomplicated by the potential for large intraoperative blood loss; a red cell

salvage device is often used Excessive distraction during spinal instrumentation(Harrington rod or pedicle screw fixation) can injure the spinal cord

Transthoracic approaches to the spine require one-lung ventilation

Anterior/posterior approaches require the patient to be repositioned in the middle

Positioning

Most spine surgical procedures are carried out in the prone position The supineposition may be used for an anterior approach to the cervical spine, makinganesthetic management easier, but increasing the risk of injury to the trachea,esophagus, recurrent laryngeal nerve, sympathetic chain, carotid artery, or

jugular vein A sitting (for cervical spine procedures) or lateral decubitus (forlumbar spine procedures) position may occasionally be used

Following induction of anesthesia and tracheal intubation in the supine

position, the patient is turned to the prone position Care must be taken to

maintain the neck in a neutral position Once in the prone position, the head may

be turned to the side (not exceeding the patient’s normal range of motion) or(more commonly) can remain face down on a cushioned holder or secured bypins or tongs Caution is necessary to avoid corneal abrasions or retinal ischemiafrom pressure on either globe, or pressure injuries of the nose, ears, forehead,chin, breasts, or genitalia The chest should rest on parallel rolls (“chest rolls” offoam, gel, or other padding) or special supports—if a frame is used—to facilitateventilation The arms may be tucked by the sides in a comfortable position orextended with the elbows flexed (avoiding excessive abduction at the shoulder).Turning the patient prone is a critical maneuver, sometimes complicated byhypotension Abdominal compression, particularly in obese patients, may

impede venous return and contribute to excessive intraoperative blood loss fromengorgement of epidural veins Prone positioning with chest rolls that permitsthe abdomen to hang freely can mitigate this increase in venous pressure

Deliberate hypotension has been advocated in the past to reduce bleeding

associated with spine surgery However, this should only be undertaken with afull understanding that controlled hypotension may increase the risk of

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Specialized head positioning pillows (eg, Covidien, ProneView) are oftenused when patients are placed in the prone position, and the face must be

checked periodically to verify that the eyes, nose, and ears are free of pressure.Even foam cushions can exert pressure over time on the chin, orbit, and maxilla.Turning the head is not easily accomplished when the head is positioned on acushion; therefore, if prolonged procedures are planned, the head can be securedwith pins keeping the face free from any pressure

Monitoring

When major blood loss is anticipated or the patient has preexisting cardiac

disease, intraarterial pressure monitors should be considered prior to

“positioning” or “turning.” Sudden, massive blood loss from injury to thegreat vessels can occur intraoperatively with adjacent thoracic or lumbar spineprocedures

Instrumentation of the spine requires the ability to intraoperatively detectspinal cord injury Intraoperative wake-up techniques employing nitrous oxide-narcotic or total intravenous anesthesia allow the testing of motor function

following distraction Once preservation of motor function is established, thepatient’s anesthetic can be deepened Continuous monitoring of somatosensoryevoked potentials and motor evoked potentials provides alternatives that avoidthe need for intraoperative awakening These monitoring techniques requiresubstitution of propofol, opioid, or ketamine infusions for deep levels of

inhalation anesthetics and avoidance of neuromuscular paralysis

CASE DISCUSSION

Resection of a Pituitary Tumor

A 41-year-old woman presents to the operating room for resection of a 10-mm pituitary tumor She complains of amenorrhea and

galactorrhea, and had recently noticed a decrease in her visual acuity, with bitemporal hemianopsia.

Functionally and anatomically, the pituitary is divided into two parts:anterior and posterior The latter is part of the neurohypophysis, which alsoincludes the pituitary stalk and the median eminence

The anterior pituitary is composed of several cell types, each secreting aspecific hormone Anterior pituitary hormones include adrenocorticotropichormone (ACTH), thyroid-stimulating hormone (TSH), growth hormone(GH), the gonadotropins (follicle-stimulating hormone [FSH] and

luteinizing hormone [LH]), and prolactin (PRL) Secretion of each of thesehormones is regulated by hypothalamic peptides (releasing hormones) thatare transported to the adenohypophysis by a capillary portal system Thesecretion of FSH, LH, ACTH, TSH, and their respective releasing

hormones is also under negative feedback control by the products of theirtarget organs For example, an increase in circulating thyroid hormoneinhibits the secretion of TSH-releasing factor and TSH

The posterior pituitary secretes antidiuretic hormone (ADH, also calledvasopressin) and oxytocin These hormones are actually formed in

supraoptic and paraventricular neurons, respectively, and are transporteddown axons that terminate in the posterior pituitary Hypothalamic

osmoreceptors, and, to a lesser extent, peripheral vascular stretch receptors,regulate secretion of ADH

What is the function of these hormones?

ACTH stimulates the adrenal cortex to secrete glucocorticoids Unlikeproduction of mineralocorticoids, production of glucocorticoids is

dependent on ACTH secretion TSH accelerates the synthesis and release ofthyroid hormone (thyroxine) Normal thyroid function is dependent onproduction of TSH The gonadotropins FSH and LH are necessary for

normal production of testosterone and spermatogenesis and cyclic ovarianfunction GH promotes tissue growth and increases protein synthesis aswell as fatty acid mobilization Its effects on carbohydrate metabolism are

to decrease cellular glucose uptake and utilization and increase insulinsecretion PRL functions to support breast development during pregnancy.Dopamine receptor antagonists are known to increase secretion of PRL.Through its effect on water permeability in renal collecting ducts, ADHregulates extracellular osmolarity and blood volume Oxytocin acts onareolar myoepithelial cells as part of the milk letdown reflex during

suckling and enhances uterine activity during labor

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The pituitary gland is attached to the brain by a stalk and extends

downward to lie in the sella turcica of the sphenoid bone Anteriorly,

posteriorly, and inferiorly, it is bordered by bone Laterally, it is bordered bythe cavernous sinus, which contains cranial nerves III, IV, V1, and VI, aswell as the cavernous portion of the carotid artery Superiorly, the

diaphragma sella, a thick dural reflection, usually tightly encircles the stalkand forms the roof of the sella turcica In close proximity to the stalk lie theoptic nerves and chiasm The hypothalamus lies contiguous and superior tothe stalk

Tumors less than 10 mm in diameter are usually approached via thetranssphenoidal route, whereas larger tumors and those with significantsuprasellar extension are approached via a bifrontal craniotomy With theuse of prophylactic antibiotics, morbidity and mortality rates are

significantly less with the transsphenoidal approach; the operation is carriedout with the aid of a microscope through an incision in the gingival mucosabeneath the upper lip The surgeon enters the nasal cavity, dissects throughthe nasal septum, and finally penetrates the roof of the sphenoid sinus toenter the floor of the sella turcica

What are the major problems associated with the

transsphenoidal approach?

containing solution to reduce bleeding, (2) the accumulation of blood andtissue debris in the pharynx and stomach, (3) the risk of hemorrhage fromaccidental entry into the cavernous sinus or the internal carotid artery, (4)cranial nerve damage, and (5) pituitary hypofunction Prophylactic

Problems include (1) the need for mucosal injections of epinephrine-administration of glucocorticoids is routinely used in most centers Diabetesinsipidus develops postoperatively in up to 40% of patients but is usuallytransient Less commonly, the diabetes insipidus presents intraoperatively.The supine and slightly head-up position used for this procedure may alsopredispose to venous air embolism

What type of tumor does this patient have?

Tumors in or around the sella turcica account for 10% to 15% of

intracranial neoplasms Pituitary adenomas are most common, followed bycraniopharyngiomas and then parasellar meningiomas Primary malignant

hormones (functional tumors) usually present early, when they are stillrelatively small (<10 mm) Other tumors present late, with signs of

increased ICP (headache, nausea, and vomiting) or compression of

contiguous structures (visual disturbances or pituitary hypofunction)

Compression of the optic chiasm classically results in bitemporal

hemianopia Compression of normal pituitary tissue produces progressiveendocrine dysfunction Failure of hormonal secretion usually progresses inthe order of gonadotropins, GH, ACTH, and TSH Diabetes insipidus canalso be seen preoperatively Rarely, hemorrhage into the pituitary results inacute panhypopituitarism (pituitary apoplexy) with signs of a rapidly

expanding mass, hemodynamic instability, and hypoglycemia This patienthas the most common type of secretory adenoma, producing

Adenomas that secrete GH are often large and result in either gigantism(prepubertal patients) or acromegaly (adults) Excessive growth prior toepiphyseal fusion results in massive growth of the entire skeleton Afterepiphyseal closure, the abnormal growth is limited to soft tissues and acralparts: hands, feet, nose, and mandible Patients develop osteoarthritis,which often affects the temporomandibular joint and spine Diabetes,

myopathies, and neuropathies are common Cardiovascular complicationsinclude hypertension, premature coronary disease, and cardiomyopathy insome patients The most serious anesthetic problem encountered in thesepatients is difficulty in intubating the trachea

Are any special monitors required for transsphenoidal surgery?

Monitoring should be carried out in somewhat the same way as forcraniotomies Visual evoked potentials may be employed with large tumorsthat involve the optic nerves Precordial Doppler sonography may be usedfor detecting venous air embolism Venous access with large-bore catheters

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What modifications, if any, are necessary in the anesthetic

technique?

The same principles discussed for craniotomies apply; however, patientsrarely have evidence of increased ICP Intravenous antibiotic prophylaxisand glucocorticoid coverage (hydrocortisone, 100 mg) are usually given

prior to induction Many clinicians avoid nitrous oxide to prevent problemswith a postoperative pneumocephalus (see earlier discussion) Effective

neuromuscular blockade is important to prevent movement while the

surgeon is using the microscope A lumbar drain is often placed to reduceICP, facilitate surgical exposure, and reduce the likelihood of CSF leaks

after closure of the dura

SUGGESTED READINGS

Bell R, Vo A, Vexnedaroglu E, et al The endovascular operating room as anextension of the intensive care unit: Changing strategies in the management

2002;13:120

Huh J, Raghupathi R New concepts in treatment of pediatric traumatic brain

28

Anesthesia for Patients with

Neurological & Psychiatric Diseases KEY CONCEPTS

Induction of anesthesia in patients receiving long-term levodopa therapymay result in either marked hypotension or hypertension

In patients with multiple sclerosis, increases in body temperature causeexacerbation of symptoms

The major risk of anesthesia in patients with autonomic dysfunction issevere hypotension, compromising cerebral and coronary blood flow Autonomic hyperreflexia should be expected in patients with spinal

cord lesions above T6 and can be precipitated by surgical

manipulations

The most important interaction between anesthetic agents and tricyclicantidepressants is an exaggerated response to both indirect-acting

vasopressors and sympathetic stimulation

Patients with vascular and nonvascular neurological diseases or psychiatric

disorders are frequently encountered by anesthesia providers Anesthesiologistsmust have a basic understanding of the major neurological and psychiatric

disorders and their drug therapy Failure to recognize potential adverse anestheticinteractions may result in avoidable perioperative morbidity

Cerebrovascular Disease

Preoperative Considerations

transient ischemic attacks (TIAs) or stroke Patients with TIAs undergoing

surgery for other indications have an increased risk of perioperative stroke

Asymptomatic carotid bruits occur in up to 4% of patients older than age 40years, but do not necessarily indicate significant carotid artery obstruction

Fewer than 10% of patients with completely asymptomatic bruits have

hemodynamically significant carotid artery lesions An asymptomatic carotidbruit may not increase the risk of stroke following surgery, but it increases thelikelihood of coexisting coronary artery disease Moreover, the absence of a bruitdoes not exclude significant carotid obstruction

The risk of perioperative stroke increases with patient age and varies with thetype of surgery Although the overall risk of stroke associated with surgery islow, it is greater in patients undergoing cardiovascular or cerebrovascular

surgery Rates of stroke after general anesthesia and surgery range from 0.08% to0.4% Even in patients with known cerebrovascular disease, the risk is only 0.4%

to 3.3% Patients at greatest risk of postoperative stroke are those undergoingopen heart procedures for valvular disease, coronary artery disease with

ascending aortic atherosclerosis, and diseases of the thoracic aorta Stroke

following open heart surgery is usually attributed to embolism of air, clots, oratheromatous debris In one study, 6% of patients experienced an adverse

neurological outcome following cardiac surgery Stroke following thoracic aorticsurgery may be due to emboli or ischemia secondary to prolonged circulatoryarrest or a clamp placed close to the origin of the carotid artery

The pathophysiology of postoperative strokes following noncardiovascularsurgery is less clear but may involve severe sustained hypotension or

hypertension Hypotension with severe hypoperfusion can result in so-called

“watershed” zone infarctions or thrombosis of cerebral arteries, whereas

hypertension can result in intracerebral hemorrhage (hemorrhagic stroke)

Sustained hypertension can disrupt the blood–brain barrier and promote cerebraledema Perioperative atrial fibrillation can likewise lead to atrial clot formationand cerebral embolism The period of time during which anesthesia and surgeryshould best be avoided following a stroke is not clear Abnormalities in regionalblood flow and metabolic rate usually resolve after 2 weeks, whereas alterations

in CO2 responsiveness and the blood–brain barrier may require more than 4weeks However, urgent surgery is performed for acute intracranial hemorrhage,symptomatic carotid disease, and cardiac sources of emboli

Patients with TIAs have a history of transient (<24 h) impairment, and, bydefinition, no residual neurological impairment These attacks are thought to

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extracranial vessels Unilateral visual impairment, numbness or weakness of anextremity, or aphasia is suggestive of carotid disease, whereas bilateral visualimpairment, dizziness, ataxia, dysarthria, bilateral weakness, or amnesia is

suggestive of vertebral–basilar disease Patients with TIAs have a 30% to 40%chance of developing a frank stroke within 5 years; 50% of these strokes occurwithin the first year Patients with TIAs should not undergo any elective surgicalprocedure without an adequate medical evaluation that generally includes at leastnoninvasive (Doppler) flow and imaging studies The presence of an ulceratedplaque of greater than 60% occlusion is generally an indication for endovascularintervention or less commonly an open carotid thromboendarterectomy

PREOPERATIVE MANAGEMENT

Preoperative assessment requires neurological and cardiovascular evaluations.The type of stroke, the presence of neurological deficits, and the extent of

residual impairment should be determined Thromboembolic strokes usuallyoccur in patients with generalized atherosclerosis Most patients are elderly andhave comorbid conditions, such as hypertension, hyperlipidemia, and diabetes.Coexisting coronary artery disease and renal impairment are common Followingnonhemorrhagic strokes or TIAs, many patients are placed on long-term

anticoagulant or antiplatelet therapy, or both Management of antiplatelet therapyand antithrombotic therapy should be reviewed by the anesthesia and surgicalteams, often guided by the physician who prescribed the therapy, to determinethe risks and benefits of discontinuation or maintenance of such therapy

Patients with acute strokes secondary to carotid and intracranial occlusivearterial disease present for carotid endarterectomy and endovascular procedures

placement of a stent When general anesthesia is used, electroencephalography,evoked potentials, carotid stump pressure, near-infrared cerebral oximetry, ortranscranial Doppler may be used to estimate the adequacy of cerebral oxygendelivery During open carotid thromboendarterectomy the surgeon may place ashunt to deliver blood to the brain around the cross-clamped vessel Despiteadequate cerebral blood flow, perioperative stroke can occur during carotidsurgery secondary to emboli

Management of patients following thrombotic or hemorrhagic stroke fornonneurological surgery must be individualized Cerebral autoregulation ofblood flow may fail, leaving flow directly dependent upon cerebral perfusionpressure (Figure 28–1) The penumbra of potentially salvageable neurologicaltissue may therefore be very sensitive to injury from the effects of both

hypotension and hypertension (Figure 28–2) We advocate tight control of bloodpressure in these patients

the patient with acute ischemic stroke Semin Cardiothorac Vasc Anesth 2010 Mar;14(1):62-63.)

Patients taken to surgery following administration of thrombolytic therapy are

at increased risk of cerebral hemorrhage, and tight blood pressure control mayreduce the likelihood of cerebral bleeding

INTRACRANIAL TUMORS

Patients with intracranial mass lesions frequently present to their primary carephysicians with complaints of headache, visual disturbances, or seizures

Families may have noticed behavioral changes in patients with frontal lobe

masses Imaging studies confirm the presence of a mass, and initial treatmentwith dexamethasone is aimed at decreasing cerebral edema Electrolytes should

be reviewed perioperatively in all patients undergoing cranial surgery, as bothhyponatremia and hypernatremia can develop secondary to cerebral salt wasting,inappropriate antidiuretic hormone secretion, or central diabetes insipidus (Table 28–1; see also Chapter 49) Patients with altered mentation preoperatively may

TABLE 28–1 Fluid and electrolyte disorders associated with intracranial pathology 1,2

Seizure Disorders

Preoperative Considerations

Seizures represent abnormal synchronized electrical activity in the brain Theymay be a manifestation of an underlying central nervous system disease, a

systemic disorder, or idiopathic Up to 2% of the population may experience aseizure in their lifetime Epilepsy is a disorder characterized by recurrent

paroxysmal seizure activity Healthy individuals who experience an isolatednonrecurrent seizure are not considered to have epilepsy

Seizure activity may be localized to a specific area in the brain or may begeneralized Moreover, initially localized (focal) seizures can subsequently

spread, becoming generalized A simple classification scheme is presented in

Table 28–2 Partial seizures (also called focal) are clinically manifested by

motor, sensory, autonomic, or psychiatric symptoms, depending on the brainregion affected Focal seizures associated with impairment in consciousness aretermed “complex partial” (psychomotor or temporal lobe) seizures Generalizedseizures characteristically produce bilaterally symmetric electrical activity

without local onset They may result in abnormal motor activity, loss of

consciousness, or both Absence (petit mal) seizures produce generalized activityresulting in isolated, transient lapses in consciousness Other generalized

seizures are usually classified according to the type of motor activity Tonic–clonic (grand mal) seizures are most common and are characterized by a loss ofconsciousness followed by clonic and then tonic motor activity

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