Anesthesia for neurosurgery

Intracranial compartments

The skull is a closed compartment containing brain parenchyma (intracellular and extracellular), blood (arterial and venous), and cerebrospinal fluid (CSF). As first described in the Monro-Kellie doctrine, during times of normal physiology, these three components exist in equilibrium with each other via complex interactions ( ). Any increase in volume of one of these three components, along with an increase in intracranial pressure (ICP), will result in a compensatory decrease in volume of the other components ( ). In neonates and infants, unfused cranial sutures and an open fontanel result in a compliant intracranial space ( Fig. 31.1 ). Cranial sutures normally fuse and the fontanel closes by 2 years of age. A space-occupying lesion with mass effect can be masked by an increase in head size in infants. Once infants present with evidence of intracranial hypertension (ICH), they often have progressed to advanced pathology requiring intervention. The caudal extent of the conus medullaris (L2 to L3) and dural sac (S3) is lower in infants and does not progress to that of an adult, with conus medullaris at L1 and dural sac at S1, until 1 year of age ( Fig. 31.2 ).

Cerebral parenchyma makes up approximately 80% of the intracranial space, and a large portion of the cerebral tissue is composed of brain water content. CSF accounts for approximately 10% of the intracranial space. It is an ultrafiltrate of plasma found within the ventricles of the brain and throughout the subarachnoid spaces of the spine and cranium. CSF is produced by the choroid plexus and absorbed through arachnoid villi and the ependymal lining of the ventricles. In adults, CSF helps provide protection via buoyancy, delivery of vital nutrients, and endogenous waste product removal to the central nervous system ( ). Its role in individuals less than 2 years of age is less understood. Recently studies on various interactions occurring within the choroid plexus-CSF system demonstrate its larger role in the development, homeostasis, and repair of the CNS ( ). The ventricular system is made up of four ventricles interconnected to allow the free flow of CSF throughout the system. Paired lateral ventricles connect to the third ventricle via the foramen of Monro. The third ventricle is subsequently connected to the fourth ventricle via the aqueduct of Silvius. The fourth ventricle communicates via the paired foramen of Luschka and the foramen of Magendie to a system of cisterns. In adults, the normal volume of CSF is approximately 150 mL, of which 25% is within the ventricular system. In term neonates, this volume is only 40 mL. The CSF volume increases to 65 to 150 mL in children ( ). CSF volume-to-weight ratio has historically been described as larger in infants and neonates (4 mL/kg) compared with adults (2 mL/kg). Some references even suggested the volume of CSF in neonates was as high as 10 to 11 mL/kg. An MRI study investigating the CSF volume in neonates 30 to 60 weeks postconceptual age (PCA) contradicts this. Rochette and colleagues described a linear relationship between weight and PCA. CSF volume in this study is approximately 2 mL/kg regardless of weight or prematurity ( ). Finally, approximately half of the CSF volume in neonates and infants is in the spinal subarachnoid space compared with about 25% for adults. Some have argued this may account for the higher local anesthetic requirements for spinal anesthesia and the shorter duration of action in infants ( ), but other factors are likely to play a role, including a faster CSF turnover rate in neonates, delayed myelination of the spinal cord, and immaturity of alpha-2 receptors ( ).

The remaining 10% of the intracranial space is made up of cerebral blood volume, which is normally described in terms of mL/100 g brain tissue. Various modalities have been used over the years to measure and estimate cerebral blood volume, including magnetic resonance imaging (MRI), computed tomography (CT), and near-infrared spectroscopy (NIRS) ( ; ).

Intracranial pressure (ICP)

ICP describes the pressure exerted within the craniospinal compartment. The range of normal ICP found in children and adults is 0 to 15 mm Hg. Under normal circumstances, premature infants exhibit a slightly lower ICP compared with full-term infants (2 to 6 mm Hg) ( ). A linear relationship exists between ICP and the reabsorption of CSF, limiting abrupt increases in ICP under normal physiologic states. Conditions that decrease the absorption of CSF may, therefore, lead to elevations of ICP. In the pediatric population, those disease states include intracranial hemorrhage, infection, cerebral inflammation, tumors, and congenital malformations ( ). Intracranial compliance represents the change in intracranial volume per unit change in pressure, and it determines the ability of the intracranial compartment to accommodate an increase in volume without significant increases in ICP ( Fig. 31.3 ) ( ). Compliance of the intracranial compartment is increased at normal volumes and allows ICP to remain low despite small increases in volume (point 1). The ability to compensate for increases in intracranial volume may become diminished when volume increases quickly or intracranial compliance becomes low (point 2). When ICP is already high, a threshold is reached where further increases in intracranial volume lead to rapid ICP elevation (point 3). Prolonged elevation of ICP may lead to focal or global ischemic events. The neonatal cranial vault is unique compared with older children and adults. Disease states causing slow increases in ICP, such as a slow-growing tumor, may go unrecognized, as their effects are often offset by the increase in intracranial volume as the head grows. There is also the potential of a compensatory increase in intracranial volume via open fontanelles and widening of sutures. However, acute rises in ICP can overwhelm these mechanisms and lead to critically high ICP in infants that may become life-threatening. The threshold level of ICP that necessitates treatment is not clearly defined in the pediatric population. Brief increases that return to baseline in <5 minutes may be of low clinical significance; however, increases >20 mm Hg for >5 minutes are generally accepted to indicate the need for treatment ( ). Disruptions to the flow of CSF or massive intracranial hemorrhage are clinical examples that can lead to critical ICP. Upon closure of the fontanelles and sutures, children have a relatively smaller intracranial volume and lower intracranial compliance compared with adults, leading to an increased risk of critical ICP ( ).

Cerebral blood volume (CBV)

Approximately 10% of the intracranial space is made up of cerebral blood volume (CBV), which is usually described in terms of mL/100 g brain tissue. CBV is determined by cerebral blood flow (CBF) and the capacitance of the intracranial vasculature beds ( ). CBV decreases with vasoconstriction and increases with vasodilation of the cerebral vessels. The majority of CBV is contained within the venous system, secondary to its low pressure and high capacitance. Alterations in intracranial volume will lead to compensatory changes in CBV. When intracranial volume increases, such as in the case of hydrocephalus, CBV will decrease under normal physiologic conditions. This is accomplished by two mechanisms: shifting blood outflow from the intracranial to extracranial vasculature beds or restricting the inflow of cerebral blood via the constriction of feeding arteries ( ). The relationship between CBV and CBF is a highly complex process. CBF-CBV coupling within one vascular compartment may differ from that in another, leading to the overall relationship between CBV and CBF differing depending on the specific physiologic situation ( ). Various forms of magnetic resonance imaging (MRI), computed tomography (CT), and near-infrared spectroscopy (NIRS) have all been used to measure CBV ( ; ).

Cerebral blood flow

Cerebral blood flow (CBF) is defined as the blood volume that flows per unit mass per unit time in brain tissue. It is typically conveyed using the units of blood mL/100 g/min ( ). Under normal circumstances, the brain receives approximately 15% of total cardiac output. This translates to approximately 50 mL/100 g/min of CBF in healthy adults ( ). Although a number of studies have demonstrated that CBF is age dependent, the association between the two variables during early development, compared with that in adults, is poorly defined ( ).

Various techniques exist to estimate CBF, each with its own strengths and drawbacks. Broadly speaking, these can be broken down into the following categories: direct intravascular measurements, nuclear medicine modalities, x-ray imaging, magnetic resonance imaging, ultrasound techniques, thermal diffusion, and optical methods, including near-infrared spectroscopy ( ). Transcranial Doppler (TCD) ultrasonography is commonly used because of its noninvasive nature and the ease with which it can be performed at bedside. This modality measures cerebral blood flow velocity (CBFV) of the basal cerebral arteries and is not a direct measure of CBF. Its utility derives from the fact that changes in CBFV generally correlate well with changes in CBV, except under specific circumstances, such as vasospasm ( ). Well-cited studies using TCD ultrasonography demonstrated that CBFV is approximately 24 cm/sec in healthy newborns and increases until 6 to 9 years of age (97 cm/sec) ( ) ( Fig. 31.4 ). After 10 years of age, CBFV decreases, approximating adult values of about 50 cm/sec ( ). Gender differences in CBFV have also been observed, which are likely due to variability in hematocrit, hormones, vessel size, and/or cerebral metabolism ( ). Table 31.1 lists mean CBFV estimates for middle cerebral artery (VMCA; anterior circulation) and basilar artery (VBAS; posterior circulation) by age and gender ( ; ; ). In certain patient groups, such as those with sickle cell disease (SCD), recent reports demonstrate that CBFV in the VMCA is not an accurate marker for CBF. Other modalities, such as magnetic resonance imaging, might play a role in helping to estimate CBF in this specific patient group ( ).

A variety of homeostatic mechanisms are known to regulate the cerebral circulation. These influences include (1) metabolism, (2) partial pressure of arterial carbon dioxide (Pa co ₂ ), (3) partial pressure of oxygen in arterial blood (Pa o ₂ ), (4) blood viscosity, and (5) cerebral autoregulation ( ). The relationship between CBF and Pa co ₂ has been documented for decades ( ; ). Hyper- and hypocapnia result in dilation and constriction of the cerebral vasculature, respectively. In healthy adults, CBF increases linearly by 2% to 4% per mm Hg Pa co ₂ within the range of 25 to 75 mm Hg, making Pa co ₂ the most potent physiologic cerebral vasodilator ( ). The change in CBF occurs within seconds, and complete equilibration is reached within 2 minutes ( ). There is limited data of age-related changes in CO ₂ vasoreactivity in healthy awake children. Studies from healthy anesthetized children suggest carbon dioxide (CO ₂ ) vasoreactivity is higher in children compared with adults (13.8% vs. 10.3% change in mean CBFV per mm Hg change in end-tidal CO ₂ ) during propofol administration and up to 1.0 MAC of volatile anesthetics ( ). It is believed that reactivity to CO ₂ is well developed in healthy preterm infants ( ) and that CO ₂ reactivity in newborns correlates with the lowest pH encountered and may reflect the severity of perinatal asphyxia ( ).

The influence of Pa o ₂ on cerebral blood flow is much less pronounced compared with Pa co ₂ and has less clinical significance ( ). At Pa o ₂ levels above 50 mm Hg, changes to the cerebral circulation are minimal. When Pa o ₂ is below 50 mm Hg, CBF increases, but the changes are slow and can take more than 6 minutes ( ).

Viscosity of blood also plays a role in the regulation of cerebral blood flow. Blood viscosity is primarily a function of hematocrit (Hct), with hemodilution resulting in decreased blood viscosity. During anemic states, the brain compensates for decreased oxygen delivery by increasing cerebral blood flow ( ). Improved rheology of blood flow through the cerebral vessels also helps to increase the effects of anemia. Multiple studies have investigated the optimal duration for maintaining a specific Hct level and the relationship between various target transfusion levels and neurologic outcomes but no current consensus exists in the pediatric setting ( ; ).

Cerebral metabolic rate

Brain metabolism in children changes with advancing age. For decades it has been known that global cerebral metabolic rate of oxygen (CMRO ₂ ) and glucose (CMR _glu ) is higher in children than adults (oxygen 5.8 vs. 3.5 mL/100 g brain tissue/min and glucose 6.8 vs. 5.5 mL/100 g brain tissue/min, respectively) ( ). This is due to a variety of factors, but increasing myelination and synaptogenesis seem to play a major role in the changes occurring during the first 8 years of life ( ; ). The higher CMRO ₂ and CMR _glu may also be secondary to age-related changes in CBF related to flow-metabolism coupling ( ). CMR _glu starts at low rates at birth (approximately 60% of adult values, 13 vs. 25 µmol/100g/min), rapidly increases to over 200% of adult values by age 5, peaks around age 9 (49 to 65 µmol/100g/min), and thereafter slowly decreases to adult levels by the time of adolescence ( ). Studies of healthy anesthetized children also suggest age-related increases in CMRO ₂ : 104 µmol/100 g/min in infants and 135 µmol/100 g/min in children aged 3 weeks to 14 years old ( ). Fig. 31.4 demonstrates how changes in CMRO ₂ and CMR _glu mirror age-related changes to CBF.

CBF is tightly coupled to cerebral metabolism and CMRO ₂ under normal circumstances and is perhaps the most important control of the cerebral circulation ( ; ). Flow-metabolism coupling is preserved during both sleep ( ) and general anesthesia ( ) and occurs at both global and local levels of the cerebral circulation ( ). During times of rest, CBF correlates well with CMRO ₂ . During instances when the central nervous system is highly activated, the fraction of cerebral oxygen extraction is decreased because of greater CBF compared with CMRO ₂ ( ).

The mediators that regulate flow-metabolism coupling in the cerebral vasculature are well studied. These include nitric oxide (NO), adenosine, prostaglandins, vasoactive intestinal peptide, and lactate, as well as ions such as hydrogen, potassium, and calcium ( ). NO is a potent vasodilator that can be produced by cells lining the cerebral vessels. During increased brain activation and metabolism, the lactate produced may cause functional hyperemia and vasodilation via increasing H+ concentration ( ). Hypothermia causes a reduction in CMRO ₂ , thereby decreasing CBF. CBF decreases approximately 5% to 7% per °C, and reduction of the brain temperature to 15 °C will decrease CMRO ₂ % to 10% of normothermic values ( ). Hypothermia causes a reduction in the functional metabolism of the CNS as well as the basal metabolism required for maintenance of cellular integrity.

Cerebral perfusion pressure

Cerebral perfusion pressure (CPP), grossly defined as the mean arterial pressure (MAP) minus ICP, defines the pressure gradient driving CBF. Normal CPP in adults ranges from 50 to 70 mm Hg, whereas normal CPP in children younger than 5 years of age is lower than that of older adolescents or adults ( ). It is well established that secondary brain injury occurs in the setting of increased ICP and decreased cerebral perfusion ( ). Although well established in the adult population, only recently has data described age-specific CPP targets. Generalized CPP targets for children range from >50 mm Hg in 6- to 17-year olds and >40 mm Hg in 0- to 5-year olds ( ).

Cerebral autoregulation

Cerebral autoregulation is a homeostatic process that maintains nearly constant CBF over a range of different blood pressures. In the seminal work by Lassen, it was shown that CBF is maintained constant at changes in MAP between 60 and 160 mm Hg in healthy adults, and the classic triphasic curve of CBF was presented ( ) ( Fig. 31.5 ). Changes in CPP between 50 to 150 mm Hg in healthy adults also produce little or no change in CBF ( Fig. 31.6 ) ( ). This autoregulation occurs via adjustments to the diameter of cerebral vessels ( ). An increase in MAP/CPP will lead to vasoconstriction and a decrease will lead to vasodilatation, protecting the brain from brain ischemia and edema/hemorrhage, respectively ( ). Outside these limits of autoregulation, CBF depends on MAP/CPP, and hypo- or hypertension may lead to irreversible injury to the brain.

Data is scarce regarding cerebral autoregulation in healthy children, and its mechanism and development is not fully understood ( ). By 6 months of age, children are believed to autoregulate CBF, although the lower limit of autoregulation (LLA) in healthy neonates is not fully clear ( ). Data from healthy children anesthetized with low dose sevoflurane demonstrates no age-related differences in autoregulatory capacity ( ). However, this range has also been shown to be narrower in children aged 6 months to 2 years ( ). One study found that during 1 MAC sevoflurane anesthesia in healthy infants, maintaining MAP beyond 35 mm Hg was safe and sufficient ( ). Similar to adults, variability in LLA likely exists in the pediatric population ( ). This all leads to uncertainty about the lower limit of blood pressure that should be tolerated in both the operating room and critical care settings, especially in patients with underlying neurologic conditions. Neonates are also thought to be especially vulnerable to cerebral ischemia and intraventricular hemorrhage because of a narrow autoregulatory range. Tight blood pressure control is paramount during neonatal management ( ) ( Fig. 31.7 ). Critically ill premature neonates have CBF pressure passivity resulting in a linear correlation between CBF and systemic blood pressure. Thus knowing age and gestational-related changes in blood pressure is essential. Techniques such as deliberate hypotension may, therefore, not be tolerated in this patient population ( ).

The exact mechanisms of normal cerebral autoregulation in healthy children are not fully understood. Similar to changes in CBF, both anatomic and physiologic maturation might play a role in fully developing the cerebral autoregulatory response ( ). A combination of metabolic, myogenic, and neurogenic processes likely work together to orchestrate cerebral autoregulation. The metabolic mechanism stipulates that autoregulation is mediated by the release of vasodilator substances that maintain CBF constant by regulating cerebrovascular resistance. Proposed mediators of cerebral autoregulation include adenosine, NO, protein kinase C, melatonin, prostacyclin, activated potassium channels, and other intracellular second messengers ( ). Pressure-dependent myogenic tone in the systemic resistance vessels was first proposed by Bayliss in 1902 but was not experimentally verified until 50 years later. The myogenic theory states that the basal tone of the vascular smooth muscle is affected by change in perfusion or transmural pressure, and the muscle contracts with increased MAP and relaxes with decreased MAP ( ). Vascular smooth muscle, endothelium, and neighboring astrocytes and neurons play direct and modulatory roles in establishing the tone of cerebral vessels ( ). Emerging evidence implicates astrocytes as one of the key contributors to neurovascular coupling via glutamate receptors and calcium signaling pathways ( ). Some investigators believe that metabolic mediators are responsible for autoregulation itself, whereas the myogenic mechanism sets the limits of autoregulation ( ). The central nervous system exerts control on the cerebral vasculature via neurotransmitters interacting at specific perivascular innervation sites. These perivascular neurotransmitters include acetylcholine, norepinephrine, neuropeptide Y, cholecystokinin, vasoactive intestinal peptide, and calcitonin gene-related peptide ( ). Acetylcholine is the most abundant of these compounds and the specific neurotransmitter contained within a perivascular nerve fiber may modulate the specific response to a change in blood pressure. Experimentally sympathetic stimulation leads to a shift of the autoregulatory curve to the right, thus protecting the brain against severe elevation of MAP ( ).

History and physical examination

Many children presenting for neurosurgical procedures are either preverbal, nonverbal, have altered mental status ( Table 31.2 ), or do not fully understand their medical condition, all of which necessitates carefully reviewing the patient’s medical record and interviewing the parents, legal guardians, and/or primary caregivers to gather information about comorbidities and relevant symptoms. Frequency and timing of home medications, such as antiepileptic drugs and chronic steroid therapy, should also be verified to ensure that patients are optimized prior to surgery. In patients with epilepsy, it is also important to note if they are on a ketogenic diet, as these patients will most likely have a chronic metabolic acidosis, and dextrose containing intravenous (IV) fluids and medications should be avoided ( ).

In addition to a routine preoperative assessment and physical exam, a focused neurologic evaluation should include determining evidence for increased ICP, mental status changes, motor weakness, or nerve damage/injury. Neonates and infants with intracranial hypertension (ICH) might present with irritability, an enlarged head, bulging fontanel, poor appetite, or lethargy ( ). Children with ICH ( Fig. 31.8 , Table 31.3 ) might present with vomiting, headache, blurry vision, or papilledema. Repeated vomiting may lead to dehydration, electrolyte abnormalities, and could increase the risk of aspiration. Infants may also present with an ocular finding characterized by a fixed down-ward gaze referred to as the “setting-sun sign” ( ).

In infants and children with craniofacial abnormalities, a thorough airway evaluation and plan is beneficial since difficulty with airway management is a key concern, often necessitating advanced techniques to secure the airway ( ). Observing for signs of airway obstruction and reviewing prior anesthetic and intubation records will aid in formulating the airway approach. Common perioperative concerns for children with specific neurologic conditions are listed in Table 31.4 .

Laboratory results and imaging

Preoperative laboratory investigations should be tailored to the patients’ underlying pathology and the scheduled surgery and may include a complete blood count, coagulation profile, and a type and crossmatch if considerable blood loss and need for transfusion is expected. Additionally, serum electrolytes might also be useful in determining sodium and potassium levels, especially in the setting of vomiting. In patients with a hypothalamic or pituitary lesion, a full endocrine workup, along with pertinent labs, are essential. In patients on chronic antiepileptic drug therapy, liver function tests should also be reviewed.

Almost all neurosurgical patients will have a preoperative MRI or computed tomography (CT) of the head available for review. A primary lesion or progression of neurologic conditions, such as in subdural hematomas (SDH) ( Fig. 31.9 ) and hydrocephalus, can be identified. Reviewing these scans with the neurosurgeon prior to the operation may be useful in mitigating potential perioperative complications.

Premedication

Preoperative sedatives administered in the preoperative holding area can ease the transition for pediatric patients going to the operative room ( ). However, it may be prudent to avoid sedative and narcotic premedication in children with suspected increased ICP, as these medications often decrease respiratory drive, resulting in hypercapnia and additional increases in ICP ( ).

In patients with normal ICP, preoperative anxiolysis should be considered. Oral midazolam (0.5 to 1 mg/kg) may be beneficial in young children without IV access, as it can provide adequate sedation with minimal respiratory depression and facilitate a smooth separation from parents. In older children or those with established IV access, intravenous midazolam (0.1 mg/kg), dexmedetomidine (0.5 to 1 mcg/kg), and/or opioids may assist with decreasing anxiety and avoiding hypertension prior to induction ( ).

Induction of anesthesia

A patient’s comorbidities and neurologic function will determine the appropriate airway approach and medications for induction of anesthesia. In neurologically stable children without IV access or difficult IV access, general anesthesia is usually established via inhalational mask induction with sevoflurane and nitrous oxide. While volatile anesthetics are cerebrovasodilators, controlled hyperventilation and opioid administration prior to airway manipulation can limit the effects on ICP. After IV access is obtained, a nondepolarizing muscle relaxant can be given to optimize intubation conditions. Alternatively, if the patient has an IV and is hemodynamically stable, anesthesia can be promptly induced with propofol (3 to 5 mg/kg). Children at risk for aspiration should undergo a rapid-sequence induction (RSI) with propofol followed immediately by a rapid-acting muscle relaxant such as succinylcholine (1 to 2 mg/kg) or rocuronium (1 mg/kg) prior to tracheal intubation.

In patients with elevated ICP, the main objective during induction is to minimize any further increase in ICP. These patients are also at greater risk for aspiration pneumonitis and typically require an RSI. Succinylcholine should be avoided in patients with spinal cord injuries or paralysis resulting from stroke or significant nerve damage, as it can cause devastating hyperkalemia. Rocuronium can be used when succinylcholine is contraindicated. Since propofol can cause hypotension, etomidate (0.2 to 0.4 mg/kg) and ketamine (1 to 3 mg/kg) are frequently used for induction in the setting of hemodynamic instability. The specific effects of anesthetic medications on cerebral hemodynamics is summarized in Table 31.5 and Table 31.6 and discussed later in this chapter.

Airway considerations

Airway and respiratory complications result in significant morbidity and mortality for pediatric patients in the perioperative period. Comprehensive knowledge of functional pediatric airway anatomy is imperative when administering anesthesia and managing the airway of a child. For a complete discussion of pediatric airway anatomy and physiology, see Chapter 4 .

Nasotracheal intubation can be advantageous in situations where the patient will be in the prone position during surgery or in patients where postoperative mechanical ventilation is foreseen. In complex craniofacial surgery, the surgeon will often wire or suture the endotracheal tube in place intraorally to prevent inadvertent extubation during the operation. After final positioning of the patient, prior to the start of surgery, breath sounds should be rechecked to ensure that mainstem intubation has not occurred or that the endotracheal tube is not kinked, especially when the head is in the flexed position.

Vascular access

Sufficient vascular access prior to the start of surgery is crucial, and this is particularly important in pediatric neuroanesthesia. In many cases, the head of the bead is rotated 90 to 180 degrees to accommodate neurosurgical equipment and trying to obtain additional vascular access under the surgical drapes without contaminating the surgical field can be quite challenging, especially in infants and small children. In general, two large-bore IV catheters are adequate for craniotomies, craniofacial surgery, vascular malformations, or other procedures where significant blood loss is anticipated. Central venous access should be considered in hemodynamically unstable patients requiring a vasopressor infusion and in patients undergoing high-risk neurosurgical procedures where adequate peripheral access cannot be obtained. Cannulation of the femoral vein is preferred in these cases, since internal jugular catheters can interfere with venous return to the head, and there is a risk of pneumothorax with attempting subclavian venous access. However, routine use of central venous catheters in the pediatric neurosurgical population is debated and usually not warranted. Although cannulation of the jugular or subclavian veins with multiorifice catheters in adults is often preferred, particularly when venous air embolism (VAE) is anticipated, these catheters are too large to be used in infants and small children. In fact, even when VAE occurs in infants, a central venous catheter is not usually successful for aspirating air, likely because of the high resistance of the small-gauge catheters used in these patients ( ). An arterial catheter should be used in cases where there is potential for blood loss, hemodynamic instability, and where beat-to-beat blood pressure monitoring is essential. Arterial catheters are also indicated for blood sampling for perioperative labs.

Positioning

Patient positioning should be discussed with the neurosurgeon in advance of the operation. The position of the patient during surgery can have certain physiologic effects ( Table 31.7 ). The prone position is most commonly used for spinal cord surgeries and posterior fossa procedures; however, if a patient is morbidly obese or is difficult to ventilate in the prone position, the sitting position may be more beneficial. Eyes must be periodically checked when possible to ensure that they are free from direct contact with a horseshoe or Mayfield head frame or a prone-view pillow. Postoperative visual loss has been associated with operations performed in the prone position ( ). Extreme head flexion in patients with posterior fossa pathology can lead to brainstem compression, as well as endotracheal tube migration into a mainstem bronchus. Significant rotation of the patient’s head can impede venous return through the jugular veins, leading to diminished cerebral perfusion, elevated ICP, and increased venous bleeding. Extension of the patient’s head could lead to inadvertent extubation, especially in infants and small children.

It is important to prevent compression and stretch injuries associated with certain surgical positions. Padding under the chest and pelvis will support the patient’s torso and will also take pressure off of the abdomen, reducing the risk of ventilation difficulties due to increased intraabdominal pressure. Ensuring that the abdomen has the ability to move freely will also reduce potential venocaval compression and increased epidural venous pressure that could lead to bleeding. Many pediatric neurosurgical procedures are performed with the head slightly in the raised position to facilitate CSF drainage from the surgical site. It is important to note that superior sagittal sinus pressure decreased with head elevation, and this can lead to VAE ( ).

Regardless of the patient’s position for surgery, special care and attention should be paid to adequately protect pressure points and prevent peripheral nerve injury and vascular compression.

Temperature management

In most pediatric neurosurgical cases, the intraoperative goal for temperature management is to maintain normothermia, avoiding extreme hypo- or hyperthermia. Usual methods for warming should be implemented, including increasing ambient room temperature prior to the child’s arrival to the operating room when possible, infrared warming lights for infants, warm fluids, and forced air warming devices. Although hypothermia decreases ICP, CBF, and CMR in animal models ( ; ), hypothermia in pediatric neurosurgical patients in the operating room is controversial and generally not advised. Hypothermia has well-known clinical complications, including coagulopathy, and increased risk of infection ( ). It has not been shown to improve neurologic outcomes in pediatric patients following TBI, and hypothermia may increase mortality ( ). There was no reduction in mortality or improvement in global functional outcomes in pediatric patients that were treated with 48 hours of hypothermia with slow rewarming, and that study was terminated early because of lack of benefit seen in early analysis ( ).

Pharmacologic considerations

Ideal properties for anesthetics used for pediatric neuroanesthesia include rapid onset and offset with no elevation in ICP, maintenance of CPP, maintenance of CBF-CMRO ₂ coupling, and preservation of autoregulation and CO ₂ reactivity, along with no seizure activity and cerebral protective effects. Given that no agent possesses all of these properties, it is critical to understand the impact of commonly used anesthetic agents on CBF, CMRO ₂ , and CSF dynamics ( Table 31.5 ). In a study of almost 700 adult patients, induction and maintenance medications used for anesthetic care were not independent risk factors for intraoperative cerebral edema ( ); however, there remains a lack of robust data in infants and children.