Among solid tumors, those affecting the brain are the primary cause of death in children. Notably, the incidence of both primary and metastatic brain tumors continues to rise.1 It is widely known that optimal outcomes are achieved with early diagnosis and treatment. To this end, the pediatric neurosurgical patient frequently presents for surgical diagnosis or for treatment of an identified lesion. This patient population presents a unique challenge for the anesthesiologist for many reasons. First, there is a brief window of opportunity in which to establish rapport and allay the anxieties of both the parent and child. Second, a solid understanding of the intracranial process and cerebral physiology are required for optimal care. Yet at the same time, by calming the patient, facilitating a smooth induction, and maintaining optimal cerebral hemodynamics, the anesthesiologist plays an integral role in the management and immediate outcome of the patient. This chapter discusses the neuroanesthesia management of pediatric patients presenting for both surgical and diagnostic procedures.
Cerebral blood flow (CBF) in the adult is approximately 50 to 55 mL/100 g of brain tissue each minute.2 There are limited data quantifying the CBF in children; however, it is appreciated that premature and newborn infants seem to have a lower CBF (40 mL/100 g/min) than that of children and adults.3 CBF in infants and children (65 to 85 mL/100 g/min) exceeds that of adults and can consume as much as one fourth of cardiac output.4
Cerebral metabolic rate for oxygen (CMRO2) plays an important role in the regulation of CBF. In fact, there is a direct correlation, such that increases in CMRO2 result in increased CBF, whereas decreases in CMRO2 result in decreased CBF. CMRO2 is slightly higher in children (5 mL/100 g/min) than in adults.4 When cerebral autoregulation is impaired by entities like tumors, edema, and acidosis, factors other than metabolic demand play an important role in determining CBF. They include cerebral perfusion pressure (CPP), arterial oxygen (PaO2), and carbon dioxide tensions (PaCO2).
Cerebral blood flow is autoregulated, thereby remaining constant within a mean arterial pressure (MAP) range between 50 and 150 mm Hg in adults. Within this range, the cerebral vasculature dilates and constricts accordingly to maintain relatively constant CBF. However, once the MAP falls outside of that range, CBF becomes dependent on pressure. Insufficient CBF results in ischemia, whereas excessive CBF leads to edema and the potential for hemorrhage. The data on autoregulation in neonates, infant, and children have largely been extrapolated from animal studies.5 Although it appears that the autoregulatory range is lower in this population, the true range remains undefined.6,7
Cerebral blood flow is less affected by changes in PaO2, as compared with PaCO2. In adults, CBF remains constant and does not begin to increase until PaO2 falls below 50 mm Hg.8 Exponential increases start to occur at around 15 mm Hg.9 Hyperoxia can cause significant reductions in CBF. The relationship between CBF and PaCO2 is linear within the range of 20 to 80 mm Hg. For each 1 mm Hg increase in PaCO2, CBF increases by approximately 2 mL/100 g/min. Outside of this range, the sensitivity of the central nervous system (CNS) vasculature to facilitate an increase or decrease in CBF is limited.
As with all surgical patients, a thorough preoperative assessment is necessary to adequately establish a comprehensive plan tailored for the surgical procedure. The plan includes not only the possibility of a premedication, but also the induction, intra-operative, and immediate postoperative periods. The evaluation should include a careful history and review of systems, focusing on any neurologic or cognitive deficits, seizures, recent vomiting, headache, and related endocrine deficiencies. A medication review that elicits the use of steroids or antiseizure medications is important because these drugs should be continued or augmented during the perioperative period. In addition, anticonvulsant medications can alter the metabolism of drugs such as muscle relaxants.10 Questions relating to bleeding disorders and malignant hyperthermia should be asked routinely. An assessment of intracranial pressure (ICP) should be made either from objective findings (bulging fontanelle, dilated scalp veins) or gathered from a review of the chart ( Table 8.1 ). Finally, a thorough physical examination should be done, with particular attention to the cardiovascular, respiratory, and neurologic systems. Establishing a gag reflex is also important to determine whether the patient is at risk for aspiration. Exam findings that should raise alarm include the combination of a dilated pupil and hemiparesis, the triad of bradycardia, hypertension, and decreased respirations (Cushing response), and a tense open anterior fontanelle in the setting of lethargy.11 A baseline hematocrit should be obtained along with a type and cross for any major neurosurgical procedure. Additional laboratory studies (Na+, glucose) should be obtained on an individual basis, specific to the patient′s history and surgical pathology. Radiological studies should also be reviewed because the location of the lesion may have an impact on physiology (e.g., respiratory center, hypothalamus, pituitary).
Widely spaced cranial sutures
The anxiolytic effect of premedication often makes it a useful adjuvant for the induction of anesthesia. Benzodiazepines like midazolam are often used, but other choices include barbiturates and narcotics. Ketamine is another option, but careful consideration should be given before its use, especially if there is concern for increased ICP ( Table 8.2 ). Routes of administration include PO, IV, rectal, and IM, and should be chosen based on the presence of IV access, level of patient cooperation, and time until surgery. The benefit of a premedication must be weighed against the risk of causing neurologic harm from the rise in PaCO2 that can result from decreased respiratory drive. Brady-cardia can also result or be worsened from the use of narcotics. If the use of a premedicating agent is necessary, administration of doses that are lower than usual should be considered, as children with intracranial pathology can be more sensitive to standard doses.
Standard American Society of Anesthesiologists (ASA) monitors (electrocardiogram, pulsoximeter, noninvasive blood pressure, end-tidal carbon dioxide, temperature) should be used for all pediatric neurosurgical cases. Arterial blood pressure monitoring should also be used for any case with the potential for significant blood loss, such as a craniotomy. Central venous access is a reasonable option when significant volume replacement is anticipated; however, this goal can also be achieved through the use of two large-bore IVs, unless central venous pressure monitoring is required. Measurement of urine output is also necessary for any major neurologic procedure, particularly because meticulous fluid management is a key element in minimizing cerebral edema. The pediatric population presents a unique risk for hypothermia during general anesthesia. Because the head makes up a large portion of the child′s body surface area, care should be given to maintain normothermia. This often requires increasing the ambient room temperature, in addition to the use of warming blankets and radiant lights. When muscle relaxants are used, train of four should be monitored using a peripheral nerve stimulator ( Table 8.3 ).
As a result of insufficient data on the effects of anesthetic agents on CBF and CMRO2 in the pediatric population, anesthesia principles, as they relate to physiology and management, must be applied based on outcomes in the adult population. The goal during induction, particularly in the setting of presumed intracranial hypertension, is to achieve a smooth and controlled level of anesthesia with rapid control of the airway. Precautions, such as hyperventilation and carefully titrated narcotic administration, should also be taken to lower ICP. Patients with acute intracranial processes should preferentially undergo an intravenous induction, given the potential for associated ICP elevation and the risk for aspiration. In instances where establishment of intravenous access is challenging and there is concern about elevations in ICP associated with crying from multiple venous access attempts, an inhalation induction can be performed.
0.5–0.75 mg/kg PO, 0.1 mg/kg IN
5 mg/kg IM with glycopyrrolate 0.1 mg/kg