Introduction
The foundation for evaluating a child’s risk of brain injury includes frequent neurologic evaluations. If unable to conduct neurologic evaluations, the anesthesiologist must instead modulate physiologic parameters to ensure that the brain receives a constant supply of oxygen and glucose. The cerebrovascular system dilates and constricts to regulate cerebral blood flow (CBF) at the global level in pressure autoregulation. At the regional level of the neurovascular unit—the interface between neurons, vessels, and astrocytes—neurovascular coupling induces rapid and fine regional adjustments in CBF to meet local metabolic demands. Anesthesia and aberrancies in hemodynamic, blood gas, or glucose management can disrupt pressure autoregulation and neurovascular coupling. Therefore, the anesthesiologist must understand CBF regulation and the effects of anesthesia and intracranial lesions on cerebrovascular physiology.
Blood Pressure Autoregulation
Cerebrovascular autoregulation is the physiologic mechanism that maintains relatively constant CBF across changes in cerebral perfusion pressure (CPP). The CPP is calculated as the difference between the mean arterial blood pressure (MAP) and intracranial pressure (ICP). If the central venous pressure exceeds the ICP, the CPP is the difference between MAP and the central venous pressure. Cerebrovascular reactivity refers to the vasoconstriction and vasodilation of resistance vessels within the brain that constrain or increase CBF. This global autoregulatory vasoreactivity is functional in term newborns. Premature infants may have underdeveloped cerebral vasculature with limitations in vascular responsiveness.
Autoregulation functions within a specific range of CPP along the “autoregulatory plateau.” When CPP is below the lower limit of autoregulation (LLA), CBF falls in a manner that is passive to the decreasing blood pressure. This places the patient at risk of cerebral ischemia. CPP levels above the upper limit of autoregulation exceed the vasoconstrictive capacity of the vasculature, which places the brain at risk of hyperemic injury. Volatile anesthetics uncouple CPP and CBF and alter pressure autoregulation responses, thereby resulting in more pressure-passive CBF than that observed during intravenous anesthesia.1 However, no large clinical studies have compared inhaled and intravenous anesthetic techniques in children with neurologic lesions. Therefore, either an inhaled or intravenous anesthetic technique is generally considered acceptable for neurosurgical procedures that do not include a neuromonitoring method that warrants specific anesthetic regimens, such as intravenous techniques for electrophysiology monitoring.
The autoregulation curve is traditionally illustrated with (1) a horizontal CBF plateau at blood pressure levels within the range that produces pressure-reactive CBF, (2) a discrete cutoff at the LLA with a decline in CBF at pressures below the LLA, and (3) a cutoff at the upper limit of autoregulation with increasing CBF above that point. This representation is based on pooling CBF responses to fluctuations in CPP from multiple studies. In reality, the autoregulatory plateau for an individual does not have a slope of precisely zero, and the limits of autoregulation are smooth inflections on a curve (Figures 2.1 and 2.2). When blood pressure crosses below the LLA, cerebral arteries and arterioles may continue to dilate, but to a degree that is insufficient to maintain steady CBF. Likewise, when blood pressure exceeds the upper limit of autoregulation, additional cerebrovascular constriction might occur but be inadequate to maintain constant CBF. With extreme increases in arterial pressure, passive dilation of arteries can transmit pulsatile pressure to the cerebral microcirculation.
Figure 2.1. Examples of individual cerebral blood flow (CBF) autoregulation curves measured with laser Doppler flowmetry (LDF) in eight piglets as hypotension was slowly induced. The calculated cerebral perfusion pressure (CPP) lower limit of autoregulation (LLA) is demarcated with a dotted line. Variation among individual animals is observed in the CBF curve during hypotension. The left column illustrates piglets with relatively horizontal autoregulatory plateaus (panels A, C, E, and G). The right column illustrates piglets that did not have horizontal LDF curves when CPP exceeded the LLA (panels B, D, F, and H). Piglets in panels C, F, G, and H display smooth inflections in CBF that are often observed when blood pressure crosses below the LLA.
Figure 2.2. Data from the eight piglets in Figure 2.1 were combined to generate a single cerebral blood flow (CBF) autoregulation curve. Each piglet’s lower limit of autoregulation (LLA; dotted line) is centered at zero on the x-axis to permit comparison of each LLA relative to the cerebral perfusion pressure (CPP). When CBF data from multiple individuals are pooled together, the autoregulatory plateau appears horizontal, and a cut point in CBF is observed at the LLA. Data are displayed as means with standard deviations.
LDF, laser Doppler flowmetry.
The blood pressure limits of autoregulation during general anesthesia are unknown in infants and children. Available data suggest that the LLA among healthy, American Society of Anesthesiologists (ASA) level I children of different ages without brain injury may be at a MAP of approximately 50–65 mmHg.2 Young children (median age 2 years) on hypothermic cardiopulmonary bypass may have LLAs at a MAP of approximately 40 mmHg.3 The effects of acute and chronic intracranial lesions on the blood pressure limits of autoregulation are not well studied in children. Anesthesia decreases the cerebral metabolic rate, an effect that might confer some level of protection during lower blood pressures. Nonetheless, the anesthesiologist should make every effort to maintain the patient’s blood pressure close to the preoperative baseline.
Intracranial Hypertension and Pressure Autoregulation
The blood pressure limits of autoregulation are dynamic and may shift with intracranial lesions. For example, elevations in ICP with or without acute trauma shift the LLA to a higher CPP.4, 5 The treatment guidelines for pediatric traumatic brain injury provide level III recommendations that clinicians should maintain a patient’s ICP at less than 20 mmHg and CPP greater than 40–50 mmHg. The target CPP may need to be increased for older children and adolescents.6 Invasive arterial blood pressure monitoring is required to continually measure the CPP. When invasive ICP monitoring is unavailable but the anesthesiologist suspects that the patient has intracranial hypertension, he or she can estimate the ICP, for example 20–25 mmHg, and subtract this value from the MAP to obtain a rough assessment of the CPP until an ICP monitor can be placed.
The anesthesiologist must sometimes raise the arterial blood pressure to bring the CPP within a range that supports autoregulation. There is much debate about which vasopressor should be used to support CPP. Evidence in animal models suggests that sex may influence the autoregulatory response to vasopressors. In a piglet model of traumatic brain injury, dopamine supports autoregulation in both males and females after trauma,7 whereas norepinephrine and phenylephrine may affect autoregulatory function differently in males and females.8, 9 Because evidence is currently limited to preclinical models, we cannot make clinical recommendations for which vasopressor is optimal. Raising the arterial blood pressure to support CPP must be balanced against the risks of increasing myocardial oxygen demand with cardiopulmonary compromise and decreasing splanchnic perfusion. Intravenous fluid boluses, blood products, and colloids are also appropriate methods to raise the CPP. Using volume resuscitation to support the blood pressure is preferable to vasopressors in patients who have vascular malformations and are at risk of CBF dysregulation or vasospasm.
When supporting the CPP in patients with intracranial hypertension, the anesthesiologist should consider treatments to lower the ICP. The intracranial space conceptually consists of three volume compartments: the brain parenchyma, cerebrospinal or extracellular fluid, and cerebral blood volume. The rate at which ICP rises depends on how quickly the intracranial mass lesion develops. Slowly growing intracranial tumors or hydrocephalus will produce a slower rise in ICP than an acute hematoma from brain trauma. The growing cranium and widening sutures of infants and young children will allow an increase in head circumference with slowly growing intracranial lesions. It is important to note, however, that an open fontanelle and sutures do not protect an infant from intracranial hypertension or cerebral herniation. Infants and young children may have very little intracranial reserve when they become symptomatic from brain tumors or hydrocephalus. The risk of cerebral herniation after traumatic brain injury is greater in infants than in older children.10
When autoregulation is functional, there is an inverse relationship between MAP and ICP. When the arterial blood pressure increases, the cerebral vasculature constricts to constrain CBF. The consequent decrease in cerebral blood volume lowers the ICP (Figure 2.3A). Therefore, raising the blood pressure may lower the ICP when autoregulation is functional. However, when autoregulation becomes impaired, changes in blood pressure are directly transmitted as fluctuations in cerebral blood volume and ICP. In this situation, increases in arterial blood pressure will raise the ICP as well (Figure 2.3B).
Related posts:
Chapter 1 – Developmental Approach to the Pediatric Neurosurgical Patient
Chapter 4 – Neuropharmacology
Chapter 10 – Anesthesia for Fetal Neurosurgery
Chapter 12 – Anesthesia for Cerebrovascular Disease in Children
Chapter 21 – Intensive Care Considerations of Pediatric Neurosurgery
Chapter 20 – Perioperative Salt and Water in Pediatric Neurocritical Care
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