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INTRODUCTION

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Intracranial volume largely determines intracranial pressure (ICP), since the skull fixes the volume. The three intracranial components are brain, cerebrospinal fluid (CSF), and blood. The brain itself, composed of cellular components and water, comprises roughly 90% of intracranial volume and may expand from tumor growth or edema. CSF accounts for roughly 5% of intracranial volume and may expand with hydrocephalus. Lastly, blood accounts for approximately 5% of intracranial volume. Expansion of the blood compartment occurs with cerebral hemorrhage or increased cerebral blood flow (CBF) as a result of cerebral vasodilation.

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An increase in either brain, CSF, or blood volume increases ICP. For healthy individuals, elastance permits small increases in volume without increasing ICP. Initial mechanisms to prevent increases in ICP include movement of CSF through the foramen magnum, absorption of CSF, and vasoconstriction, which reduces blood in the cranium. Beyond the elastic capacity, compensatory mechanisms are exhausted such that even a small increase in intracranial volume will exponentially increase ICP.

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Normal ICP is less than 10 mmHg. A sustained increase in ICP < 15 mmHg can result in irreversible effects. First, increased ICP can reduce CBF resulting in ischemia. Cerebral perfusion pressure (CPP) is determined by mean arterial pressure (MAP) minus ICP:

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Thus, if ICP increases without an appropriate increase in MAP, brain ischemia results. The second important risk of increased ICP is herniation, either across the meninges or through the foramen magnum, leading to rapid neurologic decompensation.

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CLINICAL CONSIDERATIONS

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Increased intracranial pressure manifests with headache, nausea and vomiting, visual changes, and somnolence or mental status changes. Airway protection is paramount.

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Management goals include prevention of cerebral ischemia and herniation. Decreasing the volume of one or more intracranial components remains the primary objective to achieve the goal. Removing the cellular components of the brain is a surgical endeavor. CSF can be drained, either by the surgeon or through a lumbar puncture. Of the three intracranial components, controlling CBF is most amenable to anesthesiologist control.

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When examining the control of CBF with respect to ICP, consider blood as two separate components: venous and arterial. Engorgement of the venous circulation increases blood volume within the cranium, leading to increased cerebral volume and pressure. Elevating the patient’s head optimizes venous drainage. Potential obstruction to venous drainage, such as extreme head flexion or extension or circumferential pressure from neck collars, should be avoided. Intrathoracic pressure increases due to PEEP, kinked or obstructed endotracheal tubes, or coughing decreases venous return and increases ICP. Lidocaine administration blunts tracheal response to intubation during induction; additionally, intraoperative neuromuscular paralysis should be maintained for patients with elevated ICP to prevent coughing.

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Several pharmacologic and physiologic influences to arterial blood must be considered. Of these factors, PaCO2 is the single most important determinant of CBF and cerebral blood volume. Increasing CO2 levels linearly increases CBF between 20 and 80 mmHg. CBF increases by roughly 1 mL/100 g brain/min in this range. Physiologically, an increase in CBF results from an increase in hydrogen ...

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