Chapter 27

• Regardless of the cause, intracranial masses present according to growth rate, location, and intracranial pressure. Slowly growing masses are frequently asymptomatic for long periods (despite relatively large size), whereas rapidly growing ones may present when the mass remains relatively small.
• Computed tomographic and magnetic resonance imaging scans should be reviewed for evidence of brain edema, a midline shift greater than 0.5 cm, and ventricular displacement or compression.
• Operations in the posterior fossa can injure vital circulatory and respiratory brainstem centers, as well as cranial nerves or their nuclei.
• Venous air embolism can occur when the pressure within an open vein is subatmospheric. These conditions may exist in any position (and during any procedure) whenever the wound is above the level of the heart.
• Optimal recovery of air following venous air embolism is provided by a multiorificed catheter positioned at the junction between the right atrium and the superior vena cava. Confirmation of correct catheter positioning can be accomplished by intravascular electrocardiography, radiography, or transesophageal echocardiography.
• In a patient with head trauma, correction of hypotension and control of any bleeding take precedence over radiographic studies and definitive neurosurgical treatment because systolic arterial blood pressures of less than 80 mm Hg predict a poor outcome.
• Massive blood loss from injuries to the great vessels can occur intraoperatively with thoracic or lumbar spine procedures.

Anesthetic techniques must be modified in the presence of intracranial hypertension and marginal cerebral perfusion. In addition, many neurosurgical procedures require patient positions (eg, sitting, prone) that further complicate management. This chapter applies the principles developed in Chapter 26 to the anesthetic care of neurosurgical patients.

Intracranial hypertension is defined as a sustained increase in intracranial pressure (ICP) above 15 mm Hg. Intracranial hypertension may result from an expanding tissue or fluid mass, a depressed skull fracture, interference with normal absorption of cerebrospinal fluid (CSF), excessive cerebral blood volume (CBV), or systemic disturbances promoting brain edema (see below). Multiple factors are often simultaneously present. For example, tumors in the posterior fossa usually are not only associated with some degree of brain edema and mass effect, but they also readily obstruct CSF outflow by compressing the fourth ventricle (obstructive hydrocephalus).

Although many patients with increased ICP are initially asymptomatic, they typically 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 causes brain edema, which in turn, increases ICP, resulting in more ischemia. If left unchecked, 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 or A waves) lasting 1-15 min. This phenomenon is the result of autoregulatory mechanisms periodically decreasing cerebral vascular resistance and increasing arterial blood pressure in response to cerebral ...

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