The Monro-Kellie Doctrine states that the skull is a rigid box and that its contents (brain, cerebrospinal fluid, and blood) are incompressible (119). An increase in any one of the components will, therefore, displace another component, increase the pressure within the cranium, or cause a combination of the two. The relationship between intracranial pressure (ICP) and intracranial volume is often referred to as the intracranial "compliance" curve (Fig. 3). In that the relationship is really defined as the change in pressure for a given change in volume (dP/dV), the curve would more appropriately be referred to as the intracranial or "elastance" curve (120). The "compliance" curve illustrates the fact that the body is able to compensate for changes in intracranial volume without a concomitant change in pressure, to a degree; once the capacity to compensate for the change in volume is exceeded, the pressure begins to increase. It is at the high-end of intracranial volume that even small increases in volume lead to large increases in ICP.
Patients who experience large strokes that involve the entire territory of the middle cerebral artery (MCA) or internal carotid artery (ICA) are at risk for developing cerebral edema, especially with delayed reperfusion. When the amount of edema exceeds a critical level, cerebral herniation and death can occur (121-123). To decrease the risk of edema formation, occluded vessels should be recanalized early after stroke onset. Predictors of massive brain edema following hemispheric infarction include recanalization, National Institutes of Health Stroke Scale (NIHSS) >20 for left hemispheric strokes, NIHSS > 15 for right hemispheric strokes, a history of hypertension or heart failure, increased baseline white blood cell count, major early computed tomography hypodensity involving >50% of the MCA territory and involvement of additional vascular territories (124,125).
Cerebral edema can be attenuated by a number of medical interventions, including administration of mannitol, glycerol, and hypertonic saline. These drugs increase the osmolality of the blood and facilitate the exchange of free water from the interstitial to the intravascular space; they produce their effect primarily in regions of the brain where the BBB is intact. When the BBB is impaired, the drugs can "leak" into ischemic brain tissue and theoretically lead to intracranial compartmental shift and increased risk of herniation, although these fears do not seem to be borne out clinically (126). Despite the fact that mannitol, glycerol, and hypertonic saline all decrease ICP, no data suggest that their use improves outcome in large hemispheric stroke (127-131). The benefit of corticosteroids in acute stroke is unproven, and corticosteroids do not attenuate edema associated with cerebral infarction; their use should, therefore, be avoided (132). Hypothermia might attenuate cerebral edema or, at least, delay its onset (64,133 ). The role of hypothermia in acute stroke therapy is discussed in Chapter 30. Finally, indometha-cin is unique among the nonsteroidal antiinflammatory agents, in that it causes cerebral vasoconstriction and can decrease ICP (134-137).
Despite the presence of cerebral edema and the risk of herniation in malignant MCA/ICA infarcts, no clear role for ICP monitoring has been established for the treatment of stroke (138). Transtentorial herniation is the major risk associated with hemispheric infarction, and it is possible for the temporal lobe to slip over the tentorium without a documented increase in ICP. Thus, close and frequent neurologic examination is imperative (139). For patients who progress to herniation or are at risk of imminent herniation, emergent intubation for control of the airway and ventilation is necessary. Prolonged hyperventilation can worsen cerebral ischemia by causing arterial vasoconstriction, and prolonged hyperventilation was associated with worse clinical outcome in patients with traumatic brain injury; therefore, indefinite hyperventilation cannot be recommended in patients with stroke (140). Transient hyperventilation in the setting of acute herniation, however, might be a lifesaving measure. Mannitol at a dose of 1 g/kg is also an effective acute therapy for reversing herniation. Aggressive medical intervention for transtentorial herniation might produce reasonable clinical outcomes and should be pursued when more definitive therapy is available (141). One such therapy, early decompressive hemi-craniectomy, might be lifesaving, but clinical data to support an effect on functional outcome are lacking (142-149).
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