Cerebral ischemia frequently causes cerebral edema. Global ischemia may result from cardiac arrest or sustained hypotension, whereas focal ischemia may be the product of thromboembolic occlusion of a cerebral artery. Tissue hypoxia that results from ischemic conditions triggers a cascade of events that leads to cellular injury. The immediate effect of hypoxia is energy depletion with resultant failure of the Na + /K + ATPase pump. The onset of ischemic edema initially manifests as glial swelling occurring as early as 5 min following interruption of the energy supply. This cytotoxic phase of edema occurs when the BBB remains intact, although continued ischemia leads to infarction and the development of vasogenic edema after 48-96 hr. The development of vasogenic edema usually occurs only after reperfusion or in the setting of transient ischemia. Elevations of systemic arterial pressure with a loss of cerebral autoregulation may further the development of cerebral edema by increas ing hydrostatic pressure gradients across a disrupted BBB. Conversely, a reduction in CPP coupled with changes in the microcirculation, including elevation of cerebrovascular resistance, may induce detrimental effects by limiting the distribution of essential nutrients. Secondary ischemia may also result from BBB breakdown or from the effects of free radical-related amplification of neuronal injury. Clinical symptoms are initially representative of neuronal dysfunction within the ischemic territory, although the spread of edema may elicit further neurological deficits in patients with large hemispheric infarction. This clinical syndrome involves increasing lethargy, asymmetrical pupillary examination, and abnormal breathing. The mechanism of neurologic deterioration appears to involve pressure on brain stem structures due to the mass effect of infarcted and edematous tissue. Elevation of ICP may be generalized or display focal gradients that precipitate herniation syndromes. Her-niation may lead to compression and infarction of other vascular territories, in turn initiating a new cycle of infarction and edema.
Hemorrhagic infarction is frequently the cause of elevations in ICP, but the contribution of cerebral edema has been controversial. Intracerebral hemorrhage presents with focal neurologic deficits, headache, nausea, vomiting, and/or evidence of mass effect. The edema associated with intracerebral hemorrhage is predominantly vasogenic (Fig. 3), climaxing 48-72 hr following the initial event. Secondary ischemia with a component of cytotoxic edema may result from impaired diffusion in the extracellular space of the perihemorrhage region. Expansion of the hematoma volume or extension of edema may precipitate cerebral herniation. Figure 4 demonstrates uncal herniation that resulted from expansion of a hematoma. Other forms of hemorrhage, including hemorrhagic transformation of ischemic territories and subarachnoid hemorrhage, may be associated with edema that results from the noxious effects of blood degradation products.
Cerebral venous thrombosis may lead to venous stasis and elevations of cerebral venous pressure. These conditions are attributable to the absence of an autoregulatory mechanism within the cerebral venous circulation. The effect of elevated venous pressures is therefore greater than similar increases in the arterial system. The clinical manifestations of cerebral venous thrombosis are highly variable. Individuals may be asymptomatic, and others may suffer a progressive neurologic deterioration with headaches, seizures, focal neurologic deficits, and severe
obtundation leading to death. Parenchymal venous congestion and elevation of venous pressures can lead to disruption of the BBB, the formation of vasogenic edema, and perivascular hemorrhage. Further in-
creases in venous pressure lead to a reversal of the normal hydrostatic pressure gradients, and thus reduce capillary perfusion pressure. Fluid distension of the extracellular space also impairs the diffusion of nutrients. These changes induce the formation of cytotoxic edema that may ultimately result in ischemic venous infarction (Fig. 5).
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