“Malignant” infarction refers to a large hemispheric ischemic stroke characterized by severe cerebral edema; such infarction can lead to midline shift with resultant compression of contralateral hemispheric structures and downward herniation leading to death ( Fig. 42.1 ). Edema following hemispheric stroke slowly evolves, generally peaking 3–5 days after stroke onset. The definitive therapeutic intervention is hemicraniectomy, in which a large segment of skull overlying the infarction is removed, allowing the brain to swell outward. Medical therapy with hyperosmolar agents such as mannitol and hypertonic saline also have roles as a bridge to hemicraniectomy or in those who are not surgical candidates.
Even with aggressive therapy, patients with malignant middle cerebral artery (MCA) infarction are uniformly left with long-term significant disability, with the vast majority (> 80%) dependent on others for help with activities of daily living. The severity of brain injury should be clearly communicated to family. Discuss with family the patient’s willingness to live with severe disability as expressed prior to the stroke. Rarely can the patient engage meaningfully in this discussion, as they typically are severely aphasic (dominant hemisphere involvement) or have dense neglect (nondominant hemisphere involvement), which precludes an accurate understanding of their condition. Many patients and families feel living with severe disability is a fate worse than death, and decline aggressive intervention.
Patient age has a major impact on outcome following malignant MCA infarction. In randomized trials of hemicraniectomy, younger patients (< 60 years) treated surgically have both a dramatic reduction in mortality and a significantly greater likelihood of achieving mild-moderate disability. In contrast, mortality is reduced with surgery in older patients but almost all survivors are left with moderately severe disability or worse. Given this, in combination with the invasiveness of hemicraniectomy, it is generally avoided in older patients.
Clinical criteria for predicting which acute ischemic strokes become “malignant” are imperfect. Generally, those with involvement of two-thirds or more of the MCA territory, particularly if the basal ganglia is also affected, are likely to develop severe swelling and midline shift and benefit from decompressive surgery with hemicraniectomy. In many cases the degree of infarction is only apparent on early interval follow-up head computed tomography (CT); accordingly, patients without evidence of malignant infarction on initial scan should have an interval CT 12–24 hours after the initial scan. If radiographic evidence of likely malignant infarction is present in a patient otherwise eligible for surgery within the first 24–48 hours of stroke onset, proceed to hemicraniectomy even in the absence of neurologic decline.
In patients without clear radiographic evidence to suggest a high risk of malignant infarction (e.g., smaller MCA infarctions, lack of early edema and midline shift), close neurologic monitoring is indicated. Often the earliest sign of malignant infarction is increasing somnolence. Do not wait for symptoms of uncal (anisocoria or an unreactive pupil) or transtentorial (new field cut, bilateral small fixed pupils, impaired upgaze) herniation to develop prior to considering hemicraniectomy. Should deterioration occur, administration of osmotic agents and hyperventilation can be implemented. Perform immediate repeat head CT to exclude alternative causes of worsening, such as hemorrhagic conversion. Proceed to hemicraniectomy as soon as possible.
Mannitol and hypertonic saline are osmotic therapies used to reduce cerebral edema. Mannitol is a reasonable initial choice, and is strongly preferred in volume-overloaded patients; hypertonic saline is preferred in patients with renal impairment. Administration through a central venous catheter is desirable but not essential. A bolus of 1 g/kg mannitol 20% can be given intravenously every 6 hours as needed. Determine the “osmolar gap” (calculated serum osmolarity subtracted from measured osmolarity) prior to redosing; if it exceeds 20 mOsm/L, do not give additional mannitol. Replete urine losses aggressively with normal saline to prevent hypovolemia. Hypertonic saline is an alternative to mannitol, given as a bolus (either 250 mL of 3%; 150 mL of 5%; or 30 mL of 23.4% solution) every 6 hours. Closely monitor serum sodium; if > 160 mmol/L, hypertonic saline should be stopped. Osmotic therapy is best viewed as a bridge to decompressive surgery, as it is far less effective than hemicraniectomy. However, for patients who are not candidates for hemicraniectomy, osmotic therapy may be used in an attempt to minimize the impact of cerebral edema until swelling starts to resolve on its own, usually after day 3–5. It should not be used prophylactically.