Malignant MCA Stroke: an Update on Surgical Decompression and Future Directions

Abstract

Despite a decline over the past decade in overall stroke mortality, hemispheric strokes retain a strikingly high mortality due to their potential for malignant edema and herniation. The pathogenesis of ischemic cerebral edema is steered by disruption of ionic homeostasis in the neurogliovascular unit. Significant effort has been made to identify potential medical therapies targeting edema formation with promising results. To date, decompressive craniectomy remains the therapy with the most robust impact on mortality. Historically, patient selection for surgical treatment of malignant supratentorial strokes has focused on a strict age cutoff and hemispheric dominance. Recent evidence supports a significant mortality benefit in elderly population, although the impact in morbidity is modest. Careful patient selection for surgical treatment in conjunction with comprehensive neurocritical care and inclusion of family in the educated decision making process remain the mainstay of care for such shattering disease.

2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association

“…247 These findings were noted despite differences in the clinical trials in terms of inclusion and exclusion criteria, percent of MCA territory involved, and surgical timing. 248,249 At 12 months, moderate disability (ability to walk) or better (mRS score 2 or 3) was achieved in 43% (22 of 51) of the total surgical group and 55% (22 of 40) of survivors compared with 21% (9 of 42; P=0.045) of the total nonsurgical group and 75% (9 of 12; P=0.318) of the nonsurgical survivors. At 12 months, independence (mRS score 2) was achieved in 14% (7 of 51) of the total surgical group and 18% (7 of 40) of survivors compared with 2% (1 of 42) of the total nonsurgical group and 8% (1 of 12) of the nonsurgical survivors.…”

“…At 12 months, independence (mRS score 2) was achieved in 14% (7 of 51) of the total surgical group and 18% (7 of 40) of survivors compared with 2% (1 of 42) of the total nonsurgical group and 8% (1 of 12) of the nonsurgical survivors. 245,[247][248][249][250] See Tables LIX and LX in Hyperventilation is a very effective treatment to rapidly improve brain swelling, but it works by inducing cerebral vasoconstriction, which can worsen ischemia if the hypocapnia is sustained or profound. 256 Thus, hyperventilation should be induced rapidly but should be used as briefly as possible and avoid excessive hypocapnia (<30 mm Hg).…”

Collateral pial circulation relates to the degree of brain edema on CT 24 hours after ischemic stroke

“…Our data could have potential practical implications in clinical surveillance, as CPC assessment could allow early identification of candidates for neurointensive care unit admission, tighter vigilance and additional imaging controls, as well as consideration of early preventive medical treatment and early decompressive craniectomy, all of which can influence the prognosis of these patients. 3,[9][10][11][12]33 However, the clinical outcomes related to the various degrees of radiological CE in our study were not measured and further studies should focus on establishing this relation. Previous work 22 has shown significant association between poor CPC and development of MMI, but the impact of minor degrees of edema remains unclear.…”

“…1,9 Decompressive craniectomy is a treatment option for selected patients with increased intracranial pressure; when undertaken within 48 hours of stroke onset, it has been shown to reduce mortality and to improve outcome in patients with MMI. 3,[10][11][12] Therefore, predicting its occurrence is crucial for therapeutic management at early stages.…”

Twenty-Four-Hour Real-Time Continuous Monitoring of Cerebral Edema in Rabbits Based on a Noninvasive and Noncontact System of Magnetic Induction

“…Cytotoxic cerebral edema is most commonly observed after TBI and can include cell swelling and the intracellular accumulation of water. The blood-brain barrier (BBB) is disrupted and can cause extracellular edema in vasogenic cerebral edema [4]. The development of cerebral edema can often be observed in three ways: rapid development (within 24–36 h), gradually progressive development (over several days), or initially worsening development (about a week) [5].…”