Vikas Pandey, MD
Battey T, Karki M, Singhal A, Wu O, Sadaghiani S, Campbell B, et al. Brain Edema Predicts Outcome After Nonlacunar Ischemic Stroke. Stroke. 2014
Brain edema is the harbinger of bad things to come in patients with large volume ischemic strokes. It is the reason neurologists will order close neurochecks, follow-up imaging and intensive unit level care for patients who may initially seem rather stable. The poor outcomes related to herniation, such as delayed additional neurological deficits, altered mental sensorium or even death lead clinicians to consider tactics such as early decompressive craniectomy, or osmotic therapy in this patient cohort. Typically, these methods are reserved in those with large hemispheric strokes, however, what effect on outcome prediction does the presence of signs of swelling have even with those with “smaller volume strokes”? Battey, et al. set out to answer that question.
The group used serial research MRI scans during the first 2-5 days following stroke to investigate aspects of infarct growth as well as presence of edema via retrospective analysis of the NBO and EPITHET cohorts for which a baseline DWI and a follow up DWI were available, utilizing previously used cohorts with a broad range of stroke severities (average NIHSS 14 and 13 respectively for NBO and EPITHET subgroups). They used voxel analyzing software to calculate differences in DWI volumes on sequential scans representing infarct growth as well as subjective analysis of brain edema i.e. direct evidence of mass effect or new distortion of adjacent tissue, midline shift, or new effacement of sulci or lateral ventricles. The interrater agreement of this method had a kappa value of 0.41. The group used locations as defined by the ASPECTS criteria to define if a new anatomical territory was involved different from the baseline lesion. They found that in the cohorts, presence of swelling translated to poor 90-day outcome (mRS >2), but infarct growth itself did not predict poor 90-day outcome. This was independent of factors such as increased DWI volume, NIHSS, and age. Using volumetric analysis to differentiate between what was swelling and what increased infarct burden, swelling was still an independent predictor of poor outcome.
Neuroimaging and how neurologists in particular use different aspects (no pun intended) of the images to translate to clinical care and outcome is an ever-changing process. The group put together a study that showed that infarct growth and edema even in milder stroke severities are notions that should not be taken lightly and may reflect outcome and their study is an excellent example of how we can use currently available weapons of imaging analysis and apply them to expand how we approach stroke patient care, even in ways that are not initially intended. The use of unique volumetric and voxel analysis also provides the possibility of using more advanced sequences during MRI scans to extract more information during these scans that can aid the patient and dictate pathways of stroke care.
But is the infarct growth as a result of the 5 possible causes of the neuronal cascade of death? Rather than this edema?
1. glutamate poisoning
3. Capillaries that don't open due to pericytes
4. Inflammatory action leaking through the blood brain barrier.
5. Lysosomal Membrane Permeabilization as a Key Player in Brain Ischemic Cell Death
How do you tell which one causes the infarct growth?