Contrast staining mimicking hemorrhage post-thrombectomy
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Dialysis-dependent chronic renal failure patient with acute right sided hemiplegia
Acute Stroke Cerebral CTA
Code stroke Cerebral CT Angiography demonstrated a complete segmental occlusion of the left M1. No hemorrhage or large territory infarction was seen on noncontrast CT. The patient was immediately brought to the angiography suite for mechanical thrombectomy.
Mechanical thrombectomy was complicated by dissociation of Solitaire stent-retriever in the left MCA. High volume of Omnipaque contrast was used during the prolonged procedure. Noncontrast CT head 6-hours post thrombectomy (above) demonstrates the metallic stent in the left MCA, as well as large region of hyperdensity mimicking hemorrhage in the left frontal lobe MCA territory, involving the left basal ganglia, insula, and frontal operculum. There was no significant mass effect.
2-day later NCCT head
The patient underwent a CTA in the interval to assess for stent patency (not shown). Noncontrast CT head 1 day later (above) demonstrates increased size of the region of hyperdensity in the left MCA territory, as well as new region of hyperdensity in the left ACA territory (medial frontal lobe). There was mild mass effect around the regions of hyperdensity.
3-day later NCCT head
Noncontrast CT head 3 days later (post-dialysis) was performed. The large regions of hyperdensity in the left ACA and MCA territories are significantly less dense, indicating interval washing out of contrast. Small residual foci of hyperdensity are seen in the left lentiform nucleus and subinsular region are suspicious for hemorrhage.
5-day later NCCT head
Noncontrast CT head 5 days post-thrombectomy demonstrates further resolution of contrast staining in the left MCA and ACA territories. Stable foci of hyperdensity remain in the left basal ganglia and subinsula in keeping with parenchymal hemorrhage.
This case illustrates the dramatic appearance of prolonged and intense contrast staining in a patient who received high contrast volume during DSA and who could not excrete contrast due to chronic renal failure. The initial appearance could easily be mistaken for parenchymal hemorrhage in the region of infarct, and lead to erroneous termination of anticoagulation.
Contrast staining is most commonly seen in gray matter (cortex and deep gray matter) but can involve white matter in up to 20% of patients. Unlike hemorrhage, contrast staining demonstrates lack of surrounding edema and mass effect, and returns to normal structural appearance after hours to days. Of interest, contrast staining may be a prognostic indicator of brain injury, and there were likely ischemic changes in both ACA and MCA territories in this patient. According to Amans et al., the majority of patients (86%) with contrast staining progress to ischemic infarction, but very few (6%) progress to true hemorrhagic transformation. Furthermore, contrast staining is more likely to occur in patients with prolonged period between stroke symptom onset and diagnostic angiogram, i.e. established region of infarction.
Contrast staining usually resolves by 24 hours post-DSA, but can be significantly prolonged (as in our case) in patients with renal failure.