Hemorrhage - Case 9 MR SWI
Claim CME CreditPOINT OF CARE INFORMATION
This CME activity consists of the student reviewing the video of the professor reviewing the case as well as the associated DICOM image set related to the case in question.
Learning Objectives
As a result of participation in this activity, participants should be able to:
- Provide improved patient care.
- Greater knowledge of the imaging characteristics of the patient's disease.
- Understand a better approach to interpretation of studies.
Faculty Disclosure
Mehmet Albayram, MD, Ivan Davis, MD, Mariam Hanna, MD, Anthony Mancuso, MD, Ronald Quisling, MD, Dhanashree Rajderkar, MD, Priya Sharma, MD, Roberta Slater, MD and Joann Stamm, MBA have disclosed that they have no relevant financial relationships. No one else is a position to control content have any financial relationship to disclose.
CME Advisory Committee Disclosure:
Conflict of interest information for the CME Advisory Committee members can be found on the following website: https://cme.ufl.edu/disclosure/.
Continuing Medical Education Credit
Accreditation: The University of Florida College of Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
Credit: The University of Florida College of Medicine designates this enduring material for a maximum of 0.5 AMA PRA Category 1 Credits. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
CB1719-Hemorrhage - Case 9 MR SWI
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CB1719-Hemorrhage - Case 9 MR SWI
Case ReportHistory
Exam
Prior Study
1. There is evidence of concurrent subarachnoid hemorrhage with subarachnoid clot concentrated in the proximal segment of the sylvian fissure and right lateral suprasellar space plus a large intraparenchymal hematoma in the adjacent mesial right temporal lobe. This complex of SAH & adjacent intraaxial is consistent with a sentinel hemorrhage condition where pial adhesions from prior hemorrhage (which this patient had from the left MCA aneurysm bleed) cause the hemorrhage direction to bleed into brain and subarachnoid space at the same time.
2. There is minimal to moderate external hydrocephalus and papiiledema.
3. There is early downward uncal herniation compressing the right cerebral peduncle.
CT head: CTA
1. There is no residual aneurysm in the left MCA treatment area.
2. There is a right P-com saccular aneurysm with a relatively wide neck for fundal size. There is no vasospasm nor incorporation of the parent artery in the aneurysm neck. It has a small apical daughter aneurysm.
3. There is a small basilar apex pre-aneurysm.
MR T1-w pre contrast
1. The right temporal hematoma is virtually isointense to brain indicating it is in a hyperacute to acute timeframe (2 hrs to 2 days). The existing vasogenic perilesional edema is hypointense on T1 and surrounds the parenchymal hematoma.
2. There is a right posterior saccular aneurysm. It is not as well seen on MRA than on the CTA. There is no residual left MCA aneurysm, and the basilar tip pre-aneurysm is not evident.
3. The large right temporal mass reduces venocapillary filling, But this could be just delay in filling and not necessarily infarction.
MR T1-w post contrast/MRA
1. There is no residual aneurysm in the left MCA treatment area.
2. The active P-com aneurysm is present but is detail concerning the aneurysm is clearer on the CTA.
T2-w spin echo
1. The right temporal hematoma age is in the hyperacute to early acute timeframe.
MR flair
1. MR flair demonstrates that the degree of actual transependymal fluid migration is minimal. Most of the periventricular hyper intense signal is likely age-related leukomalacia.
2. The age of the hematoma also matches the hyperacute phase on MR flair.
Findings
MR susceptibility (SWI)
There is abnormal susceptibility without appreciable blooming in the acute SAH and acute right temporal lobe hematoma. However, the is extensive pial susceptibility artifact with blooming consistent with diffuse prior SAH leaving residual hemosiderin within the pial surface along the right insula, right mesial temporal lobe, superior and middle cerebellar sulci, and within the right ventricular trigones. There is also chronic hemosiderin around the treated left MCA aneurysm. This chronic hemosiderin the right mesial temporal region would indicate prior post hemorrhage pial inflammation and adhesions. This would be the cause of the current sentinel hemorrhage complex where a cisternal right P-com saccular aneurysm would bleed concurrently into the adjacent subarachnoid space and adjacent mesial temporal parenchyma.
There is a right temporal hematoma, as discussed previously.
There is intraventricular blood, as discussed previously.
Impression
2. SWI also reveals evidence of wide spread, but mainly right temporal pial surface chronic hemosiderin, which would likely provide the pial adhesions necessary for the right P-com aneurysm to rupture into both the subarachnoid and the mesial right temporal lobe concurrently.
