Thank you in advance for any general comments you could make, I am most grateful to you and this wonderful service you provide the public.
I realize you are giving general comments with out all the information you would need to comment directly about my Wifes case.
My 35 year old Wife who was healthy not overweight, never smoked, with normal BP and taking no meds whatsoever other than vioxx prescibed for minor back twinges, experienced headaches and fatigue while on the vioxx, and then had a SAH... I got her to the hospital very quickly as I live next to a very good one. She died after 6 days. My general question is related to CT report showing areas of opercular ischemia on the first hour of her admission... her SAH was in the sylvan fissure. Is it not unusual to see ischemia prior to SAH, as I have been told it would take at least 24 hours for ischemia to form and show on the CT scan... it would appear she had ischemia in a region outside of the area of the SAH for at least 24 hours prior to the SAH.. I know vioxx has been associated with ischemia, also raise in BP...and I know that drugs that raise BP can cause hemorrhage. .... could she have had and ischemic attack or stroke and then a SAH? Three days later another report reffered to "lucency in the left frontal opercular region".... after another 3 days another report refers to "There is a new wedge shaped area of hypodensity in the left frontal lobe, infarct"
I have include the first CT report to give you more background:
On the CT brain, diffuse subarachnoid hemorrhage was demonstrated. Oval focus of hypodensity in the region of anterior communicating artery measuring 1.2 cm was also demonstrated which could represent the ruptured aneurysm itself. Based upon report of the angiogram, lumen of the aneurysm was supposed to be on the order of 2 mm. This hypodensity measuring 1.2 cm may therefore represent CLOT around the aneurysm itself or could represent partial THROMBOSIS of the aneurysm with 2 mm residual lumen.
MRI demonstrates diffuse subarachnoid hemorrhage with flair hyperintensity in the sulci throughout. Hyperintensity completely fills the suprasellar cistern. There is moderate dilatation of the lateral ventricles and mild dilatation of third ventricle. Mild degree of periventricular flair signal abnormality suggests transependymal resorption related related to hydrocephalus which is likely communicating.
Layering hemorrhage in the occipital horns present.
There are areas of increased diffusion weighted signal throughout left sylvian fissure or opercular distribution. I suspect this could be related to subarachnoid hemorrhage although I can not exclude sites of OPERCULAR ISCHEMIA. There is no ADC map for correlation. There is also increased flair signal as well as increased diffusion weighted signal in the distribution of pericallosal focus. I suspect again that this is related to hemorrhage particularly given the high T1 signal on saggital series. This distribution of hemorrhage is somewhat unusual unless an aneurysm of the anterior circulation such as anterior communicating artery were present.
The axial and coronal T2 weighted series demonstrates mixed intermediate to high signal in the region of anterior communicating artery measuring on the order of 1.2 x 0.9 cm. This is in the same location as the focal hyperdensity suggested by CT. Again I am uncertain whether this represents CLOT
around the aneurysm or partial thrombosis of the aneurysm since good flow void and significant enhancement are not demonstrated within this apparent focal hematoma.
Moderate communicating hydrocephalus suggested with transependymal resorption. Diffuse subarachnoid hemorrhage related to aneurysm bleed suggested. When corelation is made to the CT brain, I suspect the aneurysm is in the level of anterior communicating artery. This was verified by report of the angiogram. There may be CLOT surrounding the anterior comunicating artery itself or partial thrombosis of the aneurysm itself.
Subarachnoid hemorrhage in the left sylvan fissure producing increased diffusion weighted signal versus OPERCULAR ISCHEMIA on the left.
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