e******e
发帖数: 118 | 1 a 70 y/o female with hx of ischemic stroke twice in the past (1st was right
CVA with residual left side weakness,2nd was left CVA with transit aphasia
resolved, previous MRA negative) on ASA 81 and aggrenox bid now presented
with AMS. she was noted to be on the floor unresponsive in the morning and
she was last time seen well the night before. Pt regained conciouness in 45
min, eyes open, moving all extremities but aphasic. She is mildly lethargic,
looked confused, but following command. positive aphasic (new), right
facial droop (new), with intact muscle strength. CT scan left side
hypodensity, suggestive acute infart.
my initial impression is left side CVA, but neurologist thought seizure is
also possible and started pt with ativan 2mg iv x1 with keppra loading. pt
then became very lethargic, hardly arousable to assess neurological function
after ativan.
My questions are:
1) is it appropriate to start pt on ativan? will it mask the neurological
change of stroke?
2) I definately think pt has acute CVA. It is possible that she has seizure,
but the only suggestive information is she was unresponsive and she might
have post ictal state? is it appropriate to start anti-epilectics right away?
3) pt has recurrent CVA on ASA and aggrenox. What is recommended for 2nd
prevention of CVA in the next step, plavix or coumadin?
thank you for your input! | A*******s
发帖数: 9638 | | e******e
发帖数: 118 | 3 i can't load it now, but the reading is L thalamocapsular hypodensity may
represent acute infarct, no ICH | A*******s
发帖数: 9638 | 4 I would not trust the reading for acute lacunar infarct on CT. MRI will be
the final answer. But apparently it is not the cause of MS change.
【在 e******e 的大作中提到】
: i can't load it now, but the reading is L thalamocapsular hypodensity may
: represent acute infarct, no ICH
| A*******s
发帖数: 9638 | 5 I would not use ativan unless an EEG shows epileptic discharges.
The causes of MS change are complicated in a patient with multiple infarcts.
I agree a TIA or stroke could trigger her symptoms since she had bilateral
old infarcts. | d**o
发帖数: 618 | 6 Just play devil's advocate, I mean, the neurologist's advocate, perhaps his
reasoning is that the pt is already out of stroke treatment window, and
antiseizure drugs do have some neuroprotective effects (lower metabo rate,
lower oxygen demand), so it's better to give something that might help than
to give nothing at all? | A*******s
发帖数: 9638 | 7 Sorry I have to disagree with you on this one.
For a confused patient, you always try not to give sedation if possible. You
may assume she is having seizure, but where is evidence?
Assumptions are always wrong, believe it or not.
his
than
【在 d**o 的大作中提到】
: Just play devil's advocate, I mean, the neurologist's advocate, perhaps his
: reasoning is that the pt is already out of stroke treatment window, and
: antiseizure drugs do have some neuroprotective effects (lower metabo rate,
: lower oxygen demand), so it's better to give something that might help than
: to give nothing at all?
| d**o
发帖数: 618 | 8 I said I'm just playing devil's advocate ... I agree with you.
Now can you please answer the question #3 in the original post?
You
【在 A*******s 的大作中提到】
: Sorry I have to disagree with you on this one.
: For a confused patient, you always try not to give sedation if possible. You
: may assume she is having seizure, but where is evidence?
: Assumptions are always wrong, believe it or not.
:
: his
: than
| A*******s
发帖数: 9638 | 9 I even don't know the final diagnosis.
【在 d**o 的大作中提到】
: I said I'm just playing devil's advocate ... I agree with you.
: Now can you please answer the question #3 in the original post?
:
: You
| n*******c
发帖数: 501 | 10 Agree. I cannot see that neurologist's rationale of using ativan unless
there is evidence of nonconvulsive status epilepticus.If it is postictal,
the patient should improve overtime which cannot be proved while on
sedatives.
How long was CT done after onset? What is the size of left thalamocapsular
hypodensity? Lacunar infarct should not cause MS changes so even if it is
real it may not be relevant.Hard to say without imaging but should be
careful about post circulation infarct. I used to see a case of "top of the
basilar syndrome" with a CT scan showing unilateral thalamic infarct but
then bilateral thalamic infarcts were proved by MRI. | t***m
发帖数: 96 | 11 As A++ said, it is usually recommended to initiate AED based on the evidence
of sz by either diagnostic method or symptoms.Even sometimes there is
witnessed sz, the neurologists don't always start AED right away until the
second occurance. As a physician, you are more likely to wonder what's the
cause...(Keppra itself could result in drowsiness.)
Due to the fact that the pt had had recurrent CVA, what is the possible
cause, Afib, plaque, or vasculitis, etc? What are her risk factors? | e******e
发帖数: 118 | 12 as a followup,
pt had 24h continous EEG, no evidence of seizure, keppra d/c
too agitated to MRI, had repeated CT, showed more defined subacute left
thalamic CVA (sorry, don't know how to upload the image)
her speech improved, she is oriented, and able to speak simple word, such as
her name, and answer simple questions
the reason that neurologist started on keppra is because he thought the
aphasia, lethargy and facial droop was likely 2 nonconvulsive complex
partial seizure.
again, i feel if I can't tell exactly if it is seizure vs CVA, i would not
rush to give antiepileptics especially pt has no hx of seizure. | e******e
发帖数: 118 | 13 she has no afib.her coagu panel is nl. previous MRA was negative for vasular
deficit.
we consider to repeat MRA if pt can tolerate. I think she may also need some
work up to r/o vasculitis or hypercoagulabe state.
as for 2nd prevention of stroke, there is no data suggesting which is
superior among ASA, plavix vs aggrenox. In practice, physician alternatively
choose them. eg, if one fails on asa, physician may change it to plavix or
aggrenox.
coumadin,it is only indicated in pts with afib or intracranial thrombosis | A*******s
发帖数: 9638 | 14 I believe the MS change was from the stroke.
as
【在 e******e 的大作中提到】
: as a followup,
: pt had 24h continous EEG, no evidence of seizure, keppra d/c
: too agitated to MRI, had repeated CT, showed more defined subacute left
: thalamic CVA (sorry, don't know how to upload the image)
: her speech improved, she is oriented, and able to speak simple word, such as
: her name, and answer simple questions
: the reason that neurologist started on keppra is because he thought the
: aphasia, lethargy and facial droop was likely 2 nonconvulsive complex
: partial seizure.
: again, i feel if I can't tell exactly if it is seizure vs CVA, i would not
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