[##]-year-old [male/female] with [headache/weakness/slurred speech] with
history and exam consistent with [acute/subacute] ischemic stroke [involving
NAME territory].
Initial considerations in this patient included cerebrovascular accident
(CVA) from ischemic and hemorrhagic etiologies, metabolic etiologies including
hypoglycemia, hyponatremia, and hyperglycemia amongst others, intracranial mass
including tumor, seizure, systemic infectious processes, and conversion
disorder among others.
Patient presented with complaint of [headache/weakness/slurred
speech/facial droop/vision loss] with reported onset of symptoms [## hours
prior to presentation/unknown]. Patient
noted to have an NIH stroke scale of [##] on arrival in the ED. Patient noted to be [out of/within] window for
thrombolytics. A Code Stroke was [not]
activated in the ED. A non-contrast CT
scan of the head was obtained with no evidence of intracranial hemorrhage. Additional imaging was obtained to include [a
CTA of the head and neck/MRI] and was [notable for FINDINGS].
Patient noted to have symptoms consistent with likely [right/left anterior
cerebral artery (ACA) distribution stroke based on contralateral sensory
and motor symptoms in the lower extremities (sparing hands and face), gait
apraxia (Left ACA: akinetic mutism, transcortical motor aphasia (similar to
Broca’s aphasia); Right ACA: confusion, motor hemineglect)/right/left middle
cerebral artery (MCA) stroke based on contralateral hemiparesis, facial
plegia, and sensory loss with motor deficits affecting the face and upper
extremities more than the lower extremities (dominant hemisphere involvement
resulting in aphasia (Wernicke’s (receptive) aphasia or Broca’s (expressive)
aphasia/non-dominant hemisphere involvement resulting in dysarthria (motor
deficit of the mouth with understanding intact) and inattention and neglect on
side opposite to lesion, agnosia (inability to recognize previously known
objects)/right/left posterior circulation stroke based on dizziness,
dysarthria, dystaxia, diplopia, and dysphagia].
Labs obtained to include point-of-care glucose, CBC, chemistry,
coagulation panel [additional] and
were [unremarkable/notable for leukocytosis and left shift]. We considered stroke mimics, including Todd’s
paralysis after seizure, complex migraine, pseudoseizure and conversion
disorder, unlikely based on history, exam, labs, and imaging.
Neurology was consulted on
the patient and involved in the decision-making regarding administration of
tPA. We considered administration of tPA
in this patient, and felt it was [indicated/contraindicated] based on [presentation
within 3/4,.5 hours from onset of symptoms with no contraindications to
treatment/presentation over 3/4.5 hours from onset of symptoms/absolute evidence
of intracranial hemorrhage on CT/clinical presentation suggestive of subarachnoid
hemorrhage (SAH)/neurosurgery, head trauma or stroke within the past 3 months/uncontrolled
hypertension (≥185 mmHg systolic blood
pressure or >110 mmHg diastolic blood pressure/history of intracranial
hemorrhage/known intracranial arteriovenous malformation, neoplasm or aneurysm/active
internal bleeding/suspected or confirmed endocarditis/known bleeding diathesis
((1)platelet count <100,000; (2)patient has received heparin within 48 hours
and has an elevated aPTT (greater than upper limit of normal for lab); (3)current
use of oral anticoagulants (e.g. warfarin) and INR >1.7; (4)current use of
direct thrombin inhibitors or direct factor Xa inhibitors)/abnormal blood
glucose (<50 mg/dL)/relative presence of only minor or rapidly
improving symptoms/major surgery or serious non-head trauma in the previous 14
days/history of gastrointestinal or urinary tract hemorrhage within 21 days/seizure
at stroke onset/recent arterial puncture at a non-compressible site/recent
lumbar puncture/post myocardial infarction (MI) pericarditis/pregnancy]. We discussed risks, benefits and alternatives
to administration of tPA with the [patient/family] and they [provided
verbal/written consent/wished to refuse this treatment].
Prior to treatment with tPA,
blood pressure was noted to be [less than 185 mmHg systolic and 110 mmHg
diastolic/noted to be greater than 180 mmHg systolic/110 mmHg diastolic which
prompted treatment with Nicardipine/Labetalol with/without noted improvement in
blood pressure]. We monitored the
patient for complications post-tPA administration, and discussed with ICU team
for admission.
https://wikem.org/wiki/Ischemic_stroke
https://www.mdcalc.com/nih-stroke-scale-score-nihss
https://www.mdcalc.com/modified-nih-stroke-scale-score-mnihss
https://www.mdcalc.com/hat-hemorrhage-thrombolysis-score-predicting-post-tpa-hemorrhage
https://www.mdcalc.com/sedan-score-post-tpa-hemorrhage
https://www.mdcalc.com/tpa-tissue-plasminogen-activator-dosing-stroke-calculator
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