A 59 year old white male with history of CAD, HTN, DMII, and remote TIA (15 years ago) was brought to the University Hospital ER with 8/10 chest pain that was relieved by nitroglycerin. The patient then became confused, unable to speak, and weak on the left side of his body.

http://www.uptodate.com/contents/im age?imageKey=EM/77387&topicKey=E M%2F289&source=outline_link&search =altered+mental+status&utdPopup=tru

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Drug-related (Intoxication vs. Withdraw) Hypoxia Hypo/Hyperglycemia Neoplasm (Primary vs. Metastatic) Infectious (Meningoencephalitis, Sepsis, etc.) Seizure (Generalized, Partial, Absence) Stroke (Ischemic vs. Hemorrhagic) or TIA Trauma (Epidural, Subdural, Subarachnoid, Diffuse Axonal Injury, or Parenchymal damage)

Immediately after presentation the Neurology team administered Alteplase (recombinant tPA)…

Indications • Clinical diagnosis of ischemic stroke with measurable neurologic deficit with onset of symptoms < 4.5 hours

Contraindications Contraindications in PE Contraindications in Labs/Imaging in Hx


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• Spontaneous clearing of stroke Stroke/head • trauma/MI within last • Only minor and isolated • neurologic signs 3 mo. • Seizure at onset of stroke • Hx of intracranial and impairments are due hemorrhage to postictal phenomenon Major surgery in last • Clinical symptoms suggest • 14 days GI and/or Urinary tract intracranial hemorrhage active bleeding/acute • bleeding in last 21 trauma (fracture) days • Persistant BP above 185 systolic and/or 110 diastolic • NIH scale score > 25 for treatment for 3-4.5 hours

Platlets < 1,000,000 mm Serum glucose < 50mg/dl INR > 1.7 if on Warfarin and/or anticoaggulation Tx regardless of INR Elevated aPTT if on heparin Evidence of multilobar infarction with hypodensity involving > 33% of cerebral hemisphere

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PMH PSH
 CAD, HTN, DMII, TIA (1997)
 None

Social Hx
 Lives with mother. No history of smoking or alcohol abuse. History of crack

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Family Hx

cocaine use but quit 10 years ago.

Medications
 At home:  Hospital:

 DM in grandfather, mother, brother, and sister. CAD in father and brother.

▪ ASA, Ergocalciferol, Glipizide, Lisinopril, Niacin, Nitroglycerin, Tramadol, Simvastatin ▪ Alteplase, Rosuvastatin, Famotidine, Fondaparinu

Allergies
 None

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Vitals General HEENT Cardio GI
 T: 98.2, BP: 168/88, P: 68, RR: 16, Ht: 5’2”, Wt:202, BMI: 36.9
 Pt. is confused, dysarthric, and appears to be in mild distress. Pt. able

to nod and shake his head.

 Atrauamtic and normo-cephalic, no carotid bruits, no JVD, no masses,

neck non-tender to palpation.

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 Regular rate and rhythm, normal S1 and S2, no clicks, rubs, or murmurs.  Soft, non-tender, non-distended. Normal bowel sounds.  No clubbing, cyanosis, edema, or rashes. Pulses symmetric and +2 in all

Ext

extremities.

Mental Status
 Patient is gradually becoming more oriented to person, place, and date. He is now able

to name objects after a short delay with soft and slightly uncoordinated phonation.

Cranial Nerves
 Pupils are equal and reactive to light. Fundoscopic examination reveals no papilledema

or retinal hemorrhages. Extra-ocular movements are intact. Tongue was slightly deviated to the left and there was a slight facial droop on the left.

Motor
 Strength 5/5 RUE and RLE, 4/5 LUE and LLE with positive drift  DTRs symmetric and 2+ bilaterally.  Plantar response are normal.

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Coordination
 No dysdiadochokinesia. No asterixes. No essential, intention, or resting tremor.

Sensory
 Pt. can distinguish b/w sharp and dull and also vibration in all extremities.

Gait
 Non-ambulatory

Neurological Exam
 NIH stroke scale ▪ 0= no stroke ▪ 1-4= minor stroke ▪ 5-15= moderate stroke ▪ 15-20= moderate/severe stroke ▪ 21-42= severe stroke

Diagnostic Imaging
 Head CT w/o contrast ▪ Order this study first ▪ DDX ischemic vs. hemorrhagic  Brain MRI ▪ More sensitive than CT and reveals infarcts sooner

https://online.epocrates.com/u/29111078/Ischemic+stroke/Summary/Highlights http://www2.massgeneral.org/stopstroke/inpatientconsultations.aspx http://www2.kumc.edu/coa/Education/AMED900/Neurology.htm

Investigating Underlying Causes
 EKG and ECHO  A-fib embolization of mural thrombi  Paradoxical emboli via ASD  Carotid Duplex (ultrasound)  Degree of atherosclerosis in carotids  CT Angiography  Aneurysms, AVMs, or stenosis of head or neck vessels  Blood test  Bleeding disorders, hypercoagulable states  History  Glucose and Blood Pressure control

Head CT w/o contrast (x2):
 No infarction, hemorrhage, or interval change from

previous CTs.

Head CTA:
 Small, non-stenotic plaque in right common

carotid. Otherwise normal for age.

Brain MRI w/o contrast:
 Pending

14.4 7.9 41.6 197 2.2

8.7
3.0 10.4 1.0 27.6

140
3.7

108
25

15
101

147

TB
0.4

TP
7

Alb
3.7

AST ALT
18 19

ALP
56

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BNP = <20 Troponin I = 0.02 (x3) 12 lead ECG = normal in all leads Urinary tox screen = negative WBC diff = normal

Patient is a 59 y/o WM with h/o

CVA

 Since tPA treatment upon admission the patient has been steadily improving. He

HTN

regained the ability to speak soon after treatment and as of today appears to have no cognitive dysfunction. He still has slight weakness in left arm and leg, however there is steady day to day improvement. Brain MRI w/o contrast is pending. Continue to monitor improvement.  Continue taking ASA and Fondaparinux for anticoagulation.  Start inpatient rehab.
 Continue to monitor and maintain tight BP control. No permissive hypertension is


CAD

required post-tPA administration.  Continue Lisinopril.
 Continue Rosuvastitin.  Monitor glucose levels.  Continue Glipizide.

DMII

AMS
 Think drugs, bugs, sugar, stroke, neoplastic, and traumatic.

tPA
 Indications: best results are seen when given within the first 3 hours of

symptom onset  Contraindications: hemorrhage (intracranial or other), recent surgeries/procedures, low platelets/serum glucose, high INR

Stroke Work-up
 History and Neurological Exam
▪ NIH stroke scale

 Diagnostic Imaging
▪ CT vs. MRI

 Diagnosing Underlying Causes
▪ U/S, EKG, ECHO, angiographic studies, blood test, history

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