Carotid Stenosis Algorithm

NASCET (North American Symptomatic CEA Trial) – CEA vs medical reduced risk of stroke (17%) and death (7%) at 2 years for stenosis >70%.

ACAS (Asymptomatic Carotid Artery Stenosis Trial) – CEA vs medical reduced risk of stroke or death (6%) at 5 years for stenosis >60%.

CREST (Carotid Revascularization Endarterectomy vs Stenting Trial) – CEA vs CAS in both symptomatic and asymptomatic – comparable rates of primary outcome measures (death, stroke, MI, stroke at 4 years).  Periop stroke more in stenting, periop MI more in CEA.  **NB Periopr stroke more disabling (based on 1 year in QOL assessment).


ICA Stenosis Algorithm



Experiences with carotid endarterectomy at Sree Chitra Tirunal Institute.  Unnikrishnan M, Siddappa S, Anto R, Babu V, Paul B, Kapilamoorthy TR, Sivasankaran S, Sandhyamani S, Sreedhar R, Radhakrishnan K – Ann Indian Acad Neurol (2008)


Lee, Kiwon. The Neuroicu Book. 1st ed. Print.

Checklist: Autoimmune Encephalitis Work-up

Serum studies:

  • C3 C4 CH50
  • ANA
  • RF
  • sjogren’s SSA SSB
  • SPEP
  • Thyroid peroxidase, thyroglobulin antibody
  • Glutamic acid-decarboxylase antibody
  • paraneoplastic panel (includes VGKC and NMDA)


MRI brain w/wo con
CTA head/neck


Lumbar Puncture

  • opening pressure
  • CSF protein, glucose, cell count
  • CSF IgG index, oligoclonal bands (check in serum as well)
  • CSF myelin basic protein
  • Gram stain and bacterial culture
  • Fungal culture

*withdraw at least 30 cc of CSF and save extra for additional studies if necessary



CHECKLIST: tPA Eligibility Criteria + sample consent form

From ENLS / ACC/AHA 2013

Algorithm for TIA/AIS:


  • Diagnosis of ischemic stroke causing measurable neurological deficit. Neurological signs should not be minor and isolated. Neurological signs should not be clearing spontaneously
  • Onset less than 3 h before initiating alteplase
  • Patient is at least 18 years old (see section on special considerations: pediatric stroke)

Absolute exclusion criteria if positive

  • No major head trauma or prior stroke in the previous 3 months
  • Symptoms of stroke should not be suggestive of subarachnoid hemorrhage
  • No arterial puncture at a non-compressible site or lumbar puncture in the previous 7 days
  • No history of previous intracranial hemorrhage
  • No history of intracranial neoplasm, aneurysm, or arteriovenous malformation
  • No intracranial or intraspinal surgery in the previous 3 months
  • Blood pressure not elevated (systolic <185 mmHg and diastolic <110 mmHg)
  • No evidence of active bleeding or acute trauma (fracture) on examination
  • Platelet count <100,000 mm3
  • If receiving heparin in previous 48 h, aPTT must be in normal range
  • Not taking an oral anticoagulant or, if anticoagulant being taken, INR < 1.7 or PT > 15 s
  • No dabigatran, apixaban, or rivaroxaban use for chronic anticoagulation for conditions such as atrial fibrillation. There is still little information on assessing influence or levels of these medications in patients with acute stroke. There are suggestions to check an activated thromboplastin time (aPTT), INR, platelet count, thromboplastin time (TT), ecarin clotting time (ECT) and anti factor 10a level (if available). Without normalized special tests (as listed), use of alteplase is NOT recommended in patients with recent use (within 48 h) of these products
  • Blood glucose concentration <50 mg/dL (2.7 mmol/L)
  • CT does not show a multilobar infarction (hypodensity >1/3 cerebral hemisphere)

Relative exclusion criteria if positive—use caution if recommending alteplase if one or more are positive

  • Stroke symptoms are rapidly improving or only minor
  • Pregnancy
  • Seizure with postictal residual neurological impairments
  • Major surgery or major trauma in the previous 14 days
  • Gastrointestinal or urinary tract hemorrhage in the previous 21 days
  • Myocardial infarction in the previous 3 months

Some additional considerations

  • Caution should be exercised in treating a patient with major deficits
  • Caution using alteplase in patients treated with low molecular weight heparin in the past 24 h
  • Patient or family members understand the potential risks and benefits from treatment. No written consent is required but the conversation should be documented in the clinical notes. Do not delay IV therapy if a surrogate is not readily available as this can lead to worse outcomes
  • Alteplase is not FDA approved for treatment of patients under the age of 18. However, alteplase has been used off-label in selected pediatric patients with strokes, following careful counseling of parents and using identical eligibility and contraindication criteria to those used in adults.


Inclusion criteria

  • Clinical diagnosis of ischemic stroke causing measurable neurologic deficit
  • Onset of symptoms <4.5 hours before beginning treatment; if the exact time of
  • stroke onset is not known, it is defined as the last time the patient was known to be normal
  • Age ≥18 years

Exclusion criteria

  • Historical
    • Significant stroke or head trauma in the previous three months
    • Previous intracranial hemorrhage
    • Intracranial neoplasm, arteriovenous malformation, or aneurysm
    • Recent intracranial or intraspinal surgery
    • Arterial puncture at a noncompressible site in the previous seven days
  • Clinical
    • Symptoms suggestive of subarachnoid hemorrhage
    • Persistent blood pressure elevation (systolic ≥185 mmHg or diastolic ≥110 mmHg)
    • Serum glucose <50 mg/dL (<2.8 mmol/L)
    • Active internal bleeding
    • Acute bleeding diathesis, including but not limited to conditions defined in ‘Hematologic’
  • Hematologic
    • Platelet count <100,000/mm3*
    • Current anticoagulant use with an INR >1.7 or PT >15 seconds*
    • Heparin use within 48 hours and an abnormally elevated aPTT*
    • Current use of a direct thrombin inhibitor or direct factor Xa inhibitor with evidence of anticoagulant effect by laboratory tests such as aPTT, INR, ECT, TT, or appropriate factor Xa activity assays
  • Head CT scan
    • Evidence of hemorrhage
    • Extensive regions of obvious hypodensity consistent with irreversible injury
  • Relative exclusion criteria¶
    • Only minor and isolated neurologic signs
    • Rapidly improving stroke symptoms
    • Major surgery or serious trauma in the previous 14 days
    • Gastrointestinal or urinary tract bleeding in the previous 21 days
    • Myocardial infarction in the previous three months
    • Seizure at the onset of stroke with postictal neurologic impairments
    • Pregnancy
  • Additional relative exclusion criteria for treatment from 3 to 4.5 hours from symptom onset
    • Age >80 years
    • Oral anticoagulant use regardless of INR
    • Severe stroke (NIHSS score >25)
    • Combination of both previous ischemic stroke and diabetes mellitus

<Eligibility criteria for tPA in PDF format>

Written consent is no longer required for tPA as this treatment is considered standard of care for acute ischemic stroke. That being said, the verbiage on this old consent form is a reminder of the information necessary for informed consent for tPA.

I have been clearly and fully informed by Dr._ that I am having a stroke. It has been explained to me that the Intravenous Thrombolytic Therapy using the drug t-PA, administered promptly after the onset of symptoms of a stroke may dissolve the clot and restore blood flow which may lessen the amount of damage to my brain.

I have been made aware that there are common risks and complications of Intravenous Thrombolytic Therapy as well as risks and complications of not having the therapy done. I have been told that the major risks from the use of t-PA are the possibility of internal bleeding including the stomach or intestinal tract and brain. The risk of bleeding in the brain is about 6%. If bleeding into the brain occurs my condition could worsen and may even result in death. I understand that some of the other possible reactions to t-PA include: temporary bruising or bleeding in the mouth, nose, skin, urinary tract or arm. If I refuse therapy my stroke could worsen or not improve.

I have received no guarantees as to results of Intravenous Thrombolytic Therapy. I understand that the alternative is to not receive t-PA and receive only supportive treatment.

In 1996, t-PA was approved by the Food & Drug Administration (FDA) for treatment of stroke within the first 3 hours after onset. In 2009, national guidelines concluded that this treatment could be helpful up to 4.5 hours after the onset of an acute stroke. Currently, the FDA has not approved t-PA for the treatment beyond 3 hours of symptom onset.

The nature and purpose of this therapy and the risks involved have been explained to me by the physician. I have been given an opportunity to ask any questions I may have, and all such questions or inquiries have been answered to my satisfaction. I have read this form and understand it fully.


1. Use actual body weight

2. Alteplase dose is 0.9mg/Kg, max dose not to exceed 90mg.

3. Mix by swirling, rather than shaking

4. 10% of total dose bolused over 1 min, remainder infused over 1 hour

5. Administer 100ml bag of saline after 1 h infusion to flush IV line and ensure entire dose is administered, use same rate to avoid terminal alert please bolus

Comparison of AHA/ASA acute stroke management guidelines (2013) and 2015 FDA prescribing information for alteplase treatment of acute ischemic stroke

Post TPA Orders:

  1. Neurochecks q15mins x 2h, then q30mins x 6h, then q1h there after
  2. Supplemental oxygen to keep O2 says >94%
  3. Check BP q15mins x2h, then q30mins x 6h, then q6 x 16h
  4. SBP goal <180/105
  5. Bedside swallow test (30 mL water PO) before anything else PO
  6. Keep glucose 140-180mg/dL, consider insulin get if Glu persistently >200 (hyperglycemia worsens outcomes, increases risk of ICH after ischemic strokes)
  7. Administer IV fluids (NS at 1.5 mL/Kg/hr), to goal of euvolemia
  8. Bedside telemetry / cardiac monitoring to detect atrial fibrillation, continue x at least 72h
  9. Treat fever source, avoid hyperthermia
  10. Avoid indwelling urinary catheter, NGT, intra-arterial catheters x 4 hours; avoid urinary catheters unless absolutely needed
  11. No anticoagulant / antiplatelet therapy x 24h


Gross, Hartmut, and Noah Grose. 2017. “Emergency Neurological Life Support: Acute Ischemic Stroke”. Neurocritical Care 27 (S1): 102-115. doi:10.1007/s12028-017-0449-9.

EKG findings in CNS Disorders

What is the relationship between acute CNS events and cardiovascular abnormalities? 

CNS events can induce cardiac abnormalities in EKG morphology and rhythm.  Most commonly, these abnormalities involve the T wave (diffuse, deep inversions).  Minor ST segment elevation have also been reported in leads with abnormal T waves.  T wave asymmetric, characteristic outward bulge in the ascending portion.  ST elevation usually less noticeable, and <3mm in most instances.    T inversions are more pronounce din midprecordial and lateral precordial leads.  May be found to a lesser extent in limb leads. Other EKG features in acute CNS injury include prominent U waves and QT prolongation.

Explanation for EKG findings – may involve CNS-mediated increases in sympathetic adn vagal tone, as well as actual myocardial damaage termed contraction band necrosi.

EKG changes with these disease processes can include ST segment depression, T wave inversion, PR shortening, QT prolongation, accentuation of U wave, bradyarrhythmia, and tachyarrhythmia (both ventricular and supraventricular). Derangement of autonomic nervous system activity may be responsible for these.


CNS modulates cardiac function via two pathways:

  1. indirect effect via humoral mediators (E and NE)
  2. direct effect via afferent and efferent connections with SNS and pSNS

Damage to hypothalamus may be the primary cause of autonomic dysfunction.

Hypothalamic dysfunction –> excessive humoral catecholamine production and autonomic tone –> HTN, inc cardiac O2 demand, vasospasm, ??direct toxic insult to cells –> subendocardial ischemia, microhemorrahges, focal myonecrosis –>  EKG changes / enzymologic and histopathologic changes


Classic EKG changes with SAH

  • first described by Byer (1947)
  • symmetric, deep T-wave inversion with QT prolongation
  • EKG changes seen in 72% of SAH
  • arrhythmias in 91% of cases, 41% of which were serious
  • subendocardial damage with myocytolysis, myofibrillar degeneration, fuchsinophilic degeneration
  • CPK elevations in 40-50%
  • focal or global wall motion abnormalities in ~50%




Most common EKG morphologic abnormalities associated with SAH:



Arrythmias associated with SAH:



EKG changes with acute thromboembolic stroke

  • morphologic changes
    • QT interval prolongation
    • ST segment, and T wave abnormalities
    • prominent U waves
  • Rhythm abnormalities
    • atrial fibrillation
    • sinus tachycardia
    • premature ventricular contractions
    • premature atrial contractions


Cushing response

  • sinus bradycardia + increased SBP + widened pulse pressure
  • EKG changes include prominent U waves, ST segment changes, notched T waves, and prolongation of the QT interval
  • result of compressive forces on the brainstem and diencephalic structures –> induces vagal and sympathetic discharges that can trigger either bradycardias or supravent / ventricular tachy-dysrhythmias



Perron, Andrew D., and William J. Brady. “Electrocardiographic Manifestations Of CNS Events”. The American Journal of Emergency Medicine 18.6 (2000): 715-720. Web.