Tract Hemorrhage Grading Scale

Tract hemorrhage grading scale adapted from Ko et al. 

Tract hemorrhag grading: grade 0 a—no hemorrhage, grade I b—minimal intraventricular hemorrhage or hematoma <1 cm, grade II c—hematoma ❤ cm, grade III d—massive IVH, hematoma >3 cm

Reference:

Ko JK, Cha SH, Choi BK, Lee JI, Yun EY, Choi CH. Hemorrhage rates associated with two methods of ventriculostomy: external ventricular drainage versus ventriculoperitoneal shunt procedure. Neurol Med Chir. 2014;54:545–51.

Checklist: PRIS Labs

Labs to request for patients on high doses of propofol, and at risk for Propofol Infusion Syndrome

  • ABG
  • CPK levels
  • Lactic acid
  • Triglycerides
  • Amylase and Lipase

Monitor cardiovascular function carefully

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

 

References:

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:

  • ESR CRP
  • 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

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>

 

REFERENCE:

http://www.uptodate.com/contents/image?imageKey=NEURO%2F71462&rank=1~51&search=tpa&source=image_view&view=print&topicKey=NEURO/1124&source=outline_link&rank=1~51&elapsedTimeMs=1

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%

c.JPG

 

 

Most common EKG morphologic abnormalities associated with SAH:

a.PNG

 

Arrythmias associated with SAH:

b.JPG

 

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

 

Reference:

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

Pathogenic agents of bacterial meningitis according to age group


Reference: 

Textbook of Neurointensive Care, 2nd ed. A.JosephLayon et al.