Data Collection Sheet for AVMs

I created this form based on the article from Stroke Journal referenced below.  Next step is to create a public Excel template or REDCap database template that each neurocritical care unit can use for their own AVM database. Figure below shows screen capture from first page (form is 2 pages long).  PDF and DOCX versions of the form area available (see bottom for links to files.)


Data Collection Sheet for Brain AVM (pdf)

Data Collection Sheet for Brain AVM (docx)



  1. BAVM (brain AVM) – preferred over cerebral AVM (CAVM), abnormal tangle of vessels that results in arteriovenous shunting (nonutritive blood flow) demonstrated by 4-vessel cerebral contrast angiography.
  2. Date of presentation – date on which patient experienced signs or symptoms that led to the medical evaluation
  3. Index date – medical encounter through which the date of presentation was learned
  4. diagnosis date – date of definitive diagnosis of BAVM (i.e. date of contrast angiography)
  5. language cortex – the left hemisphere unless additional clinical data suggets otherwise
  6. eloquence – locations as per Spetzler-Martin score, plus the thalamus/hypothalamus/basal ganlgia;  ??nondominant parietal lobe may be considered eloquent as visuospatial deficits may be under-recognized but disabling
  7. diffuse nidus – has peninsula or islands of intervening brain
  8. old BAVM hemorrhage – all instances of CT or MR evidence of bleeding that is not temporally related to imaging for current signs and symptoms
  9. superficial drainage – all drainage from BAVM is through cortical venous system
  10. deep drainage – if any of all of drainage is through deep veins
  11. deep veins – internal cerebral v., basal v., precentral cerebral v.; in the posterior fossa, only cerebellar hemispheric veins that drain directly into straight sinus, torcula or transverse sinus are considered superficial
  12. venous stenosis – narrowing of any draining vein outflow pathway in 2 angiographic views; %stenosis – narrowest diameter of vein (in mm) divided by largest diameter of vein prox to stenosis (in mm)
  13. venous ectasia – any change in venous caliber in the venous runoff or drainage from BAVM with a >2-fold caliber change in any draining venous channel.
  14. sinus thrombosis – defect in dural venous sinus, excludes arachnoid granulations
  15. feeding vessel – arterial structure that angiographically demonstrates a contribution of flow to the AV shunt
  16. feeding arteries – parent arteries that give rise to vessels that supply flow to BAVM
  17. penetrators / perforators – vessels that are normally end arteries
  18. flow-related aneurysm – aneurysm lies on a pathway that carries non-nutritive blood flow supplying BAVM
  19. nidal aneurysm – aneurysm contiguous with the vascular mass
  20. proximal – located on the vessel or branch points of circle of Willis or proximal to it
  21. distal – refers to more distal locations beyond the circle of Willis


“Reporting Terminology For Brain Arteriovenous Malformation Clinical And Radiographic Features For Use In Clinical Trials”. Stroke 32.6 (2001): 1430-1442. Web.

Curriculum Vitae (CV) and Resume

CV is a more exhaustive document, intended to list all academic and professional accomplishments in detail.  A resume as compared to a CV is a shorter document, and will present your education and accomplishments strongly, but briefly and can be reviewed by the employer quickly.

*taken from article by Patrick C. Alguire, MD FACP (Cover Letter, Resume and Curriculum Vitae)

HIT (Heparin-Induced Thrombocytopenia) Form

HIT Algorithm:

Full anticoagulation with argatroban / lepirudin until platelet count rises above 150,000/uL


– synthetic analogue of L-arginine

-reversibly binds active site of thrombin

– rapid onset, given by drip

– goal is PTT 1.5-3x control

– cleared by liver

– ok to use in renal insufficiency (no dose adjustment)


– recombinant form of hirudin (anticoagulant in leech saliva), binds irreversibly to thrombin

– given as drip

– give bolus i life-threatening thrombosis

– goal: PTT 1.5-3x control

– cleared by kidneys.

– re-exposure can produce life-threatening anaphylaxis: ONE TIME TREATMENT ONLY


Start coumadin for long-term anticoagulation if HIT associated with thrombosis.

Do not start coumadin until platelet count increases >150,000/uL.

Initial dose of coumadin should not exceed 5mg. (Reduce risk of limb gangrene during active phase of HIT)

Continue antithrombin agents until coumadin achieves full anticoagulation


Kiwon Lee NeuroICU Book.

(Marino, 2014)