Edward Fohrman discusses what to take into consideration during vascular neurosurgery. Dr. Fohrman is the CEO of Fohrman Anesthesia Services & Consulting, Inc., which he founded in 2010. Visit EdwardFohrman.com for more.

1. Anesthetic Considerations in
Vascular Neurosurgery
Edward B. Fohrman, M.D.
Northwestern University
Feinberg School of Medicine

2. Aneurysms vs. AVMs
Characteristic Aneurysm AVM
Pathogenesis Arterial Venous
Etiology Acquired/Familial Congenital
Prevalence 1-5% 0.001 – 0.01%
Age of presentation 40-60* 20-40
Male:Female 1:2 1:1
Stroke % 5-15% of all Strokes 2% of all Strokes
Type of ICH SAH IPH
Size:Rupture Larger = ↑Ruputure risk Smaller = ↑Rupture risk
Adjunct/Alt. Tx Coil Embo Glue Embo
Rupture Rate/yr. 0.05% - 6% 2-4%
Rebleeding Risk 50% in 6 mos., 2-4%/yr 6%/yr, then 2-4%/yr
Mortality with Rupture > 50 % 10-15%
Morbidity 25-40% 30-50%
Associated Aneurysm 20% (Multiple) 20%
Hemodyamic Goals HTN! Venous Drainage
Postoperative Complication Vasospasm NPPB
Grading System Hunt Hess Spetzler Martin

3. Note: Grade 0 = Unruptured (MORTALITY)
(2%)
(5%)
(15 - 20%)
(30 - 40%)
(50 - 80%)

4. Spetzler–Martin Grading: Cerebral AVM’s
Feature Score
Maximum Diameter
< 3 cm 1
3-6 cm 2
>6 cm 3
Location
Noneloquent Cortex 0
Eloquent Cortex 1
Venous Drainage
Superficial only 0
Deep Venous Drainage
The Sum of the scores is equal to the grade (1-5)
1

5. Anterior
Communicating
Artery 30%
Posterior
Communicating
Artery 25%
Middle
Cerebral
Artery 20%
Internal Carotid Artery
Bifurcation 7.5%
Basilar tip 7%
Pericallosal Artery 4%
Posterior Inferior Cerebellar
Artery 3%
Anterior Circulation (85-90%)
A-Comm, P-Comm, MCA, ICA Bifurcation
Posterior Circulation (10-15%)
Basilar apex, PICA

6. • Congenital/Sporadic
• Incidence = 0.5%
• Venous dz w/ art. recruitment
• Arteries lack smooth m. layer
• “Arteriolized” Veins
• Absence of autoregulation in
AVM
• Shift of autoregulation in
surrounding brain tissue…
Lack of capillary bed (SHUNT)
↑Pressure, ↑Flow, ↓Resistance

7. Common Presentation of AVM’s
• Intracranial Hemorrhage (40-70%) Most Common
Intraparenchymal (60%)
SAH (30%) from AVM or Aneurysm (10-20%)
IVH (6%)
• Seizures (20-40%)
• Headaches (1-25%)
• Neurologic deficit (<10%, extremely rare)
RM Friedlander, NEJM 2007, 356:2704
J. Zhao et al. International Congress Series 1259, (2004)

8. • Progressive decrease in arterial pressure from the Circle
of Willis to the AVM nidus…
• Circulatory beds in parallel with the AVM, will be
perfused at lower than normal pressures even if CBF
remains relatively normal.
Hashimoto & Young Neurosurg Focus, 2001
‘Steal’ Is an Unestablished Mechanism for the Clinical
Presentation of Cerebral Arteriovenous Malformations
(Mast et al., Stroke. 1995;26:1215-1220.)
From the Departments of Neurology (H.M., J.P.M., R.S.M., R.M.L.), Anesthesiology (A.O., W.L.Y.), Neurological
Surgery (J.P.-S., B.M.S., W.L.Y.), and Radiology (J.P.-S., W.L.Y.), Columbia–Presbyterian Medical Center, New
York, NY.

9. Shift of Cerebral Autoregulation
normally 50 vs. 70 -150mmHg
RIGHTLEFT
Chronic HTN
Anemia
Sympathetic Stim.
TBI
Hypotension
Carotid Stenosis
AVM adjacent

10. Common Presentation of
Aneurysms
Headache
Nausea/Vomiting
MSΔ’s/Lethargy/
Coma
Papilledema
Pupillary changes
Cushing’s Triad
H&P –
“The worst HA of my life”
Focal Neuro/CN Deficit
Fever
Nuchal rigidity
Photophobia
Hypovolemia
Electrolyte imbalance
Hyponatremia
Signs & Symptoms of ↑ ICP

11. Risk Factors for AVM Hemorrhage
• Presence of aneurysms (10-20%)
– (feeding artery, intranidal, venous)
• Prior hemorrhage
• Deep venous drainage (single draining vein or venous stenosis)
• Deep location (basal ganglia/thalamus, internal capsule, corpus callosum)
• Size? Unlike aneurysms, AVM size appears unrelated to rupture risk (?smaller
avm’s rupture more frequently?)
• Pregnancy???

12. Aneurysmal Subarachnoid
Hemorrhage
is a
MULTISYSTEM DISEASE!

13. Fluid / Electrolyte Balance
• Hypovolemia:
• 30-100% develop after SAH
– Mannitol effect
• (osmotic diuresis ↑Na+, ↓K+)
• Hyponatremia:
• Natriuretic Factor release from hypothalamus
• Rx with 0.9 NS or 3%NaCl (avoid hypotonic
solutions)
• Hypokalemia
• (50-75% of patients)
• Hypocalcemia

14. Cardiac Effects of SAH
• EKG Δ’s in > 50% of pts after SAH
– T inversion and/or ST depression most common
– U waves, Q waves, long QT,
– Rhythm disturbances (30-80%)
– Atrial and Ventricular arrhythmias, Tachy/Brady
• peak occurrence on post SAH day 2-3
– Myocardial Necrosis: ↑ Troponin-I (cTnI) 15-20% of SAH
• Zaroff et al. multiple genetic polymorphisms of the β-1, β -2 and α-
adrenergic receptors associated with cardiac injury in aSAH
• more than 10% had EF<50%
• 35% had Regional WMA

15. Pulmonary Effects of SAH
• Cardiogenic & neurogenic pulmonary edema
(age>30, worse clinical grade)
• Admission cTnI Predicts Development of Pulmonary
Edema After SAH
– Andrew M Naidech, M.D., M.S.P.H., Kiki Hurt, M.D., Bernard Bendok, M.D., Georges
Cehovic, M.D. , and Michael Ault, M.D.
• 25% of all deaths related to aSAH are from medical
complications, half of which are pulmonary.
• ARDS, pneumonia, PE

16. Other Medical Complications
• Hepatic Dysfunction
– Hepatic failure/Hepatitis (25%), grade
severity/seen in pts w/ pulm edema
• Renal Dysfunction (8%), sepsis/abx
• Coagulation Dysfunction (4% ↓PLT
sepsis (DIC, leukocytosis)
• GI Bleeding (5%) r/o in sudden
tachycardic,hypotensive pts

17. COMPLICATIONS of aSAH
1. REBLEEDING
Early vs. Late
2. VASOSPASM
Risk of cerebral infarction
3. HYDROCEPHALUS
Acute vs. Chronic
4. EPILEPSY
5% incidence after discharge

18. REBLEEDING
• 50-80% Mortality
• 4% in 1st 24 hrs (Highest risk of rebleed)
• 1-2% per day for next 2 weeks
• Cumulative Rebleeding Risk
– 20% @ 2wks
– 20-30% @ 1st month
– 50% @ 6 months
– then ↓ to 3% per yr. x 15-20 yrs.
• Cumulative untreated rebleed risk 40%-50%
OVERALL
INCIDENCE =
10.5%

19. WHEN ARE SAH PATIENTS AT
RISK FOR REBLEED???
• INDUCTION OF ANESTHESIA (0.5-2%)
• MAYFIELD PINNING
• INTRAOPERATIVE RUPTURE (6-18%)
– Depends on institution, size, location of aneurysm
– Brain retraction, Hematoma evac
– DURAL OPENING
– ARACHNOID OPENING, ANEUR. DISSECT
– CLIP PLACEMENT
75%
Mortality!!!

20. Management GOALS
• Maintain CPP and limit ↑ICP
– Maintain adequate cerebral perfusion
– CPP = MAP - (ICP or CVP)
• Control systemic BP/Avoid abrupt BP changes
• Reduce Transmural Pressure across aneurysm wall
– Maintain transmural gradient
– TMP = MAP - (ICP)
• Optimize Cerebral O2 Delivery by maintaining
adequate PaO2 and Hgb
– DO2= CaO2 x CO
– CaO2= 1.34 x Hg x SaO2
• Decrease Intracranial Volume

21. Preventing REBLEEDING
• NORMOTENSION!!!
– Control Systolic HTN (↑ Transmural pressure)
– Short acting pharmacotherapy (esmolol, labetalol,
nicardipine, propofol, remifentanil)
• NORMOCAPNIA (PaCO2 35-40) until durotomy
– Avoid oversedation/ hypoventilation
• Timing & Rate of CSF drainage
• Euvolemia (lasix / mannitol)
• Seizure ppx??? (sz causes ↑BP, ↑ ICP, ↑CMRO2)
• AntiFibrinolytics??? (Aprotinin, TXA) Short Term!

22. MONITORING
• Standard ASA Monitors
• Pre-Induction A-line
• Possible CVP or PA
• ICP monitoring
• EEG, Evoked Potentials (BAER, SSEP,
MEP, Cranial Nerve)
• Precordial Doppler

23. Anesthetic Induction
• Failure to blunt hemodynamic response
to DL= RUPTURE=75%
MORTALITY!!!
• Maintain CPP & minimize transmural
pressure
• Good grade pts (1-3) have normal
intracranial elastance - hyperventilation
is NOT necessary/
– drop of 20-30% MAP is usually o.k.
• Poor grade patients (4&5) will not
tolerate drop in MAP and usually require
moderate hyperventilation
(PaCO2=30-35, ETCO2=25-30)

24. Drugs of choice
• Cautious premed to avoid hypoventilation
• Propofol, STP > Etomidate (avoid Ketamine)
• Fentanyl 3-5mcg/kg, Remifentanil 0.5mcg/kg
• Succinylcholine? Rocuronium 1mg/kg
• “PRE”med (50-50-50 propofol,remi,esmolol 50
secs prior to pinning)
• Maintenance with 0.5 MAC volatile, propofol gtt,
fent/remi gtt (? N2O)
• ANTI-HTN Nicardipine, NTG, SNP, Labetalol

25. “ THE BRAIN IS TIGHT!!!”

26. Rx for the TIGHT BRAIN
1) CBF/Blood volume
Avoid hypoxemia/hypercapnia/hypotension
Avoid arterial vasodilators
TIVA
Promote autoregulatory vasoconstriction
↓CMRO2 (Burst suppression, Hypothermia)
Mild ↑CPP (w/in autoregulatory range)
Hyperventilate (PCO2 = 25-30mmHg)
2) Brain Interstitial Fluid
Osmotic Diuresis
Mannitol 0.25-1G/kg 2cc/kg/min of 20% Mannitol
UOP goal 4-5 cc/kg/hr max effect @ 20 min
Hypertonic 3% NaCl 50-100 ml/hr (esp. if pt. is hyponatremic)
Forced (Non Osmotic) Diuresis - Lasix 0.25-1mg/kg
Fluid Restriction

27. Rx for the TIGHT BRAIN
3) Venous Blood Drainage
– ↓Intra-Abdominal Pressure (positioning, bucking)
– ↓Intra-Thoracic Pressure (↓Vt,↑RR, avoid PEEP)
– Head Up (10-300 Reverse T-Berg/ dbl. check head position for
optimal venous drainage (straight neck veins, chin/chest room)
– Avoid Venodilators (NTG)
4) CSF
– Drain off CSF directly by surgeon, or via EVD/Lumbar drain
– 15-20 ml (per surgeon)
– Decrease CSF formation with Lasix
– Stop direct stimulants of CSF formation
(Des>>Sevo&Iso>Propofol)

28. UH OH! IntraOP RUPTURE
• Call for Help!
• Make sure PRBC’s immediately available
• Institute hypotension (MAP<50mmHg)
• Burst SUPPRESSION
• Ipsilateral Carotid Compression (3min)
• Adenosine pause
• Facilitate Temporary clips, then raise MAP

29. Retrospective analysis of over 500 cases
IntraOp Tranfusion Rate = 25%
Median # of units = 2 units (Range = 1-17 units)
PostOp Tranfusion Rate = 45%
(244 pts. including 77 patients tx intraop)
Neurosurgery 49:1068–1075, 2001

30. Predictors of tranfusion
• 1) Advanced age
• 2) Lower Hct on admission
• 3) Ruptured (vs. unruptured)
• 4) Severe IVH
• 5) Aneurysm size (Larger)
Neurosurgery 49:1068–1075, 2001

31. Temporary Proximal Occlusion
• Reduces risk of rupture during manipulation of the
aneurysm via “local hypotension”
• Before temporary clip:
– Mild hypothermia 32-34°C (+/-)
– BURST Suppression/cerebral protection and consider
controlled hypotension
• After temporary clip:
– Enhance collateral circ via ↑MAP
– Optimal duration of temp clip is <20 min. to avoid
neurodeficit/infarction. Consider unclipping to
punctuate with periods of adequate perfusion/DO2 and
reinduce burst suppression
Samson D, Batjer HH, Bowman G, et al: A clinical study of the parameters and effects of
temporary arterial occlusion in the management of intracranial aneurysms.
Neurosurgery 1994; 34:22.

32. Case Question
• A patient presents to the ER with aSAH
• Angio shows 2 aneurysms
– A-com & MCA
• Radiologist and Surgeon disagree about
which one caused the SAH
• Why does it matter?

33. Relative Contraindications to Controlled
Hypotension
• Presence of intracerebral hematoma
• Occlusive cerebrovascular dz
• Vasospasm
• CAD
• Renal dysfunction
• Anemia
• Fever

34. IHAST-2
NEJM 2005;352:135-45.

35. VASOSPASM
• Typically occurs POST aSAH
day 3-21 and peaks around day
7-10
• 50% chance of angiographic
vasospasm in all grades
• Accounts for 30% of SAH
related M&M
• 20-25% delayed ischemic sx
• Cause in >25% of SAH related
death and 40% of SAH related
disability

36. CT scan showing
multiple strokes (arrows)
caused by SAH induced
vasospasm.
Vasospasm M&M
• CT evidence of
infarction 30-50%
•5-15% mortality from
vasospastic infarction

37. Postoperative complications of AVM’s
• Bleeding
• Edema
• Normal Perfusion Pressure Breakthrough
• Occlusive Hyperemia

38. Thank You

39. Questions?