The Anesthetized Brain is less Vulnerable to ischemic injury than the awake brain. EEG changes suggestive of severe ischemia are present. Basic Methode Brain Protection are “ Corner Stone “ CPP, CBF, CBV maintained in “Normal Range”, MAP may increased up to 10 – 20 %. Anesthetics Drugs may have Brain Protectection effect. Volatile anesthetics do provide some Transient Protection (< 1,5 MAC) Barbiturates, although long considered to be the gold standard. Hypothermic methode are controversial, Hyperthermia should be avoided. Insulin is Administered if glucose values exceed 180 mg/dl. Close monitoring of BSL to ensure that Hypoglycemia does not develop

1. Intraoperative Brain Protection
INA-SNACC.

2. INTRODUCTION
Most Feared Complications in Intraoperative Anesthesia and Surgery :
CEREBRAL ISCHEMIA and NEURONAL INJURY.
Althought, The incidence quite low,
BUT certain procedure the risk can be high
The Majority of these complications occur during :
INTRAOPERATIVE PERIOD.
NOT ONLY Evaluating, BUT ALSO : Identifying
Decrease the Brain’s Vulnerability to Ischemia

3. INTRODUCTION
Normal Brain : Glial cell Maintain Imunological Integrity & Protection the Brain
Cerebtal Ischemic : Migration peripherial Imune Cell Infiltrate to the Brain
Exacerbate Neuro Degeneration, Anoxic Depolarization, Failure Glutamate up take.
Neuronal Injury

4. THE BRAIN THAT WOULDN’T DIE ?
May result from many Pathological Causes :
Understanding of Neuronal Death is Essential :
Designing Therapies, Prevent Neuronal death
Intraoperative Brain Protection was focused on
Balance of Supply - Demand Concept.
Rationale by reducing Brain’s ATP requirement.

5. THE BRAIN CAN BE DIE ?

6. Reperfusion
Reactive Oxygen
Species
Cytoskeleton
Breakdown
Protein
Pronecrotic
ISCHEMIC CASCADE
Hypoxia-Ischemia
Mitochondrial
Injury
Bax
Cytochrome c
release
Caspase
activation
DNA
fragmentation
NECROTIC DEATH
Depletion of energy
production
Depolarization without
Repolarization
Excess EAAs
(Glutamate)
Excess Calcium
Decrease O2
supply
NMDACalcineurin
Peroxynitrite
Bad dephospho-
rylation
Neuronal
Death
NOS
NO
PEROXYDATION
Slide Mg
BRAIN PROTECTION

7. NEUROANESTHESIA PRINCIPLE
A = Airway : Clear
B = Breathing : Normo or Slight Hypocapnia
C = Circulation. Avoid : High Increase or High Decrease of BP.
Avoid : Increase I C P. ( More 20 mmHg  Tx)
Fluid tx: Normo ( T, vol, Glycemia, Isoosmoler ).
Correction:Acidosis, Electrolyte, plas. Glucose.
D = Drugs ( Avoid drugs & Anes. Technique will increase ICP ).
Give drugs have B r a i n Protection E f f e c t.
E = Environment (temperature control, mild hypothermia avoid
hyperthermia)

8. INTRAOPERATIVE BRAIN PROTECTION
Basic Methode are “Corner Stone“ Intra Operative Brain Protection
Ensure DO2, Manipulation of PaCO2 = Normocapni/35-40mmHg.
PCO2 is a potent effect to CBF & CBV.
Hypocapnia Reduce CBF, CBV and ICP. to produce Brain Relaxation.
CBF Reduction enhance injury in Ischemic or Traumatic CNS injury
Prophylactic Hyperventilation has not any benefit in ischemic Injury.
BTF; Prophylactic hyperventilation avoided during early stages TBI.
It should be applied with an understanding of its complications.
“

9. CBF is Normally Autoregulated over a MAP Range of 50 to 150 mmHg.
Maintenance of CBF with a CPP in excess of 60 mmHg.
Adequate CPP is to Maintain Perfusion in a Brain Ischemic Injury.
TBI: Higher than normal CPP (>70 mmHg) to maintain normal CBF.
Patients who have Sustained an Ischemic cerebral injury may benefit from :
Induced Hypertension; Increase MAP > 20% baseline, Augmentation CBF
Hypotension to be Deleterious to ischemic or traumatic injured brain.

10. Targets Blood Sugar Levels between 100-180 mg/dl.
• Anaerobic Glucose metabolism product Lactic Acid and ATP.
• The Lactic Acid contributes to the Tissues Acidosis.
Brain Does Not have Glucose Stores : If During Hyperglycemia.
• Increased Neuronal Glucose, Increase Lactic Acid.
• Promote tissue Acidosis, contributes Neuronal Death.
During Hypoglycemia is also associated with Cerebral Injury.
• 40 mg/dl, Shift or Changes EEG Wave .
• 20 mg/dl, Suppression of the EEG (flat).
• Persistence of this level: Seizure and Neuronal Death.
glucose glucose 6-phosphate
ATP ADP
pyruvateCO2
ATP
ADP
ATP
H2O Oxygen
lactate
glucose glucose 6-phosphate
ATP
ADP
pyruvateCO2
ATP
ADP
ATP
H2O
X
XOxygen
lactate

11. INFLUENCE OF ANESTHETICS
ON THE ISCHEMIC BRAIN
BARBITURAT
Produce isoelectricity EEG extensively, (Gold Standard C. Protectants)
Have been efficacious in the treatment of Focal ischemia
Reduce of cerebral injury produced by M C A Occlusion.
Would not be to provide much benefit in Global ischemia.
Warner et. al;
Approximately a third of the dose required to achieve EEG
suppression, can a reduction in injury that is of similar
achieved with much larger doses.

12. INFLUENCE OF ANESTHETICS
ON THE ISCHEMIC BRAIN
PROPOFOL : ( Shares a number of properties with Barbiturates ).
In Particular :
Produce burst suppression of the EEG, reducing CMRO2 > 50%.
In Focal Ischemia, Reduced the E x t e n t of Cerebral Infarction.
Gelb’s Group Study Suggest :
Propofol NP Is not sustained beyond a period of One Week.
Provided that the severity of injury is Very Mild.
Efficacy of propofol is Similar to Volatile agents.

13. INFLUENCE OF ANESTHETICS
ON THE ISCHEMIC BRAIN
ETOMIDATE :
Reduce CMRO2 by up to 50% by producing EEG Burst Suppression.
Cleared rapidly, does not cause myocardial depression or hypotension.
In Global Ischemia :
Reduce Ischemic Injury. (hippocampus).
Reduce nitric oxide levels by inhibiting NOS or directly scavenging NO
In Focal Ischemia :
Actually Increased the volume brain infarction.

14. INFLUENCE OF ANESTHETICS
ON THE ISCHEMIC BRAIN
VOLATIL AGENT :
Isoflurane, Sevoflurane and Desflurane can EEG burst-suppression in
<1.5 MAC.
Isoflurane : to be neuroprotective in models of hemispheric, focal and
near complete ischemia.
Similarly, both sevoflurane and desflurane can reduce ischemic
cerebral injury.
There does not substantial difference among the volatile agents with
regard to neuroprotective efficacy.

15. INFLUENCE OF ANESTHETICS
ON THE ISCHEMIC BRAIN
VOLATIL AGENT :
Produce Neuroprotection after : S h o r t Recovery Periods.
Produce Long Term N P in the severity of injury is Very Mild.
Efficacy was not sustained when was : Extended to 2 weeks.
Volatile anesthetics Delay but do not prevent neuronal death.
Delaying Neuronal, Increase Duration Therapeutic Window.
For the administration of other agents that have N P Efficacy.

16. INFLUENCE HYPOTHERMIA
ON THE ISCHEMIC BRAIN
Hypothermia :
Hypothermia Protective Effect Greater in Restored After Ischemia.
Temperature (34 - 35°C) reduce the brain’s vulnerability to Ischemic Injury.
Induction Mild Hypothermia did not reduce Incidence New Cerebral Injury.
Mild Hypothermia inTBI: Reduced ICP and Improved Neurologic Outcome.
Hyperthermia :
Increases Brain Temperature During and After Ischemia : Aggravate Injury.
An Increase of 1° C can dramatically increase injury

17. HYPOTHERMIA
13th Congress of Neuro Anesthesiologist 2016,
Ujung Pandang – Indonesia

18. INFLUENCE OF SEIZURE
ON THE ISCHEMIC BRAIN
Seizures :
Intracranial Pathology : (Increased neuronal activity, Increased CBF and
CBV (consequently increased ICP) and Cerebral acidosis).
Untreated Seizures produce neuronal necrosis even with normal CPP.
Prevention and Rapid Treatment of seizures is an Important Goal.
Can be Rapidly Treated : BZD, Barbiturates, Etomidate and Propofol.
Antiepileptic : Phenytoin, Pentobarbital are often use.

19. SUMMARY
The Anesthetized Brain is less Vulnerable to ischemic injury than the awake brain.
EEG changes suggestive of severe ischemia are present.
Basic Methode Brain Protection are “ Corner Stone “
CPP, CBF, CBV maintained in “Normal Range”, MAP may increased up to 10 – 20 %.
Anesthetics Drugs may have Brain Protectection effect.
Volatile anesthetics do provide some Transient Protection (< 1,5 MAC)
Barbiturates, although long considered to be the gold standard.
Hypothermic methode are controversial, Hyperthermia should be avoided.
Insulin is Administered if glucose values exceed 180 mg/dl.
Close monitoring of BSL to ensure that Hypoglycemia does not develop

20. REFERENCE
1. Vincent AM1, McLean LL, Backus C, Feldman EL; FASEB J. 2005. “, Short-term
hyperglycemia produces oxidative damage and apoptosis in neurons.
Apr;19(6):638-40. Epub 2005 Jan 27
2. Malone JI, Hanna S, Saporta S, Mervis RF, Park CR, Chong L, Diamond DM;
Pediatr Diabetes. 2008 Dec;9(6):531-9. doi: 10.1111/j.1399-5448.2008.00431.x.
“Hyperglycemia not hypoglycemia alters neuronal dendrites and impairs
spatial memory.”
3. Sharma R, Buras E, Terashima T, Serrano F, Massaad CA, Hu L, et al. (2010)
Hyperglycemia Induces Oxidative Stress and Impairs Axonal Transport Rates
in Mice. PLoS ONE 5(10): e13463. doi:10.1371/journal.pone.0013463
4. Sang Won Suh et al; The Journal of Neuroscience, 19 November 2003, 23(33):
10681-10690;Hypoglycemic Neuronal Death and Cognitive Impairment Are
Prevented by Poly(ADP-Ribose) Polymerase Inhibitors Administered after
Hypoglycemia.