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BASIC CONCEPT ON
NEUROANESTHESIA
ISNACC
Objective
•To understand technique and anesthetic effect to reach
slack brain.
•To understand technique and anesthetic effect to CBF,
ICP, autoregulation, CO2 reactivity, CMRO2.
•To understand perioperative management.
•To understand mechanism of brain protection and how to
give brain protection.
Cotrell J.E. : Anesthesia for
Neurosurgery, 1994
 New diagnostic equipment
 New monitoring equipment
 New anesthetics
 New understanding common drugs for
neuroanesthesia.
Will be improve outcome in patient with intracranial
disorder.
Anesthesiologist target in
neurosurgery
 Control ICP and brain volume.
 Brain protection from ischemia and injury.
 Less bleeding
Nancye Edwards : Principles and Practice of Neuro anaesthesia,
1991
The relation ICP and mortality
in brain injury
Mean ICP (mm Hg) Mortality (%)
0 - 20 19
21 - 40 28
41 - 80 79
Miller JD : Head injury and brain ischemia
implication for therapy
Br. J Anaesth. 57 : 120 - 129 , 1985
Figure: Idealized intracranial pressure volume relationships. From: Shapiro, H.M.
Intracranial hypertension: Therapeutic and anaesthetic considerations.
Anesthesiology 43: 445-471, 1975
Autoregulation:
• Keep until 1,5 MAC Sevoflurane
Gupta et al, Br.J.Anaeth,1997
Summors et al, Anesth Analg , 1999.
• Autoregulation loss at 1,5 MAC Isofluran.
Matta et al, Anesth Analg, 1999.
• One of reasoning: effect dilatation Sevo < Iso
Lam JMK et al, J. Neurosurg, 1997
auto regulation + 5/10 Good outcome
auto regulation + 4/10 Good outcome
auto regulation – severe disability 2
death 9
Mild head injury : 9/29 impairment autoregulation
Methods of brain protection
•Basic methods
•Hypothermia - low normothermia
•Pharmacology
Intravenous Anesthetic : pentothal
Inhalation anesthetics: Sevoflurane
Lidocaine
Mannitol, Magnesium
Erythropoietin
Alpha 2 agonists dexmedetomidine
Basic methods
• Control airway, adequate oxygenation, avoidance
hypoxia, hypercapnia (keep normocapnia).
• Hyperventilation only if herniation present.
• Control of BP/Maintenance of CPP normotension or
induce hypertension 10-20%. CPP >70 mmHg.
• Control ICP (CPP = MAP – ICP). Therapy if ICP 20
mmHg.
• Correction of acidosis, electrolyte imbalance,control
plasma glucose concentration
Mortality:
Head injury with :
Hypoxia : 56%
Hypovolemia : 64%
Hypoxia + Hypovolemia : 76%
Without hypoxia+Hypovolemia : 27%
Asean Congress of Anaesthesiologist, Singapore, 1995.
Anesthesia management :
b
 A = Clear airway
 B = Control ventilation, normocapnia at TBI and slight
hypocapnia at brain tumor.
 C = Avoid high increase or decrease of BP, avoid
increase of cerebral venous pressure. normovolemia,
iso-osmoler.
 D = Avoid drugs & anesthesia technique will increase
ICP, give drugs with brain protection effect.
 E = environment (temperature control) target 35
degree C in OR
Airway
•Clear airway at all the operation and anesthesia.
•Non kinking ETT
•hypoxia or hypercarbia dangerous to patient.
Ventilation to reach :
PaO2 : 100 - 200 mmHg
PaCO2 : 25 - 30 mmHg
for brain tumor surgery
PaCO2 : Normocapnia
in brain injury
Avoid PaCO2 < 20 mmHg
Control ventilation
Regulation BP
 Hypotension :
CPP = MAP - ICP
prefer systolic 90 - 100 mmHg (tumor)
Normotension (trauma)
 Hypertension :
- increase CBV, ICP, edema, blood loss.
- during laringoscopy/intubation,
inserting head pin, skin incision, extubation
Mechanical factor which increase
cerebral venous pressure
 Coughing, bucking
 Trendelenburg
 Neck large vein obstruction
 Abdominal pressure
 PEEP
 internal jugular vein / subclavia vein canulation
Preoperative evaluation
 Similar with routine assessment
 Add : - evaluation ICP, side effect therapy
- CT Scan, MRI
 Premedication :
- avoid narcotic
- diazepam 0,15 mg/kg po
- midazolam 0,025 - 0,05 mg/kg im
Intraoperative anesthetics
1. Monitoring
2. Induction of anesthesia
3. Maintenance of anesthesia :
- inhalation anesthetics (Sevoflurane, isoflurane)
- intra venous anesthetics (pentothal)
- brain relaxation
- Fluid management
4. Emergence and immediate postoperative
Monitoring
 Routine monitoring
 ECG, non invasive BP, CVP, invasive BP (artery line),
FiO2, pulse oximetry, temperature, peripheral nerve
stimulator, catheter urine.
Indication for inserting
artery line
 Rapid changes of BP
 Risk of rapid blood loss.
 Hypotension technique
 Pathologic condition
 Need postoperative ventilation.
Indication for CVP monitoring
 Severe blood loss
 Measurement status volume
 Sitting position / fossa posterior surgery
 vasoactive drugs route
ICP Monitoring
 still controversial
 tumor > 3 cm Need ICP monitoring
 Edema
Target induction of anesthesia
 Control of PaCO2
 Control of BP
 Avoid drainage obstruction of cerebral vein
 Adequate oxygenation & ventilation
 Avoid awareness
Induction of anesthesia
 O2 100%
 Fentanyl 1 - 3 ug/kg
 Pentothal 5 mg/kg 2,5 mg/kg
 Lidocaine 1 - 1,5 mg/kg
 Norcuron 0,1 - 0,15 mg/kg
 oropharyngeal airway
 eye ointment; paper tape.
Technique to avoid increase BP
 Deeper anesthesia: Pentothal
 Narcotic : Fentanyl, Sufentanil
 Nitroprusside ?
 Glyseril trinitrat ?
 Lidocaine 1-1,5 mg/kg iv
 Alpha 2 agonist dexmedetomidine
Hypotension during induction of
anesthesia :
 Elevation extremities, not trendelenburg
 Give crystalloid, colloid
 Vasopressor : if under lower limit of autoregulation
Choice of induction agent
Smooth induction more important than really
drugs combination
Pentothal 3 - 4 mg/kg
Fentanyl 3 - 5 ug/kg
Vecuronium 0,1 - 0,15 mg/kg
or Rocuronium 0,6 - 0,8 mg/kg
or Atracurium 0,5 mg/kg
Maintenance of anesthesia
 Less effect to cerebral autoregulation and response to
CO2
 Stable cardiovascular
 Capable to decrease ICP and increase CPP
 One of choice : pentothal, O2 + Sevoflurane, fentanyl,
relaxant.
Choice of inhalation anesthetics
•Inhalation anesthetic should be evaluated effect on ICP
and cerebral vasculature.
•All inhalation anesthetic has cerebral vasodilatation effect,
will increase CBF, CBV and ICP.
•Must be know the effect on cerebral autoregulation,
response to CO2 reactivity and CMRO2, brain protection
effect.
Variable Halothane Enflurane Isoflurane Sevoflurane
BP
Vascular resistance
Cardiac output
Cardiac contraction
CVP
Heart rate
Sensitization of the
heart to epinephrine
↓ ↓
0
↓ ↓
↓
↑
0
↑ ↑ ↑
↓ ↓
↓
↓ ↓
↓ ↓
↑
↑
↑
↓ ↓
↓ ↓
0
0
0
↑ ↑
0?
↓
↓ ↓
0
0
0
0 ↑
0
Cardiovascular effect of volatile inhalation
anesthetics at 1-1,5 MAC
0 = no change (<10%)
↓ = 10-20% decrease
↓ ↓ = 20-40% decrease
↑ =
Anoxia NMDA/AMPA
Protect
Response
Improve
NA+
Improve
ATP
Improve
Ca+
Protect
Response
Thiopental (600 μM) Yes Yes No/Yes
1
Yes Yes
Midazolam (100 μM) Yes - Yes Yes -
Propofol (20 μg/ml) No Yes Yes Yes No
Lidocaine (10 μM) Yes Yes Yes No -
Isoflurane (1,5%) No No No No -
Sevoflurane (4%) Yes Yes Yes Yes -
Etomidate
3 μg/ml No No No - -
30 μg/ml No Yes No - -
Nitrous oxide (50%) No No No No -
1
Worsens ATP after 3.5 minutes of anoxia:
improves ATP after 10 minutes of anoxia.
Effect of Anesthetics on Physiological ResponsesEffect of Anesthetics on Physiological Responses
and Ion and Metabolite Levelsand Ion and Metabolite Levels
Cottrell JE. ESA, 2004,Lisbon
Maintenance of anesthesia :
 First choice : Sevoflurane
 Second choice : Isoflurane
 TOF : 0
 fluid : 2/3 diuresis
 Mannitol : 0,25 - 1 gr/kg
 Lasix : 0,5 - 1 mg/kg
Fluid
 Stable circulation
 To avoid : hypovolemia, hypervolemia, hypoosmoler,
hyperglycaemia
 First choice NaCl 0,9%, avoid RL, no dextrose: 1-1,5
ml/kg/h or 2/3 diuresis.
 Dextrose : only for therapy hypoglycaemia (blood sugar <
60 mg%)
Extubation
 Be carefully : increase of BP, leading to hyperaemia,
edema, increase of ICP.
 Lidocaine 1 - 1,5 mg/kg, alpha 2 agonist
dexmedetomidine.
 End of surgery increase TOF = 1
 Et CO2 normal
 Difficult to make decision criteria when extubation.
Postoperative periode
 Avoid coughing, bucking, stretching, increase BP.
 Neurological evaluation immediately.
 Mostly extubated at OR
 Lidocaine 1,5 mg/kg, dexmedetomidine, vasodilator,
esmolol to avoid increase BP.
 Analgetics : avoid ketorolac
Immediate or delayed recovery?
• Delayed recovery cannot be recommended as a mechanism of
limiting the metabolic and hemodynamic consequences from
emergence after neurosurgery
Bruder N et al, Anesth Analg 1999; 89(3)
• Awake craniotomy have less PONV than GA.
Manninen P et al. J.of Clin Anesth 2002;14(4)
• Fast-track NA including local anesthetic, combined GA and
local anesthetic, GA with SAFE drug.
Advantages Early awakening
• Earlier neurological examination.
• Earlier indications for further investigations.
• Less hypertension, less catecholamine burst.
• Lower cost
Disadvantages early awakening
• Increased risk of hypoxemia, hypercarbia
• Difficult respiratory monitoring during transfer to the ICU.
• Hypothermia?
Condition for early emergence: systemic
homeostasis
•Normothermia (>36o
C).
•Normovolemia, normotension
(70mmHg<MAP<120mmHg)
•Mild hypocapnia (PaCO2 35 mmHg)
•Normoglycemia (glucose 4-8 mmol/l)
•No hypoosmolality (285 ±5mOsm/kg)
•Hematocrit > 25%
•No coagulation disorder
Conditions for early emergence : brain
homeostasis
• Normal CMRO2 and CBF
• Normal ICP at the end of surgery
• Antiepileptic prophylaxis
• Adequate head up position
• Intact cranial nerves for airway protection
Check-list before attempting early
extubation
Adequate pre-operative state of consciousness.
Limited brain injury, no major brain laceration.
No extensive posterior fossa surgery involving
cranial nerves IX-XII
No major AVM resection: risk of malignant post
operative edema,
Normal body temperature and oxygenation,
cardiovascular stability.
Suggested awakening sequence (1)
Prepare awakening (aim: avoid post operative
respiratory depression).
•Discontinue middle or long acting opioid approx
60 min before planned emergence.
•Stop anesthetic administration during skin
closure.
•Let neuromuscular block decrease to 2/4 if
myorelaxation used. Antagonise myorelaxant
before extubation.
•Progressive rise of PaCO2 to normoventilation
Suggested awakening sequence (2)
•Avoid unnecessary painful stimuli: remove
head pins as early as possible, remove packing
—performed adequate suctioning before the
patient is fully awake.
•Treat BP bursts: treat hypertension due to
nociception, goal MAP < 120 mmHg
(dexmedetomidine, lidocaine, beta blocker).
•Transfer to PACU or ICU: O2, continuous
monitoring (ECG,BP, SpO2)
Systemic and cerebral condition
making delayed emergence
systemic cerebral
Hypothermia (<35,5oC)
Hypertension ( SBP > 150
mmHg)
Hypotension-hypovolemia
Hematocrit < 25%
Hypoxia or hypercapnia
Ineffective spontaneous
ventilation
Hypoosmolality (<280 mOsm/kg)
Disorder of coagulation
Residual neuromuscular block
Preoperative altered
consciousness
Large tumor resection with midline
shift
Long lasting surgery (>6 hours)
Intraoperative brain swelling
Injury to cranial nerves (IX,X,XII)
Convulsions during emergence
Summary
1. Avoiding secondary brain injury will decrease
morbidity and mortality.
2. Choice of anesthetics and technique of anesthesia will
improve outcome.
3. knowledge neurophysiology and neuropharmacology
fully help in patient management.
Lecture 1 basic  concept  on neuroanesthesia 2

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Lecture 1 basic concept on neuroanesthesia 2

  • 2. Objective •To understand technique and anesthetic effect to reach slack brain. •To understand technique and anesthetic effect to CBF, ICP, autoregulation, CO2 reactivity, CMRO2. •To understand perioperative management. •To understand mechanism of brain protection and how to give brain protection.
  • 3. Cotrell J.E. : Anesthesia for Neurosurgery, 1994  New diagnostic equipment  New monitoring equipment  New anesthetics  New understanding common drugs for neuroanesthesia. Will be improve outcome in patient with intracranial disorder.
  • 4. Anesthesiologist target in neurosurgery  Control ICP and brain volume.  Brain protection from ischemia and injury.  Less bleeding Nancye Edwards : Principles and Practice of Neuro anaesthesia, 1991
  • 5. The relation ICP and mortality in brain injury Mean ICP (mm Hg) Mortality (%) 0 - 20 19 21 - 40 28 41 - 80 79 Miller JD : Head injury and brain ischemia implication for therapy Br. J Anaesth. 57 : 120 - 129 , 1985
  • 6. Figure: Idealized intracranial pressure volume relationships. From: Shapiro, H.M. Intracranial hypertension: Therapeutic and anaesthetic considerations. Anesthesiology 43: 445-471, 1975
  • 7.
  • 8.
  • 9. Autoregulation: • Keep until 1,5 MAC Sevoflurane Gupta et al, Br.J.Anaeth,1997 Summors et al, Anesth Analg , 1999. • Autoregulation loss at 1,5 MAC Isofluran. Matta et al, Anesth Analg, 1999. • One of reasoning: effect dilatation Sevo < Iso
  • 10. Lam JMK et al, J. Neurosurg, 1997 auto regulation + 5/10 Good outcome auto regulation + 4/10 Good outcome auto regulation – severe disability 2 death 9 Mild head injury : 9/29 impairment autoregulation
  • 11. Methods of brain protection •Basic methods •Hypothermia - low normothermia •Pharmacology Intravenous Anesthetic : pentothal Inhalation anesthetics: Sevoflurane Lidocaine Mannitol, Magnesium Erythropoietin Alpha 2 agonists dexmedetomidine
  • 12. Basic methods • Control airway, adequate oxygenation, avoidance hypoxia, hypercapnia (keep normocapnia). • Hyperventilation only if herniation present. • Control of BP/Maintenance of CPP normotension or induce hypertension 10-20%. CPP >70 mmHg. • Control ICP (CPP = MAP – ICP). Therapy if ICP 20 mmHg. • Correction of acidosis, electrolyte imbalance,control plasma glucose concentration
  • 13. Mortality: Head injury with : Hypoxia : 56% Hypovolemia : 64% Hypoxia + Hypovolemia : 76% Without hypoxia+Hypovolemia : 27% Asean Congress of Anaesthesiologist, Singapore, 1995.
  • 14. Anesthesia management : b  A = Clear airway  B = Control ventilation, normocapnia at TBI and slight hypocapnia at brain tumor.  C = Avoid high increase or decrease of BP, avoid increase of cerebral venous pressure. normovolemia, iso-osmoler.  D = Avoid drugs & anesthesia technique will increase ICP, give drugs with brain protection effect.  E = environment (temperature control) target 35 degree C in OR
  • 15. Airway •Clear airway at all the operation and anesthesia. •Non kinking ETT •hypoxia or hypercarbia dangerous to patient.
  • 16. Ventilation to reach : PaO2 : 100 - 200 mmHg PaCO2 : 25 - 30 mmHg for brain tumor surgery PaCO2 : Normocapnia in brain injury Avoid PaCO2 < 20 mmHg Control ventilation
  • 17. Regulation BP  Hypotension : CPP = MAP - ICP prefer systolic 90 - 100 mmHg (tumor) Normotension (trauma)  Hypertension : - increase CBV, ICP, edema, blood loss. - during laringoscopy/intubation, inserting head pin, skin incision, extubation
  • 18. Mechanical factor which increase cerebral venous pressure  Coughing, bucking  Trendelenburg  Neck large vein obstruction  Abdominal pressure  PEEP  internal jugular vein / subclavia vein canulation
  • 19. Preoperative evaluation  Similar with routine assessment  Add : - evaluation ICP, side effect therapy - CT Scan, MRI  Premedication : - avoid narcotic - diazepam 0,15 mg/kg po - midazolam 0,025 - 0,05 mg/kg im
  • 20. Intraoperative anesthetics 1. Monitoring 2. Induction of anesthesia 3. Maintenance of anesthesia : - inhalation anesthetics (Sevoflurane, isoflurane) - intra venous anesthetics (pentothal) - brain relaxation - Fluid management 4. Emergence and immediate postoperative
  • 21. Monitoring  Routine monitoring  ECG, non invasive BP, CVP, invasive BP (artery line), FiO2, pulse oximetry, temperature, peripheral nerve stimulator, catheter urine.
  • 22. Indication for inserting artery line  Rapid changes of BP  Risk of rapid blood loss.  Hypotension technique  Pathologic condition  Need postoperative ventilation.
  • 23. Indication for CVP monitoring  Severe blood loss  Measurement status volume  Sitting position / fossa posterior surgery  vasoactive drugs route
  • 24. ICP Monitoring  still controversial  tumor > 3 cm Need ICP monitoring  Edema
  • 25. Target induction of anesthesia  Control of PaCO2  Control of BP  Avoid drainage obstruction of cerebral vein  Adequate oxygenation & ventilation  Avoid awareness
  • 26. Induction of anesthesia  O2 100%  Fentanyl 1 - 3 ug/kg  Pentothal 5 mg/kg 2,5 mg/kg  Lidocaine 1 - 1,5 mg/kg  Norcuron 0,1 - 0,15 mg/kg  oropharyngeal airway  eye ointment; paper tape.
  • 27. Technique to avoid increase BP  Deeper anesthesia: Pentothal  Narcotic : Fentanyl, Sufentanil  Nitroprusside ?  Glyseril trinitrat ?  Lidocaine 1-1,5 mg/kg iv  Alpha 2 agonist dexmedetomidine
  • 28. Hypotension during induction of anesthesia :  Elevation extremities, not trendelenburg  Give crystalloid, colloid  Vasopressor : if under lower limit of autoregulation
  • 29. Choice of induction agent Smooth induction more important than really drugs combination Pentothal 3 - 4 mg/kg Fentanyl 3 - 5 ug/kg Vecuronium 0,1 - 0,15 mg/kg or Rocuronium 0,6 - 0,8 mg/kg or Atracurium 0,5 mg/kg
  • 30. Maintenance of anesthesia  Less effect to cerebral autoregulation and response to CO2  Stable cardiovascular  Capable to decrease ICP and increase CPP  One of choice : pentothal, O2 + Sevoflurane, fentanyl, relaxant.
  • 31. Choice of inhalation anesthetics •Inhalation anesthetic should be evaluated effect on ICP and cerebral vasculature. •All inhalation anesthetic has cerebral vasodilatation effect, will increase CBF, CBV and ICP. •Must be know the effect on cerebral autoregulation, response to CO2 reactivity and CMRO2, brain protection effect.
  • 32. Variable Halothane Enflurane Isoflurane Sevoflurane BP Vascular resistance Cardiac output Cardiac contraction CVP Heart rate Sensitization of the heart to epinephrine ↓ ↓ 0 ↓ ↓ ↓ ↑ 0 ↑ ↑ ↑ ↓ ↓ ↓ ↓ ↓ ↓ ↓ ↑ ↑ ↑ ↓ ↓ ↓ ↓ 0 0 0 ↑ ↑ 0? ↓ ↓ ↓ 0 0 0 0 ↑ 0 Cardiovascular effect of volatile inhalation anesthetics at 1-1,5 MAC 0 = no change (<10%) ↓ = 10-20% decrease ↓ ↓ = 20-40% decrease ↑ =
  • 33. Anoxia NMDA/AMPA Protect Response Improve NA+ Improve ATP Improve Ca+ Protect Response Thiopental (600 μM) Yes Yes No/Yes 1 Yes Yes Midazolam (100 μM) Yes - Yes Yes - Propofol (20 μg/ml) No Yes Yes Yes No Lidocaine (10 μM) Yes Yes Yes No - Isoflurane (1,5%) No No No No - Sevoflurane (4%) Yes Yes Yes Yes - Etomidate 3 μg/ml No No No - - 30 μg/ml No Yes No - - Nitrous oxide (50%) No No No No - 1 Worsens ATP after 3.5 minutes of anoxia: improves ATP after 10 minutes of anoxia. Effect of Anesthetics on Physiological ResponsesEffect of Anesthetics on Physiological Responses and Ion and Metabolite Levelsand Ion and Metabolite Levels Cottrell JE. ESA, 2004,Lisbon
  • 34. Maintenance of anesthesia :  First choice : Sevoflurane  Second choice : Isoflurane  TOF : 0  fluid : 2/3 diuresis  Mannitol : 0,25 - 1 gr/kg  Lasix : 0,5 - 1 mg/kg
  • 35. Fluid  Stable circulation  To avoid : hypovolemia, hypervolemia, hypoosmoler, hyperglycaemia  First choice NaCl 0,9%, avoid RL, no dextrose: 1-1,5 ml/kg/h or 2/3 diuresis.  Dextrose : only for therapy hypoglycaemia (blood sugar < 60 mg%)
  • 36. Extubation  Be carefully : increase of BP, leading to hyperaemia, edema, increase of ICP.  Lidocaine 1 - 1,5 mg/kg, alpha 2 agonist dexmedetomidine.  End of surgery increase TOF = 1  Et CO2 normal  Difficult to make decision criteria when extubation.
  • 37. Postoperative periode  Avoid coughing, bucking, stretching, increase BP.  Neurological evaluation immediately.  Mostly extubated at OR  Lidocaine 1,5 mg/kg, dexmedetomidine, vasodilator, esmolol to avoid increase BP.  Analgetics : avoid ketorolac
  • 38. Immediate or delayed recovery? • Delayed recovery cannot be recommended as a mechanism of limiting the metabolic and hemodynamic consequences from emergence after neurosurgery Bruder N et al, Anesth Analg 1999; 89(3)
  • 39. • Awake craniotomy have less PONV than GA. Manninen P et al. J.of Clin Anesth 2002;14(4) • Fast-track NA including local anesthetic, combined GA and local anesthetic, GA with SAFE drug.
  • 40. Advantages Early awakening • Earlier neurological examination. • Earlier indications for further investigations. • Less hypertension, less catecholamine burst. • Lower cost
  • 41. Disadvantages early awakening • Increased risk of hypoxemia, hypercarbia • Difficult respiratory monitoring during transfer to the ICU. • Hypothermia?
  • 42. Condition for early emergence: systemic homeostasis •Normothermia (>36o C). •Normovolemia, normotension (70mmHg<MAP<120mmHg) •Mild hypocapnia (PaCO2 35 mmHg) •Normoglycemia (glucose 4-8 mmol/l) •No hypoosmolality (285 ±5mOsm/kg) •Hematocrit > 25% •No coagulation disorder
  • 43. Conditions for early emergence : brain homeostasis • Normal CMRO2 and CBF • Normal ICP at the end of surgery • Antiepileptic prophylaxis • Adequate head up position • Intact cranial nerves for airway protection
  • 44. Check-list before attempting early extubation Adequate pre-operative state of consciousness. Limited brain injury, no major brain laceration. No extensive posterior fossa surgery involving cranial nerves IX-XII No major AVM resection: risk of malignant post operative edema, Normal body temperature and oxygenation, cardiovascular stability.
  • 45. Suggested awakening sequence (1) Prepare awakening (aim: avoid post operative respiratory depression). •Discontinue middle or long acting opioid approx 60 min before planned emergence. •Stop anesthetic administration during skin closure. •Let neuromuscular block decrease to 2/4 if myorelaxation used. Antagonise myorelaxant before extubation. •Progressive rise of PaCO2 to normoventilation
  • 46. Suggested awakening sequence (2) •Avoid unnecessary painful stimuli: remove head pins as early as possible, remove packing —performed adequate suctioning before the patient is fully awake. •Treat BP bursts: treat hypertension due to nociception, goal MAP < 120 mmHg (dexmedetomidine, lidocaine, beta blocker). •Transfer to PACU or ICU: O2, continuous monitoring (ECG,BP, SpO2)
  • 47. Systemic and cerebral condition making delayed emergence systemic cerebral Hypothermia (<35,5oC) Hypertension ( SBP > 150 mmHg) Hypotension-hypovolemia Hematocrit < 25% Hypoxia or hypercapnia Ineffective spontaneous ventilation Hypoosmolality (<280 mOsm/kg) Disorder of coagulation Residual neuromuscular block Preoperative altered consciousness Large tumor resection with midline shift Long lasting surgery (>6 hours) Intraoperative brain swelling Injury to cranial nerves (IX,X,XII) Convulsions during emergence
  • 48. Summary 1. Avoiding secondary brain injury will decrease morbidity and mortality. 2. Choice of anesthetics and technique of anesthesia will improve outcome. 3. knowledge neurophysiology and neuropharmacology fully help in patient management.

Editor's Notes

  1. Teknik dan obat anestesi dapat mempengaruhi outcome pasien. Oleh karena itu pengertian mengenai patofisiologi kelainan serebral, teknik dan obat anestesi serta alat pantau yang yang digunakan untuk mngetahui keadaan pasien sangat memegang peranan penting.
  2. Tujuan dari topik ini adalah untuk mengerti tentang pengaruh dari teknik dan obat anestesi untuk mendapatkan otak yang kempis (slack brain) selama tindakan pembedahan, pengaruhnya pada aliran darah otak, tekanan intrakranial, autoregulasi, reaktivitas pembuluh darah terhadap CO2, serta pada metabolisme otak. Tujuan lain adalah untuk mengerti pengelolaan pasien pada periode perioperatif (prabedah, slama pembedahan, dan pascabedah, dan untuk mengerti bagaimana membverikan protekasi otak selama periode perioperatif.
  3. Professor James Cottrell dari SUNY (State University of New York) dalam Anesthesia for Neurosurgery mengatakan bahwa dengan ditemukannya alat diagnostik yang baru (misalnya CT-scan, MRI, MRI kontras ), alat pantau yang baru (SJO2 untuk memantau oksigenasi otak), obat anestesi yang baru (Sevofluran), serta pengertian baru mengenai obat yang bisas dipakai (RL bersifat hipoosmoler yang dapat meningkatkan edema otak), akan memperbaiki pasien dengan kelainan serebral.
  4. Sasaran ahli anestesi dalam memeberikan anestesi pada pasien bedah saraf adalah untuk mengendalikan tekanan intrakranial serta volume otak, memeberikan proterksi otak akibat iskemia dan injury, serta mengurangi perdarahan. Adanya otak yang kembung akibat peningkatan tekanan intrakranial akan menyebabkan iskemia akibat retraksi ahli bedah atau robekan jaringan otak oleh tulang selain akan menambah iskemia karena penurunan tekanan perfusi otak.
  5. Pengendalian tekanan intrakranial sangat penting dan harus segera dilakukan, karena makin tekanan intrakranial, maka makin tinggi mortalitas. Bila tekanan intrakrnial  20 mmHg maka terpai untuk menurunkan tekanan intrakranial harus segera dilakukan.
  6. Isi ringga kranium terdiri dari jaringan otak, darah,serta likuor serebrospinal. Tekanan intrakrnial normal 5-15 mmHg. Peningkatan salah satu komponen isi ronggra kranium akan dikompensasi dengan menurunkan komponen lain dan yang pertama adalah menurunkan volume likuor serebrospinal, sehingga walaupun ada penambahan komponen tersebut tekanan intrakranial masih dalam batas normal ( pada gambar adalah daerah 1 sampai 2). Akan tetapi, bila batas kompensasi dilalui maka terjadi peningkatan tekanan intrakranial (2 sampai 4).
  7. Gambar ini menunjukkan patofisiologi peningkatan tekanan intrakranial yang tidak terkendali, yang hasil akhirnya dalah kematian sel=sel otak. Kotak yang diberi tanda bintang adalah bagian dimana dokter anestesi dapat ikiut berperan. Sebagai contoh, pengaturan tekanan darah, karena hipotensi atau hipertensi akan menimbulkan keadaan yang sama walaupun mekanismenya berbeda. Demikian juga posisi pasien, pemilihan obat anestesi akan memegang peranan penting dalam mengendalikan tekanan intrakranial.
  8. Dasar neuroanestesi adalah pengertian tentang aliran darah otak. Aliran darah otak otak dipertahankan kira-kira 50-54 ml/100 gr jaringan/menit. Faktor utama yang mengengaturnya adalah autoregulasi, PaCO2, dan PaO2. Aliran darah otak tetap konstan 50-54 ml/100 gr jaringan/menit pada tekanan arteri rerata 50-150 mmHgkarena pembuluh darah akan berkonstriksi dan berdilatasi. Bila tekanan arteri rerata &amp;lt; 50 mmHg terjadi penurunan aliran darah otak dan kalan makin menurun terjadi iskemia dan infark otak. Peningkatan tekanan arteri rerata &amp;gt; 150 mmHg akan menyebabkan hilangnya kemampuan vasokonstriski dan terjadi kerusakan BBB dan dapat terjadi edema otak dan perdarahan otak. Perubahan 1 mmHg PaCO2 dari 24-80 mmHg akan merubah aliran darah otak sebesar 4% (kira-kira 1,75 ml/100g/menit), hiperkaribia kan menyebabkan serebral vasodilatasi dan hipokaribi akan menimbulkan serebral vasokonstriksi. Adanya hipoksia (PaO2 &amp;lt; 60 mmHg) akan meningkatkan aliran darah otak. Peningkatan aliran darah otak ini akan menyebabkan edema otak dan peningkatan tekanan intrakranial.
  9. Penagaturan PaCO2 dan PaO2 dapat diataur dengan cara melakukan ventilasi mekanis serta kadar O2 yang diberikan. Saat pemberian anestesi supaya efek autoregulasi tetap ada, maka harus dipertimbangkna penggunaan obat anestesi yang akan tetapi mem[pertthanakn autoregulasi aselama pemberain anestesi. Sebagai contok, yang disampai oleh Gupta et al, Summors etal serta Matta et al bahwa autoregulasi tetap intact bila diberikan anestesi dengan Sevofluran sampai 1,5 MAC, salah satu alasannya adalah efek serebral vasodilatasi sevofluran &amp;lt; daripada isofluran ( MAC Sevofluran 2,08) tapi hilang pada 1,5 MAC Isofluran, dengan demikian selama anestesi berikan Sevofluran &amp;lt; 3 vol % atau isofluran &amp;lt; 2 vol%).
  10. Mekanaisme mempertahankan autoregulasi selama anestesi adalah sangat penting. Lam 1997 menyampaikan bahwa pada cedera kepala, intactnya autoregulasi akan berhubungan dengan mortalitas, serta harus diingat bahwa pada cedera kepala ringanpun ternya 9 dari 29 pasien autoregulasinya terganggu. Bila autoregulasi hilang, dari 11 pasien 2 pasien dari penilaian GOS (Glasgow Outcome Scale) menunjukkan 2 severe disability dan 9 pasien meninggal.
  11. Selama periode perioperatif (prabedah di UGD, selama pembedahan, atau pascabedah di ICU atau ruangan perawatan lainnya) harus diingat untuk melakukan proteksi otak akibat cedera sekunder. Proteksi otak dapat dilakukan dengan metode dasar (ABC resusitasi), hipotermi, atau dengan obat (Pharmacological Brain Protection).
  12. Basic method merupakan ABC resusitasi. A adalah airway, jalan nafas harus bebas sepanjang waktu. B, breathing adalah mengatur ventilasi untuk mendapatkan oksigenasi adekuat/menghindari hipoksia dan menghindari hiperkapnia dengan target normokapnia. Hiperventilasi hanya dilakukan bila ada tanda herniasi. C, Circulation adalah untuk mengenedalikan tekanan darah dengan target normotensi atau menaikkan tekanan darah 10-20% dari tekanan darah asal, target CPP &amp;gt; 70 mmHg. Terapi bila ICP &amp;gt; 20 mmHg. Koreksi asidosis, ketidak seimbangan elektrolit, guladar jangan &amp;gt; 150 mg%. Bila &amp;gt; 200 mg% beri insulin, Bila &amp;lt; 60 mg&amp; beri glukosa.