BASIC CONCEPT ON NEUROANESTHESIA

Tatang Bisri

Objective

To understand technique and anesthetic effect to reach slack brain. To understand technique and anesthetic effect to CBF, ICP, 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)
0 - 20 21 - 40 41 - 80

Mortality (%)
19 28 79

Miller JD : Head injury and brain ischemia implication for therapy Br. J Anaesth. 57 : 120 - 129 , 1985

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

Intravenous anesthetics
Barbiturate Ca influx Block Na channel Free radicals inhibition formation. Extracellular lactate, glutamate, aspartat Propofol: glutamate excotoxicity neuronal damage. propofol infus syndrome

Mortality:
Head injury with :

Hypoxia

: 56%

Hypovolemia
Hypoxia + Hypovolemia

: 64%
: 76%

Without hypoxia+Hypovolemia : 27%

Asean Congress of Anaesthesiologist, Singapore, 1995.

Figure: Idealized intracranial pressure volume relationships. From: Shapiro, H.M. Intracranial hypertension: Therapeutic and anaesthetic considerations. Anesthesiology 43: 445-471, 1975

FIG 2 - 4. Representation of brain function related to two measures of oxygenation ( arterial oxygen partial pressure ( Pa O2 ) and delivered oxygen ( D O2 ) ) and two measures of perfusions (cerebral blood flow ( CBF ) and cerebral perfusions pressures ( CVP ) ).

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.

Control ventilation
Ventilation to reach :
PaO2 : 100 - 200 mmHg 25 - 30 mmHg for brain tumor surgery PaCO2 :

PaCO2 : Normocapnia in brain injury Avoid PaCO2 < 20 mmHg

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 v. jugularis interna/v. subclavia 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 - children : midazolam 0,75 mg/kg po

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
Edema

Need ICP moni toring

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
Vecuronium

3 - 5 ug/kg
0,1 - 0,15 mg/kg

or Rocuronium
or Atracurium

0,6 - 0,8 mg/kg

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.

Cardiovascular effect of volatile inhalation anesthetics at 1-1,5 MAC

Variable
BP Vascular resistance Cardiac output Cardiac contraction CVP Heart rate Sensitization of the heart to epinephrine 0 = = = = no change (<10%) 10-20% decrease 20-40% decrease increase

Halothane Enflurane Isoflurane Sevoflurane

0 0 0 0 0 0? 0 0 0 0 0

N2O
60% N2O : CBF 100% CMR O2 20% Can decrease by Pentothal, Opioid, Hypocapnia. Frequent of emesis 90% Avoid in aerocele, until 5 days after pneumoencephalography, risk of air embolism, redo craniotomy < 3 weeks. Dont use N2O (Cottrell, 2001,2002)

N2O

Increases neurotoxicity of NMDA in rats Potentiated the NMDA damage Adding ketamine worsens damaged neuron.
Cottrell. ESA 2004

Adding a nontoxic dose of N2O to midazolam/isoflurane anesthetic resulted in a robust neurodegenerative reaction more severe in the thalamus and parietal cortex
Jevtovic et al. J neuroscience 2003

Halothane :
Smallest decrease CMR O2 CBF increase 3 x isoflurane With N2O, CBF increase 300% Autoregulation loss at > 1 MAC and persistent until post operative period. CSF : production and absorption increase ICP increase whereas hypocarbia BBB & B-CSF barierre : destroyed Increase brain water, permeability BBB, edema concentration 2% mitochondria destroyed myocardium sensitization to catecholamine

Stone DJ et al : The Neuroanaesthesia Hand Book, 1996 Cottrell JE : Anesthesia and Neurosurgery, 1994

Enflurane :
Can produce EEG seizure at moderate dose (1,5 - 2 MAC) and hypocapnia. CMR O2 decrease CSF : increase production, decrease absorption

cerebral ischemia protection better than halothane but less than isoflurane.
Loss autoregulation : 1 MAC

Not advised for neuroanesthesia

Isoflurane :
concentration 0,5% 0,95% CBF decrease CBF increase

Increased ICP with Isoflurane 1% easy reduce with hypocapnia / pentothal Autoregulation intact until 1,5 MAC CO2 Response intact until 2,8 MAC CSF : production : no change absorption increase Increase ICP caused by Isoflurane Enflurane/halothane

: 30 minutes : 3 hours

Stone D.J et al : The Neuroanaesthesia Hand Book, 1996 Cottrell : Anesthesia and Neurosurgery, 1994

Isoflurane

Isoflurane only transient protective against a severe focal ischemic insult. Isoflurane did not inhibit postischemic neuronal apoptosis. Conclusion: Isoflurane have not brain protection effect.
Werner C. AOSRA Nov 2003, WCA 2004, ESA 2004. Cottrell JE: WCA 2004, ESA June 2004 Kawaguchi et al. Anesth Analg 2004 Warner DS.Anesth Analg 2004

sevoflurane

Sevoflurane improves neurological outcome following incomplete cerebral ischemia in rat.

Werner C et al.Br J Anesth 1995;83

Isoflurane delay but does not prevent cerebral infarction in rats subjected to focal ischemia.
Kawaguchi et al. Anesthesiology 2000;92

Sevoflurane provides sustained anti necrotic and anti apoptotic effect.

Engelhard et al. ASA Annual meeting 2003. Abstract A 740

Sevoflurane:

Have advantages performance for Neuroanesthesi. Faster recovery Sevoflurane than Isoflurane faster neurologis evaluation post operative period. Cerebral vasodilatation effect less than halothane, isoflurane. Effect to blood circulation less than isoflurane More advantages than TIVA.
Nathanson, WCA-Montreal, 2000

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

Effect of Anesthetics on Physiological Responses and Ion and Metabolite Levels

Anoxia Protect Response Thiopental (600 M) Midazolam (100 M) Propofol (20 g/ml) Lidocaine (10 M) Isoflurane (1,5%) Sevoflurane (4%) Etomidate 3 g/ml 30 g/ml Nitrous oxide (50%)
1Worsens

NMDA/AMPA Improve + Ca Yes Yes Yes No No Yes Protect Response Yes No -

Improve + NA Yes Yes Yes No Yes

Improve ATP No/Yes Yes Yes Yes No Yes

1

Yes Yes No Yes No Yes

No No No

No Yes No

No No No

No

ATP after 3.5 minutes of anoxia: improves ATP after 10 minutes of anoxia.

Cottrell JE. ESA, 2004,Lisbon

Maintenance of anesthesia :
First choice

: Sevoflurane : 0 : 2/3 diuresis

Second choice : Isoflurane TOF fluid

Mannitol
Lasix

: 0,25 - 1 gr/kg
: 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, oedema, 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.

Tabel 4. Kondisi untuk Early Emergence (11).

Homeostasis Sistemik
Normotermi (>36oC) Normovolemia, normotensi (70 mmHg <MAP<120 mmHg) Hipokapni ringan/Normokapnia (PaCO2 35 mmHg) Normoglikemia (glukose 4-8 mmol/l) Tidak ada hipoosmoler (285 5 mOsm/kg) Hematokrit > 25% Tidak ada gangguan koagulasi

Homeostasis Otak

Metabolisme otak dan aliran darah otak : normal Tekanan intrakranial normal diakhir operasi Profilaksis antiepilepsi Posisi kepala head-up adekuat Saraf kranial untuk proteksi jalan nafas intack

Tabel 6. Check-list sebelum dilakukan ekstubasi segera (11):

No

Parameter

1. 2. 3. 4. 5. 6. 7. 8.

Kesadaran prabedah adekuat Operasi otak terbatas Tidak ada laserasi otak yang luas Bukan operasi fossa posterior yang luas yang mengenai saraf IX dan XII Bukan reseksi AVM yang besar (resiko terjadinya edema pascabedah malignan) Temperatur normal Oksigenasi normal Kardiovakuler stabil.

Tabel 7. Kondisi sistemik dan serebral yang menyebabkan pasien lambat bangun (11):
Sistemik
Hipotermi (<35,5oC) Hipertensi (tekanan sistolik > 150 mmHg) Hipotensi-hipovolemia Hematokrit < 25% Hipoksia atau hiperkapnia Nafas spontan tidak efektif Hipoosmoler < 280 mOsm/kg) Gangguan koagulasi Ada residu obat pelumpuh otot

Serebral
Perubahan kesadaran prabedah Reseksi tumor besar dengan mid line shift Operasi > 6 jam Ada pembengkakan otak selama operasi Cedera pada saraf IX, X, XII Kejang saat bangun dari anestesi

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

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.

Tatang Bisri, 2005