PERIOPERATIVE MANAGEMENT

OF
BRAIN TRAUMA

Tatang Bisri
Konsultan Neuroanestesi IDSAI

Problems in Severe Head Injury

50% mengalami hipoksia, hipotensi

memperburuk outcome.
Hipoksia: PaO2 < 60 mmHg
Hipovolemia/shock : sistolik < 90 mmHg
10-20% cervical fraktur.
Increase ICP
- Herniation
- Brain ischemia

Mortalitas :
Cedera kepala disertai :

Hipoksia

: 56%

Hipovolemia

: 64%

Hipoksia + Hipovolemia

: 76%

Tidak disertai hipoksia+Hipovolemia : 27%

Asean Congress of Anaesthesiologist, Singapore, 1995.

Kriteria Intubasi :
GCS < 8
pernafasan ireguler
frekuensi nafas < 10 atau > 40 per menit
volume tidal < 3,5 ml / kg BB
vital capacity < 15 ml / kg BB
PaO2 < 70 mmHg
PaCO2 > 50 mmHg
Sperry RJ et al : Manual of Neuroanesthesia, 1989.

Table : Suggested Choice

GCS

Hemodynamic
Stability
Yes

Hypnotic

Urgency

Neuromuscular
Blocker

Lidocaine 1,5 mg/kg

3-8

Yes

Sux 1.0 mg/kg

Thiopental 2-3 mg/kg or

propofol 1-2 mg/kg
+ lidocaine 1,5 mg/kg
Etomidate 1-2 mg/kg

Yes
No
Yes

Sux 1.0 mg/kg

Vec 1.02 mg/kg
Sux 1.0 mg/kg

Thiopental 3-4 mg/kg or

propofol 1,5-2,0 mg/kg
+ lidocaine 1,5 mg/kg
Etomidate 1-2 mg/kg

Yes
No
Yes

Sux 1.0 mg/kg

Vec 0.02 mg/kg
Sux 1.0 mg/kg

No
Yes
9 - 12
No

Yes
13 - 15
No

Sux = succinylcholine ; Vec = vecuronium ; GCS = Glasgow Coma Scale

Lam A.M. : Anaesthetic management of acute head injury, 1995

Hipotensi / Hipovolemia:
Jarang oleh karena trauma otak, kecuali:
- Infant dengan subdural hematom besar
- Stadium akhir cedera kepala
- Cedera batang otak.
Cari penyebab di tempat lain.

Cairan
Untuk mempertahankan sirkulasi stabil
Untuk mencegah : hipovolemia,
hipervolemia, hipoosmoler, hiperglikemi
Dipilih NaCl 0,9%, hindari RL, jangan
dextrose
Dextrose : hanya untuk terapi hipoglikemi
(gula darag < 60 mg%).

Pengaturan cairan
Pemeliharaan kristaloid 1 - 1,5 ml/kg/jam
Hindari larutan hipotonik (Dextrose 5%)
Balans elektrolit (RL, NaCl), batasi RL
Koloid
Darah : Hb pre op rendah, Ht < 30%,
perdarahan > 20%

Hubungan ICP dan mortalitas

pada cedera kepala
ICP rata-rata (mm Hg)

Mortalitas (%)

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

Herniasi

Trias sindroma herniasi : penurunan

kesadaran, dilatasi pupil, hemiparesis.
Bila ada gejala klinis herniasi, lakukan
hiperventilasi.
Herniasi dapat terjadi pada ICP 18 mmHg.

Pengelolaan pasien tanpa ada

tanda klinis herniasi

Beri sedasi dan pelumpuh otot saat

transportasi.
Pelumpuh otot short acting diberikan bila
dengan sedatif saja tidak efektif.
Tidak perlu mannitol
Tidak perlu hiperventilasi, asal optimal
oksigenasi dan normal ventilasi

Bila ada tanda klinis herniasi otak

Terapi agresif peningkatan tekanan

intrakranial
Hiperventilasi mula-mula sampai PaCO2
30-35 mmHg
PaCO2 < 30 mmHg harus ada
pemantauan SJO2
Manitol bila volume sirkulasi adekuat

Metode pengendalian hipertensi

intrakranial

Posisi untuk memperbaiki cerebral venous return:

netral, head up 15-30 derajat.
Ventilasi adekuat: PaO2 > 100 mmHg,
PaCO2 35 mmHg, hiperventilasi
sesuai kebutuhan.
Optimal hemodinamik (MAP, CVP, HR)
mempertahankan CPP >70 mmHg, target
normotensi.Terapi bila MAP> 120-130 mmHg
Osmotik diuretik (Mannitol, furosemid, NaCl
hipertonik)

Metode pengendalian hipertensi

intrakranial

Hindari overhidrasi, sasarannya

normovolemi.
Obat yang menimbulkan vasokonstriksi
serebral : barbiturat
Pengendalian temperatur : low
normothermia.

ANESTESI
PASIEN CEDERA KEPALA

Teknik anestesi

A = Airway : bebas sepanjang waktu

B= Breathing and ventilation : target
tdk ada hipoksia (PaO2 > 70
mmHg), Normokapni
C= Circulation
D= Drugs
E = environment / temperature control: di
OK
35oC, di ICU 36oC

Circulation

Hindari lonjakan tekanan darah

Pertahankan CPP adekuat
Target Normovolemia, Normotensi,
Isoosmoler.
Hindari posisi yang menghambat
drainase vena serebral dan
meningkatkan CBF.

Pengendalian Tekanan Darah

Hipotensi :
CPP = MAP - ICP
disukai sistolik 90 - 100 mmHg . Normotensi pada
head injury

Hipertensi :
- meningkatkan CBV, ICV, edema, perdarahan
- terjadi saat laringoskopi/intubasi,

Faktor mekanis yang meningkatkan tekanan

vena serebral
batuk, mengejan , trendelenburg, obstruksi
vena besar di leher, tekanan pada abdomen,
tahanan pengembangan dada, PEEP,
kanulasi v. jugularis interna/v. Subclavia.
Posisi head up 30o, normal, tidak fleksi,
rotasi, ekstensi.

D= drugs

Pakai obat yang berefek brain

protection
Hindari obat yang berefek
meningkatkan ICP, cerebral
vasodilator.
Hemodinamik stabil

Cardiovascular effect of volatile inhalation

anesthetics at 1-1,5 MAC
Variable

Halothane Enflurane Isoflurane Sevoflurane

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

0
0
0

0?

0
0
0
0
0

Neuroprotection properties of
volatile anesthetics

Neuroprotection in term of antinecrotic

and anti-apoptotic effect
Increase CBF in ischemic region.
Reduction of functional CMR
Suppression of convulsions
Werner C. AOSRA Nov 2003
WCA, April 2004. ESA June 2004.

Neuroprotection properties of
volatile anesthetics

Inhibition of lactic acidosis and excitatory

neurotransmitter release
Prevention of pathological Na+, Ca2+ influx.
Inhibition of lipidperoxidation.
Reduction of free radical formation.
Werner C. AOSRA Nov 2003

Volatile anesthetics

Isoflurane, sevoflurane, desflurane

produce maximum cerebral metabolic
suppression (2 MAC) correct for
imbalance between oxygen supply and
demand.

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

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

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

lidocaine

Blocking Na influx
Reduce post necrotic injury
Truncates ischemic damage in the
penumbra by blocking the apoptotic cell
death pathway that involve cytochrome
lidocaine have brain protection effect.

Effect of Anesthetics on Physiological Responses

and Ion and Metabolite Levels
Anoxia

NMDA/AMPA

Protect
Response

Improve
NA+

Improve
ATP

Improve
Ca+

Protect
Response

Thiopental (600 M)

Yes

Yes

No/Yes

Yes

Yes

Midazolam (100 M)

Yes

Yes

Yes

Propofol (20 g/ml)

No

Yes

Yes

Yes

No

Lidocaine (10 M)

Yes

Yes

Yes

No

Isoflurane (1,5%)

No

No

No

No

Sevoflurane (4%)

Yes

Yes

Yes

Yes

3 g/ml

No

No

No

30 g/ml

No

Yes

No

No

No

No

No

Etomidate

Nitrous oxide (50%)

1

Worsens ATP after 3.5 minutes of anoxia:

improves ATP after 10 minutes of anoxia.

Cottrell JE. ESA, 2004,LISBON

Pemeliharaan

1. Efek paling kecil terhadap autoregulasi

serebral dan kemampuan merespons CO2
2. Mempertahankan kestabilan kardiovaskuler
3. Mampu menurunkan ICP sehingga akan
menaikkan CPP

Periode pascabedah
Cegah batuk, mengedan, kenaikan
darah

tekanan

Segera lakukan pemeriksaan neurologi

Cedera kepala sedang (GCS 9-12) dan ringan
(GCS 13-15) kebanyakan diekstubasi di OK.
Cedera kepala berat tdk diekstubasi.
Lidokain 1,5 mg/kg, vasodilator,
dexmedetomidine, esmolol untuk mencegah
kenaikan tekanan darah

PENGELOLAAN
di ICU
Pascabedah
DAI
ABCDE (Brain protection)
Nutrition

Methods of brain protection

Basic methods
Hypothermia - low normothermia
Pharmacology
Intravenous Anesthetic
Inhalation anesthetics
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

Plasma glucose concentration

Avoidance of hyperglycemia : < 150 mg%,

Maintained 100-150 mg%, assayed every 2
hours
Hyperglycemia associated with worsened
outcome following stroke or neurotrauma.
Normoglycemia may protect neuron (decrease
intracellular lactic acidosis, decrease membrane
permeability, reduced edema of endothelial cells,
neuroglia, neuron).

Use of mild hypothermia during aneurysm

clipping by neuro-anesthesiologist (SNACC
Members)

Goal temperatures
33-35oC
35-37oC
United States
Outside US

65%
52%

33%
43%

Moore L Berkow et al
J. Neurosurgical Anesthesiology 2002

Hypothermia
499

n
Good outcome
Mortality
Bacteriemia

65,9%
28%
5%

Normothermia
501
62,7%
32%
2,5%

Conclusion: No indication that intraoperative

cooling resulted in any alteration in outcome .
Cottrell, WCA,2004. Cottrell JE at al. J Neurosurg

Hipotermia-hipertermia
Hipotermia: OK: 35o , 36o or normotermia di
ICU.
CMRO2 , pelepasan EAA , Glutamat
stabilisasi membran
mempertahankan ATP, Ca influx.
Moderate hypothermia (33o ) : komplikasi saat
rewarming (ICP ) dan pneumonia.
Hipertermia: Ca influx, mengosongkan ATP,
mengganggu pemulihan
(Cottrell, ASA Annual meeting, 2003)

Osmodiuretics

Mannitol decreases ICP, increases CPP,

improves CBF in laboratory animals and human.
This effect related to plasma expansion with
reduction of Ht, plasma viscosity, CBV.
Osmolarity must be monitored and should no
exceed 320 mOsm/l.
Rebound effects to be relevant only with a
defective BBB or treatment > 4 days.
Werner C: WCA 2004, AOSRA 2003

magnesium
Vascular : increased COP, rCBF
Neuronal: NMDA ion channel blockade,
Ca++ channel blockade, enhanced ATP
recovery.
Dose: 2 gm over 15 min and the 8 gm
over 24 hours

Sedasi

Agitasi dan nyeri akan meningkatkan ICP

Perlu diberikan yang berefek sedasi,
analgetik.
Bila pasien sadar : beri analgetik, sedasi,
anxiolitik (dexmedetomidine)
Analgetik short acting seperti fentanyl
dapat diberikan

Pengelolaan kejang

Adanya kejang akan meningkatkan

CMRO2, meningkatkan CBF dan ICP.
Terapi dengan fenitoin 10-15 mg/kg
dengan kecepatan 50 mg/menit.
Diazepam 0,2 mg/kg
Bila tetap ada kejang beri pentotal 1-3
mg/kg/jam
Pasien harus terintubasi dan ventilasi

NUTRITION
SHI : Hypermetabolic state

Estimated energy requirement vary from

140% to 200% above normal for the first 3
weeks post injury.
Direct impact to energy expenditure:
patients temperature, catecholamine
levels, severity of injury, resting muscle
tone, spontaneous muscle
activity,fluctuation of ICP

Determinant of energy
expenditure in TBI

Severity of HI
Secondary infection
Catecholamine
response
Spontaneous muscle
activity
Use of barbiturate,
sedative, paralyzing
therapy

Seizure
Elevated temperature
for brain injury
Other injury

Guidelines for predicting Energy

expenditure

Estimate energy expend 30 kcal/kg/day

Seizure: increase 20-30% over standard
estimate
Nonsedative coma: 140% basal energy
expend (BEE)
Pentobarbital coma: 100-120% BEE
Afebril non ICU patient : 120-130% BEE
Standard head injury range : 140-200% BEE

Enteral nutrition as first choice for

patients with SHI
If enteral access not successfulTPN
Hyperglycemia worsening cerebral
deficits .
Adequate nutrition will improve
outcome.
First choice : Post pyloric access /Jejunal
feeding .

Kesimpulan :
I

Pengelolaan cedera kepala yg benar

mencegah

terjadinya cedera sekunder dan menurunkan

morbiditas & mortalitas

Cedera sekunder bisa terjadi pada setiap tahapan

perawatan di Rumah Sakit.

Cedera kepala berat sering disertai hipoksia &

hipovolemia.

Hipotensi (sistolik < 90 mmHg) atau hipoksia (PaO2 <

60 mmHg) harus dihindari dan terapi sesegera
mungkin.

II Cedera kepala berat sering disertai fraktur cervical

hati-hati saat intubasi.

Harus dihindari PaCO2 < 35 mmHg selama 24 jam

pertama setelah cedera kepala..

MAP harus dipertahankan >90mmHg,

terapi bila MAP>130mmHg.

CPP harus dipertahankan minimal 70 mmHg.

III Indikasi ICP monitor :

Cedera kepala berat ( GCS < 8 ) dg CT-Scan
abnormal

Cedera kepala berat ( GCS < 8 ) dg CT-Scan normal

bila umur > 40 tahun, sistolik < 90 mmHg.

Bila ICP > 20 -25 mmHg

dimulai.

terapi harus segera

Mannitol efektif untuk mengendalikan kenaikan ICP,

dosis 0,25 - 1 g/kg.

IV

Dosis tinggi barbiturat dipertimbangkan bila

hemodinamik stabil. Pada cedera kepala berat dengan
kenaikan ICP yang tidak bisa diterapi dengan terapi
medical & bedah yang maksimal.

Tidak dianjurkan pemberian glucocorticoid.

Tujuan terapi cairan : sirkulasi stabil, cegah hipovolemia,
hipervolemia, hipoosmoler, hiperglikemia.

Jangan diberi dextrose. Gula darah jangan > 150 mg%.

Dextrose hanya untuk terapi hipoglikemia (gula darah <
60mg%).

Early nutrition akan menurunkan morbiditas dan

mortalitas.

Terimakasih
atas segala perhatiannya
Tatang Bisri
Bandung 2005