PERIOPERATIVE MANAGEMENT OF

BRAIN TRAUMA

Tatang BisriKonsultan 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.

GCS Hemodynamic Hypnotic Urgency NeuromuscularStability Blocker

Yes Lidocaine 1,5 mg/kg3 - 8 Yes Sux 1.0 mg/kg

NoThiopental 2-3 mg/kg or

Yes propofol 1-2 mg/kg Yes Sux 1.0 mg/kg9 - 12 + lidocaine 1,5 mg/kg No Vec 1.02 mg/kg

No Etomidate 1-2 mg/kg Yes Sux 1.0 mg/kg

Thiopental 3-4 mg/kg orYes propofol 1,5-2,0 mg/kg Yes Sux 1.0 mg/kg

13 - 15 + lidocaine 1,5 mg/kg No Vec 0.02 mg/kgNo Etomidate 1-2 mg/kg Yes Sux 1.0 mg/kg

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

Table : Suggested Choice

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

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.

ANESTESIANESTESIPASIEN CEDERA KEPALA 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,

pemasangan pin, sayatan kulit, bor kepala, ekstubasi

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

Variable Halothane Enflurane Isoflurane Sevoflurane

BPVascular resistanceCardiac outputCardiac contractionCVPHeart rateSensitization of the heart to epinephrine

0 0

000 0?

000

0 0

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

0 = no change (<10%) = 10-20% decrease = 20-40% decrease = increase

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.

Anoxia NMDA/AMPAProtect

ResponseImprove

NA+Improve

ATPImprove

Ca+Protect

Response

Thiopental (600 μM) Yes Yes No/Yes1 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 -

1Worsens ATP after 3.5 minutes of anoxia: improves ATP after 10 minutes of anoxia.

Effect of Anesthetics on Physiological Responses Effect of Anesthetics on Physiological Responses and Ion and Metabolite Levelsand Ion and Metabolite Levels

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 tekanan darah

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

PENGELOLAANPENGELOLAANdi ICUdi ICUPascabedahPascabedahDAIDAI

•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 temperatures33-35oC 35-37oC

United StatesOutside US

65% 33%52% 43%

Moore L Berkow et alJ. Neurosurgical Anesthesiology 2002

nHypothermia Normothermia499 501

Good outcomeMortalityBacteriemia

65,9% 62,7%28% 32% 5% 2,5%

Conclusion: No indication that intraoperative cooling resulted in any alteration in outcome . Cottrell, WCA,2004. Cottrell JE at al. J Neurosurg Anesth 2004

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

NUTRITIONSHI : 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 : • 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.

I

•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.

II

• 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 terapi harus segera dimulai.

• Mannitol efektif untuk mengendalikan kenaikan ICP, dosis 0,25 - 1 g/kg.

III

• 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.

IV

Terimakasihatas segala perhatiannya

Tatang BisriBandung 2005