Endro Basuki S.

Disampaikan pada seminar clinical update FKUGM 2012

Manajemen Penderita Cedera Kepala

dr. ENDRO BASUKI S., Sp.BS, M.Kes

Jakarta, 8 Januari, 1953Dokter Umum FK UGM, 1979Spesialis Bedah Saraf FK UNPAD, 1989 Vrije Universiteit Amsterdam, 1987 1988Magister Kesehatan FK UGM, 2000Puskesmas Kec. Lamuru, Bone, 1979 1982Staf SMF Bedah Saraf RS Dr SardjitoKPS Bedah Saraf FK UGM / RSUP Dr SardjitoBendahara CE&BU RS Dr Sardjito/FK UGMPengurus Harian Komite Medik RS Dr Sardjito/Ketua Sub Komite Disiplin ProfesiPresiden elect PERSPEBSI, 2009 2013Medical Advisory Board PT. ASKES

CEDERA KEPALATERJADI TIAP 15 DETIKMATI TIAP 12 MENIT50 % KEMATIAN PADA TRAUMA60 % KEMATIAN AKIBAT KLL

TATALAKSANAAAIRWAY & C-SPINE CONTROLBBREATHINGCCIRCULATIONPRIMARY

SURVEY

KONSEPNYARESPONSIBILITAS TERPENTINGMANAJEMEN ABC : CEGAHHIPOVENTILASI DAN HIPOVOLEMIAPOTENSIAL TERJADINYASECONDARY BRAIN DAMAGE

SCALPSKINCONNECTIVE TISSUEAPONEUROSIS/GALEALOOSE AREOLAR TISSUEPERICRANIUMvaskularisasi sangat baik, perdarahan hebat potensial menimbulkan syok ANATOMI FISIOLOGICEDERA KEPALA

SCALPSKULLMENINGESBRAINLCSTENTORIUMGCSICP

MENINGESTiga lapis : duramater, arachnoid, piamaterArteri Meningea Media, potensial terlibat pada kasus EDH

CAIRAN SEREBROSPINALDiproduksi oleh pleksus koroideusRata-rata 30 ml per jamBersirkulasi

TENTORIUMMembagi 2 ruangan intrakranialSupratentorial dan Infratentorial

CEREBRAL PERFUSION PRESSURE ( CPP )Merupakan PRIORITAS UTAMARumus : CPP = Mean Arterial Pressure - ICPCEREBRAL BLOOD FLOW ( CBF )Normal : 50 ml/100 gram otak/ menitBila mencapai 5 ml/ menit :cell death & irreversible damage

TEKANAN INTRAKRANIALNormal : 10 mmHg ( 136 mm air )Makin tinggi TIK makin jelek prognosisHUKUM MONRO-KELLIEPrinsip : total volume intrakranial bersifat TETAP,Oleh karena kranium merupakan NON EXPANSILE BOX

Vk = V darah + V likwor + V parenkimMonro Kellie

SECONDARY SURVEYWhole ExaminationANAMNESISPEMERIKSAAN FISIKPENUNJANG

INFORMASI PENTINGUSIA DAN MEKANISME TRAUMASTATUS RESPIRASI & KARDIOVASKULERKESADARAN, REAKSI PUPIL, LATERALISASIADANYA TRAUMA NON SEREBRALHASIL PEMERIKSAAN DIAGNOSTIK

TANDA TANDA PENTINGPUPIL ANISOKORLATERALISASI MOTORIKLUKA TERBUKA DGN KEBOCORAN LCSPERBURUKAN NEUROLOGISFRAKTUR DEPRESI TULANG TENGKORAKSAKIT KEPALA HEBAT

KOMPONEN GLASGOW COMA SCALEE: BUKA MATA: 1 4V: SUARA : 1 5M: GERAKAN : 1 - 6

KOMPONEN MATA

KOMPONEN MOTORIK

KOMPONEN VERBAL

KLASIFIKASIMEKANISMETUMPULTAJAM(PENETRATING)KLLTRAUMA TEMBAKTRAUMA TUSUK

SEVERITYRINGAN:GCS 14 - 15SEDANG:GCS 9 - 13BERAT:GCS 3 - 8MORFOLOGIBerdasarkan PatofisiologiFRAKTUR KRANIUM linear terbuka/tertutup depresi basis craniiLESI INTRAKRANIAL

LESI INTRAKRANIAL

1. Primary Brain Injury:a. Vocal Brain Injury:- Cerebral Contusions,- Cerebral Laceration,

b. Diffuse Brain Damage:- Diffuse Axonal Injury,- Diffuse Vascular Injury.

2. Secondary Brain Injury:a. Traumatic Intracranial Haematoma, - Extradural Haematoma,- Subdural Haematoma (Akut, Sub-akut, dan Kronik),- Subdural Hygroma,- Intracerebral Haematoma,- Intraventricular Haematoma,Subarachnoid Haemorrhage,

b. Post Traumatic Brain Swelling,

c. Focal Brain Damage Secondary to Brain Shift and Herniations

Cerebral ContusionsVocal Brain InjuryCerebral LacerationDiffuse Brain DamageDiffuse Axonal InjuryDiffuse Vascular InjuryPrimary Brain Injury:

Secondary Brain Injury:Traumatic Intracranial HaematomaExtradural HaematomaSubdural HaematomaAkutSub-akutKronikSubdural HygromaIntracerebral HaematomaIntraventricular HaematomaSubarachnoid Haemorrhage

Post Traumatic Brain SwellingFocal Brain Damage Secondary to Brain Shift and Herniations

MEMELIHARA KEBUTUHAN METABOLIK OTAK

CEGAH/OBATI HIPERTENSI INTRAKRANIALHIPOKAPNEAKONTROL CAIRANDIURETIK ( MANNITOL )

PRINSIP

MANNITOLThe mechanism by which mannitol provides its beneficial effects is still controversial, but probably includes some combination of the following:Lowering ICPSupports the microcirculation by improving blood rheologyPossible free radical scavenging

Lowering ICPA. Immediate plasma expansion: reduces the hematocrit and blood viscosity (improved rheology) which increases CBF and O2 delivery. This reduces ICP within a few minutes , and is most marked in patients with CPP < 70 mmHgB. Osmotic effect: increased serum tonicity draws edema fluid from cerebral parenchyma. Takes 15-30 minutes until gradients are established. Effect lasts 1.5-6 hrs, depending on the clinical condition.

bolus administration : onset of ICP lowering effect occurs in 1-5 minutes; peaks at 20-60 minutes.In urgent reduction of ICP : an initial dose of 1 gm/kg should be given over 30 minutes. for long-term reduction of ICP : infusion time should be lengthened to 60 minutes and the dose reduced (e.g. 0.25-0.5 gm/kg q 6 hours.

Cautions with Mannitol1. mannitol opens the BBB , and mannitol that has crossed the BBB may draw fluid into CNS (this may be minimized by repeated bolus administration vs. continous infusion) which can aggravate vasogenic cerebral edema. Thus, when it is time to D/C mannitol, it should be tapered to prevent ICP rebound

2. caution: corticosteroids + phenytoin + manitol may cause hyperosmolar nonketotic state with high mortality3. overenthusiastic bolus administration may HTN and if autoregulation is defective increased CBF which may promote herniation rather than prevent it

4. high doses of mannitol carries the risk of accute renal failure (acute tubular necrosis), especially in the following: serum osmolarity > 320 mOsm/L, use of other potentially nephrotoxic drugs, sepsis, pre-existing renal disease

5. large doses prevents diagnosing DI by use of urinary osmols or SG6. because it may further increase CBF, the use of mannitol may be deleterious when IC-HTN is due to hyperemia

RINGKASANJAGA PATENSI JALAN NAFASJAGA VENTILASIATASI SYOKPERIKSA NEUROLOGISCEGAH CEDERA OTAK SEKUNDERCARI CEDERA YANG TERKAITBILA STABIL, PERIKSA PENUNJANGBILA PERLU KONSUL BEDAH SARAFTERUSKAN ASESMENT

ILUSTRASI KASUSCEDERA KEPALA

Fraktur Impresi

CT scan Impresi Fraktur

TINDAKAN OPERATIF FRAKTUR DEPPRESI

BASILAR SKULL FRACTURES

EpiduralEPIDURALHEMATOM

PERJALANAN KLINIK EDH

ACUTE EPIDURAL HEMATOMA

Subdural hematom

IntraserebralhematomPre operasiPasca Operasi

KorpusAlienum

FUNGSI OTAK Sisi dominan untuk yang tidak kidal adl yg sebelah kiri Orang kidal, 75 % sisi dominan adalah kiri Fungsi sisi dominan adalah untuk bahasa dan memori yang berdasarkan bahasa Sisi kanan untuk memori visual

LOBUS FRONTALIS1. PRE-SENTRAL GIRUS Pusat motorik untuk muka, tangan, kaki, badan, dsb.2. AREA BROCA Pada sisi dominan adalah pusat bicara ekspresif motorik3. AREA MOTOR TAMBAHAN Untuk gerakan mata dan kepala sisi yang berlawanan4. AREA PRE-FRONTAL Untuk inisiatif dan personalitas5. PARASENTRAL LOBUS Pusat penahan BAK dan BAB

Pustaka Baru :Selladurai, Ben dan Reilly, Peter, Initial Management of Head Injury a Comprehensive Guide, McGraw-Hill Australia, 2007.

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