• Setelah menyelesaikan bab ini peserta diharapkan dapat menjelaskan: 1.Anatomi kepala & otak. 2.Patofisiologi cedera kepala. 3.Pemeriksaan pasien cedera kepala. 4.Penatalaksanaan pasien cedera kepala.


CKR 570 orang . 52 ribu meninggal . • 34 ribu meninggal dalam perjalanan ke UGD RS (data tahun 1995) . 220 ribu MRS dan 100 ribu terdapat kecacatan temporer/permanen (Data tahun 1993). • Di US 2 juta insiden kasus trauma kepala per tahun.CKS 231 dengan kematian 3 % .EPIDEMIOLOGI • Data di Bagian Syaraf RSUPNCM tahun 2000. • Sejak mulai diberlakukannya “Safety On The Road” terjadi penurunan hingga 22% lebih terhadap angka kematian trauma kepala.CKB 128 dengan kematian 50%. dari 929 penderita cedera kepala : .

EPIDEMIOLOGI • Angka Survival di UGD ( US tahun 1993) adalah : – 80% pada Cedera kepala ringan (GCS 13 – 15) – 10% Cedera Kepala Sedang (GCS 9 – 12) – 10% pada Cedera Kepala Berat (GCS ≤ 8 ) .


ANATOMI •Kulit kepala. •Tulang tengkorak. •Jaringan otak. •Kompartemen vaskuler.Kulit Kepala (SCALP) • S kin atau kulit • C onnective Tissue • A poneurosis • L oose areolar tissue • P erikranium . 1. •Selaput otak/meningen. •Cairan serebro spinal.

ANATOMI Tulang Tengkorak : 1. Calvaria 2. Arachnoid Mater 3. Basis Cranium Lapisan Meningen 1. Duramater 2. Pia mater .

Lokal 2. diffus axonal injury dan gegar otak. Direct (Langsung ) B. Difus Sekunder (Timbul dan berkembang beberapa waktu setelah trauma) 1. Difus . Indirect (Tidak Langsung) Direct --- initial impact tulang kepala dengan obyek Indirect - Robekan pembuluh darah dan terganggunya integritas akson. shg terjadi subdural hematoma. Lokal 2.MECHANISME OF BRAIN INJURY 2 Mekanisme yaitu : A. Cedera Primer dan Sekunder Primer (timbul segera pada saat terjadinya trauma): 1.

DIAGRAM MOI CEDERA OTAK TRAUMA SKULL FRACTURE CEDERA PRIMER CEDERA SEKUNDER LOKAL : DAI Kontusio Laserasi.TIK naik Difus Vaskuler Injury . Hipoksi Edema. HSD akut DIFUS : Komosio PSA EDH LOKAL : HSD subakut/kronik Infeksi Infark Batang Otak DIFUS : Iskemi.

COUP VS CONTRA COUP COUP -- Direct • Lacerasi SCALP • Fraktur tulang tengkorak • Epidural Hematoma • Contusio Otak Contra Coup - Direct & Indirect .

•Causes arterial vasoconstriction that reduces the ICP but also the CPP. EXCITOTOXICITY . •Another simple but vital principal that must be kept in mind when dealing with intracranial pathologies.PENYEBAB CEDERA OTAK SEKUNDER ISCHEMIA Cerebral Perfusion Pressure. •Hyperventilation and low C02 are no longer recommended. •The CPP is just as important as the intracranial pressure. •CPP 70mmHg> is generally associated with a poorer outcome following head injury.

CEDERA OTAK SEKUNDER Sistemik : • Hipoxemia • Anemia • Hipotensi • Hiperthermia • Hiper/hipocapnea • Komplikasi respirasi • Elektrolyte imbalance Intracranial • TIK ↑ • Edema cerebri • Lesi massa • Kejang .


GCS •E + M + V = 3 to 15 •Less than or equal to 8 at 6 hours .50% die •Initial "postresuscitation" score most accurate predictor of future outcome. .


CONT …………… .


.CASE 1 Ditemukan seorang laki laki muda terbaring dibawah tangga. lupa ingatan. mengerang kesakitan. Korban tampak pucat dan dingin dengan muka penuh darah. dan terdapat lacerasi dan udem di bagian kiri kepala. tidak ada yang mengetahui insidennya .

• How do you assess the neurological state? . • How do you assess the airway? • Rapid assessment of the neurological state.What do yo do now ? ABC’s AIRWAY / BREATHING • Most important and the primary concern is if the patient is able to maintain an airway.

Mata tidak membuka •What is his GCS ? GCS = 7 •What do you need to now ? GCS < 8 --- Intubasi pasien .•Korban suara hanya mengerang dan respon menghindari rangsangan nyeri.

– percussion may be helpful but – Auscultation – Conditions that have to be excluded: • tension pneumothorax • flail chest • massive haemothorax • open pneumothorax . • look for: – exposure – inspection of chest – chest wall movement – tracheal deviation.What do you want to check next ? Breathing: • Exclude conditions that will impair breating and rapidly correct.

• How do you deal with it? • In this category you also need to look for: – Blood volume and cardiac output. • Level of consciousness • Skin color • Pulse. .CIRCULATION • Now you can finally deal with the head laceration. – Bleeding: expose patient fully.

• Absence of neurological deficit does not exclude cervical spine injury.SPINE • What do you do to protect the C-spine? • All patients with head trauma or maxillofacial trauma should be presumed to have an unstable cervical spine injury until positively excluded. – leaving patient in hard color and on spinal board for several hours is very poor management. – Waiting for several hours to exclude c-spine injury is poor management. – Early attention to excluding c-spine injuries is important. • Examination of the c-spine is impaired in a comatosed patients.C . • Decubitus ulcers may develope quickly. Serious full thickness skin ulcers will develope. • What are the investigations you would do? .

This injury is secondary to a hyperextension mechanism and usually involves the second cervical vertebrae. • This injury is potentially unstable.FOTO CERVICAL • This injury is known as a extension teardrop fracture. . It is seen most often in the elderly.

• In this patient with little dispacement. the anterior and longitudinal ligaments are intact and the injury is relatively stable. The injury occurs with hyperextension and commonly occurs following car accidents. With marked anterior displacement. the ligaments are ruptured and the injury is unstable .• This is known as a hangman's fracture and consists of fractures through the pedicles of C-2 (traumatic • spondylolithisis of the axis).

• What is your next step? • Reassess the GCS. • pupillary changes . .(fixed. • Breathing 100% oxygen and on ventilator.THE PATIENT IS NOW STABLE • Good oxygen saturation. • Continuous Neuro OBS is vital the detect early changes in the patient. • Abdomen is soft (but this may be misleading in head trauma) • There is no x-ray finding of fracture or any clinical signs of fracture.a late finding due to brainstem compression. dilated) .

• The patient is now intubated and paralysed. you did not get a chance to do the neurological examination prior to intubation. Previously equal pupils. Your findings at this stage: • Slightly dilated pupil on the right but reactiv. • GCS of 3T • More brisk reflexes on the left. .

. • Neurosurgeon needs to be contacted at an early stage.What is the next step ? • Patient needs urgent CT scan.

• 40 mmHg < severe elevation.TEKANAN INTRA KRANIAL • Many Intracranial pathologies affects intracranial pressure • Normal ICP <10mmHg (136 mm water) • 20 mmHg < is abnormal. • The higher the ICP after head injury the worst the outcome .


• ICP value gets elevated at point of decompensation. • When ICP starts going up the patient will rapidly decompensate and herniation is imminent • Every effort should therefore be made to keep the patient on the flat part of the curve .

some carbon dioxide retention?) • Nausea and vomiting. • Drowsiness. • Papilloedema. – relieved by vomiting. (Intracranial pressure increases during sleep. .• Signs of increased ICP: • Headache: – Worse on waking in the morning. usually worse in the morning. Important clinical sign not to be dismissed.





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