cedera otak traumatik
TRANSCRIPT
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CEDERA OTAK TRAUMATIK
dr.Jimmy Eko Budi Hartono, SpS
Bag./SMF Ilmu Penyakit Saraf
Fakultas Kedokteran Universitas Diponegoro - RS. Dr. Kariadi
Semarang
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☺ Berat : 2% BB
☺ Sel otak: 100 miliar neuron, 10 miliar glia.
☺ Kebutuhan: - 15-20% cardiac output
- 15-20% oksigen tubuh
- 50% glukosa tubuh
- 15-20% energi ATP
☺ Cadangan glukosa: hanya cukup untuk 1-2 menit
☺ Reproduksi : Setelah usia 2 tahun reproduksi
sel neuron tidak terjadi lagi.
OTAK
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♣ Kelainan otak disebabkan oleh trauma mekanik eksternal
♣ menyebabkan gangguan fisik, kognitif dan psikososial
♣ sementara atau menetap
♣ berhubungan dengan berbagai tingkat kesadaran. (TraumaticBrain Injury)
3
DEFINISI
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- Berdasarkan kelainan patologis : fokal atau difus.
- Berdasarkan waktu terjadinya : primer dan sekunder.
- Mekanisme : tembus peluru atau bukan.
- Ada tidaknya fraktur.
- Derajat penurunan kesadaran (kuantitatif),
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KLASIFIKASI
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KATEGORI GCS GAMBARAN KLINIS CT Scan
MINIMAL (SIMPLE
HEAD INJURY)
15 Pingsan (-),
Defisit neurologis (-)
Normal
RINGAN (MILD
HEAD INJURY)
13–15 Pingsan < 10 menit,
Defisit neurologis (-)
Normal
SEDANG
(MODERATE
HEAD INJURY)
9 – 12 Pingsan > 10 menit
sampai 6 jam, Defisit
neurologis (+)
Abnormal
BERAT (SEVERE
HEAD INJURY)
3 – 8 Pingsan > 6 jam,
Defisit neurologis fokal
(+)
Abnormal
(Frank, 2005; Wijoto, 2008)
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Gennarelli dan Thibault :
1. Mekanisme Kontak,
2. Mekanisme Akselerasi,
- Akselerasi tranlasi : otak bergerak sesuai garis lurus - Akselerasi rotasi
- Akselerasi angulasi : merupakan kombinasi diatas.
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MEKANISME CEDERA KEPALA
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Patologi Cedera Kepala
• Primer dampak langsung benturan atau
proses mekanik1.Laserasi kulit kepala
2.Fraktur tengkorak, fraktur basis kranii
3.Cedera otak fokal
4.Cedera otak difus
5.Kontusio kortikal & laserasi
6. Lesi substansia alba difus (DAI)
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• Sekunder proses komplikasi
1. Hematom Intrakranial
Ekstra aksial : EDH, SDH, PSA
Intra aksial : PIS, PIV
2. Edema serebri :
vasogenik, sitotoksik, osmotik, hidrostatik,
interstitial atau hidrosefalik
3. Herniasi tentorial / tonsiler
4. Iskhemia serebral fokal / global
5. Infeksi
6. Hydrocephalus
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Primary Survey
• Airway maintenance with cervical spine protection
• Breathing & Ventilation
• Circulation with hemorrhage control
• Disability : Neurologic status
• Exposure / Environmental control : • completely undress the patient, but prevent hypothermia
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Airway
• Talk to the patient
• Give oxygen
• Assess airway
• Consider need for advanced airway
management
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Breathing• Inspection of RR :
• Cyanosis
• Penetrating injury
• Presence of flail chest
• Sucking chest wounds
• Use of accessory muscle
• Palpation : • Tracheal shift
• Broken ribs
• Subcutaneous emphysema
• Percussion :• Haemothorax / pneumothorax
• Auscultation :• Pneumothorax
• Resuscitation action :• Cricothyroidotomy
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Circulation
• Level of consciousness• Circulating blood volume reduced, cerebral
perfusion impaired, then resulting in altered level of consciousness
• Skin color• Pink skin, rarely hypovolemia
• Ashen gray skin, sign of hypovolemia
• Pulse• Full, slow & regular pulses : relative normovolemia
• Rapid : hypovolemia
• Irregular : cardiac dysfunction
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Disability (Neurologic Evaluation)
•A Awake
•V Verbal response
•P Painful response
•U Unresponsive
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Verbal responseOriented to person, place, and date = 5
Converses but is disoriented = 4
Says inappropriate words = 3
Says incomprehensible sounds = 2
No response = 1
Glasgow Coma ScaleEye openingSpontaneous = 4
To speech = 3
To painful stimulation = 2
No response = 1
Motor responseFollows commands = 6
Makes localizing movements to pain = 5
Makes withdrawal movements to pain = 4
Flexor (decorticate) posturing to pain = 3
Extensor (decerebrate) posturing to pain = 2
No response = 1
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Dekortikasi / deserebrasi
Dekortikasi
Deserebrasi
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Epi Dural Hematom (EDH)
• 5% - 15% dari CKB
• 70% - 80% berlokasi regio temporal
• Akibat perdarahan a. meningea media
• 85% disertai fraktur cranii
• Lucid interval
• Talk and die
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Sub Dural Hematom (SDH)
• 26% - 63% cedera kepala tertutup
• Akibat ruptur vena jembatan (bridging vein) subdural
• Kesadaran menurun sejak awal
• Mortalitas SDH > EDH, berhubungan dengan kerusakan
otak
• SDH akut < 3 hari
• SDH sub akut 4 – 21 hari
• SDH kronis > 21 hari
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Perdarahan Sub Arachnoid (PSA)
• Mortalitas 35%
• Kerusakan struktur permukaan vaskuler di
ruang subarachnoid, darah masuk lcs
• Vasospasme serebri & mengurangi CBF
mengakibatkan iskemik sekunder
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Perdarahan Intra Serebral (PIS)
• 15% dari CKB
• 80% - 90% pada regio frontal & temporal
• Kadang serebelum
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Perdarahan Intra Ventrikel (PIV)
• 1,5% - 10% CKB
• Hidrosefalus akut sehingga TIK↑
• Akibat ruptur vena subependim
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Efek tunda Cedera Kepala
• Epilepsi
• Bocornya lcs
• Post Concussion Syndrome
• Kerusakan otak kumulatif : petinju & joki
• Kerusakan saraf cranial
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MID LINE SHIFT
OBLITERASI VENTRIKEL
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OBLITERASI SISTERNA
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Epidural hematom
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Subdural Hematom Akut (SDH akut)
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SubduralHematomKronis
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Intra Serebral hematom
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Resiko terjadinya intrakranial hematom akibat Cedera kepala.
CKR (GCS 13-15) 2%CKS (GCS 9-12 ) 9 – 10%CKB (3-8 ) 50%
CKR + Fraktur linier, resiko meningkat
7 – 10 kali
CKR + Lucid interval resiko meningkat
sampai 32%
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Umur > 50 th resiko 3 – 4 kali lebih besar
dibanding < 30 tahun
Lesi fokal banyak terjadi pada trauma
dengan kecepatan rendah (terjatuh,
cedera pada olah raga, dan kegiatan
sehari-hari di rumah)
DAI terjadi pada trauma dengan
kecepatan tinggi.
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Hematom pada daerah temporal dan
temporoparietal, beresiko tinggi
menekan batang otak, melalui proses
herniasi transtentorial, sehingga perlu
evakuasi hematom segera.
Lokasi hematom :
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Diperkenalkan oleh Strich (1956) dan diuji klinis oleh Genarelli (1982).
Terdapat defisit neurologis atau kehilangan kesadaran namun tanpa lesi yang jelas pada gambaran CT-Scan
Diagnosa pasti DAI ditegakkan berdasar pemeriksaan mikroskopis.
Diffuse Axonal Injury (DAI)
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Gambaran radiologis DAI :
Kadang ditemukan patechial haemorrhage di substansia alba, corpus callosum, ganglia basalis, batang otak.
Gambaran edema diffus, traumatik PSA, traumatik IVH
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DAIHemaragik tanpa efek masa
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PERDARAHAN PADA CORPUS CALLOSUM
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PERDARAHAN PADA BATANG OTAK
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Edema cerebri difus
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TRAUMATIK PSA
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PERDARAHAN INTRA VENTRIKEL
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Hydrocephalus
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Fraktur basis cranii
Raccon eye
Battle signOtorhoea
Rhinnorhoea
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Brill hematom
Brill hematom Raccon eye
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HERNIASI SEREBRI
a. Herniasi subfalcial /
cingulate
b. Herniasi uncal
c. Herniasi transtentorial /
central
d. Herniasi eksternal
e. Herniasi tonsillar
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80% kematian Cedera Kepala disebabkan
oleh proses berkelanjutan dari iskemiotak.
Target pengelolaan adalah mencegah
proses iskemik dan kerusakan sekunderotak yang disebabkan oleh proses ekstraserebral.
Penyebab kematian pada cedera kepala
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Kematian cedera otak sekunder (9 H)
1. Hipoksemia (Hipoksia, anemia, CO)
2. Hipotensi (Hipovolemi, ggn jantung, pneumothorax)
3. Hiperkapnia (Distress pernafasan)
4. Hipokapnia (Hiperventilasi)
5. Hipertermi (Hipermetabolisme / reaksi stres)
6. Hiperglikemi (Hipotermia / dekstrose)
7. Hipoglikemia (cairan hipotonik)
8. Hipoproteinemia (malnutrisi)
9. Hiponatremia (SIADH)
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Gambaran CT scan akibat TIK :
Hilangnya gambaran ventrikel III
Hilangnya sisterna perimesensefalik
Bila TIK unilateral akan terjadi :
Pergeseran otak ke sisi berlawanan
Pelebaran ventrikel kontralateral
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Pelebaran ventrikel
kontralateral
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Pergeseran otak ke sisi berlawanan
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