trauma kepala - medula spinal
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Cedera KepalaCedera Kepala
Cedera Medulla Cedera Medulla SpinalisSpinalis (traumatic brain injury (traumatic brain injury
& spine injury)& spine injury) dr. Anna Luthfiana SpSdr. Anna Luthfiana SpS
Bagian Ilmu Penyakit SarafBagian Ilmu Penyakit Saraf
&&
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
setiap perubahan fungsi setiap perubahan fungsi
mental atau fisik yang mental atau fisik yang
diakibatkan oleh benturan diakibatkan oleh benturan
pada kepalapada kepala
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Comotio cerebri =Comotio cerebri =
pingsan sejenak, dengan atau tanpa pingsan sejenak, dengan atau tanpa
amnesia retrograd, tanpa defisit amnesia retrograd, tanpa defisit
neurologisneurologis
Contusio cerebri =Contusio cerebri =
Perdarahan permukaan otak, berupa Perdarahan permukaan otak, berupa
bintik perdarahan besar atau kecil, bintik perdarahan besar atau kecil,
tanpa kerusakan duramater, dengan tanpa kerusakan duramater, dengan
defisit neurologis yang reversibeldefisit neurologis yang reversibel
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
mekanismemekanisme severitasseveritas morfologimorfologi
Tertutup Tertutup Terbuka / Terbuka / PenetransPenetrans
RinganRingan : GCS 13-15: GCS 13-15SedangSedang : GCS 9-12: GCS 9-12Berat Berat : GCS <= 8: GCS <= 8
Fraktura tengkorakFraktura tengkorak Lesi intrakranialLesi intrakranial
Kalvaria Kalvaria - - Linear / Linear / SStelata telata - - DepressedDepressed // NNonon--ddepressedepressed
BasilarBasilar FokalFokal - - Epidural Epidural - - Subdural Subdural - - IntraserebralIntraserebral
Difusa Difusa - - Konkusi ringan Konkusi ringan - - Konkusi klasik Konkusi klasik - - Cedera aksonal Cedera aksonal ddifusaifusa
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
mekanismemekanisme
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
mekanismemekanisme
• GCS 13 - 15 GCS 13 - 15 : Mild Traumatic Brain Injury : Mild Traumatic Brain Injury (CKR)(CKR)• GCS 9 - 12 GCS 9 - 12 : Moderate Traumatic Brain Injury : Moderate Traumatic Brain Injury (CKS)(CKS)• GCS GCS ≤ ≤ 8 8 : Severe Traumatic Brain Injury : Severe Traumatic Brain Injury (CKB)(CKB)
severitasseveritas
LOC ≥ 5’ ; FND; LOC ≥ 5’ ; FND; PTA ≥ 30’PTA ≥ 30’
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
GCS GCS Good Recovery or Vegetative Good Recovery or Vegetative or or at 24 hourat 24 hour moderate disabilitymoderate disability dead dead
11-15 11-15 91%91% 6% 6%
8-108-10 59%59% 27% 27%
5-75-7 28%28% 54% 54%
3-4 13%3-4 13% 80% 80%
GCS dan Outcome (Stein, 2000)GCS dan Outcome (Stein, 2000)
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Tanpa memperdulikan nilai GCS, Tanpa memperdulikan nilai GCS, pasien digolongkan sebagai pasien digolongkan sebagai penderita penderita cedera kepala beratcedera kepala berat bila: bila:
1. 1. Pupil tak ekual Pupil tak ekual
2. 2. Pemeriksaan motor tak ekual Pemeriksaan motor tak ekual
3. C3. Cedera kepala terbuka dengan edera kepala terbuka dengan bocornya CSS ataubocornya CSS atau adanya adanya
jaringan jaringan otak yang terbuka. otak yang terbuka.
4. Perburukan neurologik. 4. Perburukan neurologik.
5. Fraktura tengkorak depressed. 5. Fraktura tengkorak depressed.
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Nyeri kepala disertai muntahNyeri kepala disertai muntah = = # #
linearlinear
# depressed = # depressed = indikasi elevasi :indikasi elevasi :
depresi > 8-10 mm (> ketebalan depresi > 8-10 mm (> ketebalan
tulang tengkorak), defisit tulang tengkorak), defisit
neurologis, bocornya LCS, open neurologis, bocornya LCS, open
depresseddepressed
mmorfologiorfologi
ffraktura tengkorakraktura tengkorak
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
# basis kranii =# basis kranii =
LCS otorrhea atau rhinorrhea, LCS otorrhea atau rhinorrhea,
hemotympanum atau lacerasi CAE, hemotympanum atau lacerasi CAE,
battle’s sign, racoon’s eyes, paresis battle’s sign, racoon’s eyes, paresis
n.VII-VIII, n.I, n.VIn.VII-VIII, n.I, n.VI
- Hati-hati pemasangan NGT- Hati-hati pemasangan NGT
- Harus diberikan antibiotika profilaksis- Harus diberikan antibiotika profilaksis
mmorfologiorfologi
ffraktura tengkorakraktura tengkorak
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
mmorfologiorfologi
ffraktura tengkorakraktura tengkorak
Standar Foto KepalaStandar Foto Kepala
• RutinRutin : AP + Lateral: AP + Lateral• OccipitalOccipital : Towne: Towne• OrbitaOrbita : Caldwell: Caldwell• ViscerocraniumViscerocranium : Waters: Waters• ZygomaticumZygomaticum : Axial: Axial• Basis Cranii dan os petrosumBasis Cranii dan os petrosum
: Stanver bilateral: Stanver bilateral
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Hematoma epidural (EDH) =Hematoma epidural (EDH) =regio temporal atau temporal-parietal regio temporal atau temporal-parietal
robeknya pembuluh meningeal mediarobeknya pembuluh meningeal media (darah (darah arterial, atau arterial, atau
sekunder dari vena (sekunder dari vena (1/3 1/3 kasuskasus) ) akibat robeknya sinus venaakibat robeknya sinus vena tt..u u
parietal-oksipitalparietal-oksipital - - fossa posterio fossa posterior)r)
0.5% dari keseluruhan atau 9% dari pasien koma0.5% dari keseluruhan atau 9% dari pasien koma cedera kepalacedera kepala
menegakkan diagnosis harus ditindaklanjuti segera menegakkan diagnosis harus ditindaklanjuti segera
interval lucidinterval lucid
kelemahan anggota gerak (& defisit neurologis) yang tidak ekualkelemahan anggota gerak (& defisit neurologis) yang tidak ekual
dilatasi pupil ipsilateraldilatasi pupil ipsilateral
OutcomeOutcome langsung bergantung pada status pasien sebelum langsung bergantung pada status pasien sebelum
operasi. Mortalitas dari hematoma epidural sekitar 0% pada operasi. Mortalitas dari hematoma epidural sekitar 0% pada
pasien tidak komapasien tidak koma, , dan 20% pada pasien koma dalamdan 20% pada pasien koma dalam
mmorfologiorfologi
Lesi intrakranialLesi intrakranial
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Hematoma subdural (SDH) =Hematoma subdural (SDH) =Jauh lebih sering dariJauh lebih sering dari hematomahematoma epidural, epidural,
sekitar 30% penderitasekitar 30% penderita dengan CKBdengan CKB
Paling sering akibat robeknya vena Paling sering akibat robeknya vena bridgingbridging antara antara
korteks serebral dan sinus korteks serebral dan sinus drainingdraining., dapat berkaitan ., dapat berkaitan
dengan laserasi permukaan atau substansi otak. dengan laserasi permukaan atau substansi otak.
UmumnyaUmumnya lebih berat dan prognosisnya lebih buruk lebih berat dan prognosisnya lebih buruk
nyeri kepala terus memberat disertai penurunan nyeri kepala terus memberat disertai penurunan
kesadarankesadaran
MMortalitasortalitas 60%,60%, diperkecil oleh tindakan operasi yang diperkecil oleh tindakan operasi yang
sangat segera dan pengelolaan medis agresifsangat segera dan pengelolaan medis agresif
mmorfologiorfologi
Lesi intrakranialLesi intrakranial
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Types of Damage in Brain Injury (Stamp, 2000)
• Shearing injury of axons • Deep cerebral cortex, thalamus, basal ganglia• Punctate hemorrhage and diffuse cerebral edema
Diffuse Axonal Injury
DIFFUSE AXONAL SHEARING
• When axons are torn or stretched as a result of the different layers moving at different speeds, this called SHEARING.
• Shear damage is microscopic
• This is a common cause of brain damage after TBI
Mild to moderate ischemiaMild to moderate ischemiaSevere ischemiaSevere ischemiaAdvanced ischemiaAdvanced ischemia
Insufficient oxygenInsufficient oxygenand glucoseand glucose
Inadequate energyInadequate energysupplysupply
Failure of neuronal activityFailure of neuronal activityRegional brain dysfunctionRegional brain dysfunction
Influx of waterInflux of waterNaNa++ Cl Cl--
Loss of functionLoss of functioncauses accumulationcauses accumulation
of glutamate of glutamate and aspartateand aspartatewhich bind towhich bind to
NMDA receptorsNMDA receptorsInflux of CaInflux of Ca2+2+
Influx of waterInflux of waterNaNa++ Ca Ca2+2+
Destruction of cellDestruction of cell
componentscomponents
Formation of Formation of
free radicals,free radicals,
eicosanoids andeicosanoids and
leukotrienesleukotrienes
Accumulation of lactic acid and HAccumulation of lactic acid and H++
compromises neuronal integritycompromises neuronal integrity
AnaerobicAnaerobicmetabolismmetabolism
Cytotoxic edemaCytotoxic edema
Irreversible cellular injuryIrreversible cellular injury
Cellular injury during ischemia - Inadequate energy Cellular injury during ischemia - Inadequate energy supplysupply
Ischemia Ischemia ( O( O22,glucose),glucose)
ATP ATP DepolarisationDepolarisation
Failed homeostatic Failed homeostatic mechanismsmechanisms
Lactic acidLactic acid
Free FeFree Fe2+2+
Free radicalsFree radicals
Glial injuryGlial injury
IRREVERSIBLE INJURYIRREVERSIBLE INJURY
ProteolysiProteolysiss
NO synthesisNO synthesisLipolysisLipolysis
GlutamateGlutamate
Arachidonic acidArachidonic acidAuto-oxidationAuto-oxidation
NA DANA DA
NeurotransmittersNeurotransmitters
[H[H++]][Na[Na++] ] ii [K[K++] ] ii [Cl[Cl--] ] ii
[Ca[Ca2+2+] ] ii
VCRVCR
LCRLCR
Free radicalsFree radicals
29.3 + 16.4Mc Laughlin, 1996
39.9 + 11.2 (Schroeder, 1995)
42.5 + 15.8 (Mc Laughlin, 1996)Vasoreactivity 0.4-9.1%
ContusionContusion
Perilesional edemaPerilesional edema
CT-normal tissueCT-normal tissue
Cerebral Blood FlowCerebral Blood Flow
TraumaIschemia
•Edema sitotoksik•Ggn membran•Ggn sintesis protein
Energi turun Depolarisasi Sel
Fe lepas
Disrupsi Ca Glutamat lepas
Radikal bebas
Destruksi sel Asidosis
Secondary Brain Injury (Cohadon, 1995)
Hipoksia/ Iskemia/ Trauma
Pelepasan neurotransmiter Penurunan ATP
Depolarisasi sel Kegagalan pompa
Ca intrasel naik Nekrosis
Ca mitokondria naik
Fx apoptogenik lepas Tranduksi signal abnormal
Pembentukan ReactiveOxygen Species
Apoptosis
Zauner, 2002
Mechanism of Cytotoxic edema in brain injury (Stamp, 2000)
CBF
MAP(mmHg)
Normal 50 - 100 ml / min
Normal 60 - 150 mmHg
Cerebral Blood Flow
Regulation of Cerebral Vascular Resistance
PaCo2 (mmHg)
Normal 30 - 50 mmHg
Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651
• Inadequate Energy supplyInadequate Energy supply
Cellular injury during ischemiaCellular injury during ischemia
• Consequences of calcium overloadConsequences of calcium overload
• Deterioration of Ion GradientsDeterioration of Ion Gradients
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Monroe-Kellie PrincipleMonroe-Kellie Principle
Brain Blood
CSF MassBone
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Management of Traumatic Head InjuryManagement of Traumatic Head Injury
• Decrease intracranial pressureDecrease intracranial pressure• Support circulation / maximize Support circulation / maximize
cerebral perfusion pressurecerebral perfusion pressure• Maximize oxygenation and Maximize oxygenation and
ventilationventilation• Decrease cerebral metabolic rateDecrease cerebral metabolic rate
MANAGEMENT OF HEAD INJURYMANAGEMENT OF HEAD INJURY
• Goals of resuscitation and treatment Goals of resuscitation and treatment is to minimize secondary ischemic is to minimize secondary ischemic brain injury by promoting and brain injury by promoting and preserving cerebral perfusionpreserving cerebral perfusion– Prevent or treat post injury Prevent or treat post injury
hypotensionhypotension– Prevent or treat hypoxemia and Prevent or treat hypoxemia and
reduce oxygen demand of the brain reduce oxygen demand of the brain – Prevent or treat intracranial Prevent or treat intracranial
hypertensionhypertension– Avoid measures that decrease Avoid measures that decrease
cerebral perfusioncerebral perfusion
TREATMENTTREATMENT
GOAL PHARMACOLOGICAL AGENT :GOAL PHARMACOLOGICAL AGENT : TO GAIN PHYSIOLOGICAL CONTROL OF THE PATIENT TO GAIN PHYSIOLOGICAL CONTROL OF THE PATIENT
IN ORDER TO OPTIMIZE SUBSTRATE DELIVERY TO IN ORDER TO OPTIMIZE SUBSTRATE DELIVERY TO THE BRAIN AND PREVENT PAROXYSMAL INCREASES THE BRAIN AND PREVENT PAROXYSMAL INCREASES IN INTRACRANIAL PRESSURE IN INTRACRANIAL PRESSURE (PARALYTIC, (PARALYTIC, ANALGESICS, PRESSORS)ANALGESICS, PRESSORS)
TO PREVENT OR TREAT BRAIN SWELLING TO PREVENT OR TREAT BRAIN SWELLING (DIURETICS, BARBITURATES)(DIURETICS, BARBITURATES)
TO DECREASE SECONDARY(OR DELAYED PRIMARY) TO DECREASE SECONDARY(OR DELAYED PRIMARY) DAMAGE DAMAGE (STEROID)(STEROID)
TO TREAT SYMPTOMS ASSOCIATED WITH BRAIN TO TREAT SYMPTOMS ASSOCIATED WITH BRAIN INJURY INJURY (SEDATIVE, STIMULANTS)(SEDATIVE, STIMULANTS)
TO PREVENT OR TO TREAT COMPLICATION OF BRAIN TO PREVENT OR TO TREAT COMPLICATION OF BRAIN INJURY INJURY (ANTIBIOTIC, ANTICONVULSANT, (ANTIBIOTIC, ANTICONVULSANT, NEUROPROTECTANT)NEUROPROTECTANT)
MonitoringMonitoring
• Serial neurologic Serial neurologic examinationsexaminations
• Circulation / RespirationCirculation / Respiration• Intracranial PressureIntracranial Pressure• Radiologic Studies Radiologic Studies • Laboratory StudiesLaboratory Studies
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Managemen di Unit Gawat DaruratManagemen di Unit Gawat Darurat
• Tanda vital:Tanda vital: – TD, N, RR, temperatur, tipe pernafasan (cheyne-TD, N, RR, temperatur, tipe pernafasan (cheyne-
stokes, cluster, apneustic, ataxic)stokes, cluster, apneustic, ataxic)
• Inspeksi kelainan sistemisInspeksi kelainan sistemis• Inspeksi kraniumInspeksi kranium
– Tanda2 # basis kraniiTanda2 # basis kranii– Tanda2 # kranium lain, # facial, dllTanda2 # kranium lain, # facial, dll– Periorbital edema, proptosisPeriorbital edema, proptosis
• Cranio-cervical auscultationCranio-cervical auscultation– Bruit a. carotis = diseksi a. carotisBruit a. carotis = diseksi a. carotis– Bruit pada mata = fistula traumatis carotis-Bruit pada mata = fistula traumatis carotis-
cavernosuscavernosus
• Tanda-tanda trauma medulla-spinalisTanda-tanda trauma medulla-spinalis• Adanya kejangAdanya kejang = tunggal, multiple, status = tunggal, multiple, status
Pemeriksaan Fisik secara umumPemeriksaan Fisik secara umum
MMaannaajemen dan Terapijemen dan Terapi
• Di Unit Gawat Darurat: Di Unit Gawat Darurat: – Riwayat: jenis dan saat kecelakaan, kehilangan Riwayat: jenis dan saat kecelakaan, kehilangan
kesadaran, amnesia, nyeri kepala kesadaran, amnesia, nyeri kepala – Pemeriksaan umumPemeriksaan umum menyingkirkan cedera menyingkirkan cedera
sistemik sistemik – Pemeriksaan neurologis Pemeriksaan neurologis – Radiograf tengkorak Radiograf tengkorak – Radiograf tulang belakang leher dan lain-lain Radiograf tulang belakang leher dan lain-lain
bilabila ada indikasi ada indikasi – Kadar alkohol darah dan skrining toksik dari urin Kadar alkohol darah dan skrining toksik dari urin
(terutama suspected) (terutama suspected) – Contoh darah untuk penentuan golongan darah Contoh darah untuk penentuan golongan darah
– Tes darah dasar dan EKG Tes darah dasar dan EKG – CT scan CT scan kepala (bila memungkinkan) kepala (bila memungkinkan) – Rawat untuk pengamatan bahkan bila Rawat untuk pengamatan bahkan bila CT scan CT scan
normalnormal
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Managemen di Unit Gawat DaruratManagemen di Unit Gawat Darurat
• Status kesadaran: Status kesadaran: – GCS, tipe pernafasan, pupil, refleks GCS, tipe pernafasan, pupil, refleks
cahaya, refleks kornea, doll’s eye cahaya, refleks kornea, doll’s eye phenomena, deviasi conjugae phenomena, deviasi conjugae tanda herniasitanda herniasi
• Saraf kranial:Saraf kranial: – t.u n.II, III, IV, VI, VII, & funduskopit.u n.II, III, IV, VI, VII, & funduskopi
• Pemeriksaan motorikPemeriksaan motorik• Pemeriksaan refleks patologis, Pemeriksaan refleks patologis,
clonus, & refleks fisiologisclonus, & refleks fisiologis• Pemeriksaan sensorisPemeriksaan sensoris
Pemeriksaan NeurologisPemeriksaan Neurologis
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Managemen di Unit Gawat DaruratManagemen di Unit Gawat Darurat
• BR dengan HOB elevasi 30-45 BR dengan HOB elevasi 30-45 derajatderajat
• Pemeriksaan neurologis tiap 2 jamPemeriksaan neurologis tiap 2 jam• OksigenasiOksigenasi• IVFD isotonik (misal: NS, RL, IVFD isotonik (misal: NS, RL,
Assering)Assering)• Analgetika ringan PO atau PRAnalgetika ringan PO atau PR• Anti-emesis (k/p)Anti-emesis (k/p)• Lain-lain Lain-lain individual individual
Cedera Kepala Ringan (CKR)Cedera Kepala Ringan (CKR)
MANAGEMENT OF MILD HEAD INJURYMANAGEMENT OF MILD HEAD INJURY
HISTORY :HISTORY :• NAME, AGE, SEX, RACE, OCCUPATIONNAME, AGE, SEX, RACE, OCCUPATION• MECHANISM OF INJURYMECHANISM OF INJURY• TIME OF INJURYTIME OF INJURY• LOSS OF CONSCIOUSNESS IMMEDIATELY LOSS OF CONSCIOUSNESS IMMEDIATELY
AFTER INJURYAFTER INJURY• SUBSEQUENT LEVEL OF ALERTNESSSUBSEQUENT LEVEL OF ALERTNESS• AMNESIA : RETROGRADE, AMNESIA : RETROGRADE,
ANTEROGRADEANTEROGRADE• HEADACHE : MILD, MODERATE, SEVEREHEADACHE : MILD, MODERATE, SEVERE• SEIZURESEIZURE
MANAGEMENT OF MILD HEAD INJURYMANAGEMENT OF MILD HEAD INJURY
• GENERAL EXAMINATION TO EXCLUDE GENERAL EXAMINATION TO EXCLUDE SYSTEMIC INJURYSYSTEMIC INJURY
• LIMITED NEUROLOGICAL EXAMINATIONLIMITED NEUROLOGICAL EXAMINATION• CERVICAL SPINE AND OTHER CERVICAL SPINE AND OTHER
RADIOGRAPHS AS INDICATEDRADIOGRAPHS AS INDICATED• BLOOD ALKOHOL LEVEL AND URINE BLOOD ALKOHOL LEVEL AND URINE
TOXIC SCREENTOXIC SCREEN• CT SCAN OF THE HEAD IN ALL PATIENT CT SCAN OF THE HEAD IN ALL PATIENT
EXCEPT COMPLETELY ASYMPTOMATIC EXCEPT COMPLETELY ASYMPTOMATIC AND NEUROLOGICALLY NORMAL AND NEUROLOGICALLY NORMAL PATIENT IS IDEAL PATIENT IS IDEAL
MANAGEMENT OF MILD HEAD INJURYMANAGEMENT OF MILD HEAD INJURY
• OBSERVE IN/ADMITTED TO HOSPITALOBSERVE IN/ADMITTED TO HOSPITAL– NO CT SCANNER AVAILABLENO CT SCANNER AVAILABLE– ABNORMAL CT SCANABNORMAL CT SCAN– ALL PENETRATING HEAD INJURYALL PENETRATING HEAD INJURY– HISTORY OF LOSS CONSCIUOSNESSHISTORY OF LOSS CONSCIUOSNESS– DETERIORATING CONSCIOUSNESSDETERIORATING CONSCIOUSNESS– MODERATE TO SEVERE HEADACHEMODERATE TO SEVERE HEADACHE– SIGNIFICANT ALCOHOLIC/DRUG SIGNIFICANT ALCOHOLIC/DRUG
INTOXICATIONINTOXICATION– SKULL FRAKTURESKULL FRAKTURE– CSF LEAK RHINORRHEA OR OTORRHEACSF LEAK RHINORRHEA OR OTORRHEA
MANAGEMENT OF MILD HEAD INJURYMANAGEMENT OF MILD HEAD INJURY
– SIGNIFICANT ASSOCIATED INJURIESSIGNIFICANT ASSOCIATED INJURIES– NO RELIABLE COMPANION AT HOMENO RELIABLE COMPANION AT HOME– UNABLE TO RETURN PROMPTLYUNABLE TO RETURN PROMPTLY– AMNESIAAMNESIA– HISTORY OF LOOS OF HISTORY OF LOOS OF
CONSCIOUSNESSCONSCIOUSNESS
MANAGEMENT OF MILD HEAD INJURYMANAGEMENT OF MILD HEAD INJURY
• DISCHARGE FROM HOSPITAL :DISCHARGE FROM HOSPITAL :– PATIENT DOES NOT MEET ANY OF PATIENT DOES NOT MEET ANY OF
CRITERIA FOR ADMISSIONCRITERIA FOR ADMISSION– DISCUSS NEED TO RETURN IF ANY DISCUSS NEED TO RETURN IF ANY
PROBLEMS DEVELOP AND ISSUE PROBLEMS DEVELOP AND ISSUE A”WARNING SHEET”A”WARNING SHEET”
– SCHEDULE FOLLOW-UP CLINIC VISIT, SCHEDULE FOLLOW-UP CLINIC VISIT, USSUALY WITHIN 1 WEEKUSSUALY WITHIN 1 WEEK
Peringatan untuk pasien cedera kepala ringan dan Peringatan untuk pasien cedera kepala ringan dan
sedang yang terpaksa dipulangkan/ menolak sedang yang terpaksa dipulangkan/ menolak
observasi observasi
di rumah sakit: di rumah sakit:
• PADA SAAT INI KAMI BELUM MENEMUKAN KELAINAN PADA SAAT INI KAMI BELUM MENEMUKAN KELAINAN
YANG MENUNJUKKAN BAHWA CEDERA KEPALA YANG YANG MENUNJUKKAN BAHWA CEDERA KEPALA YANG
ANDA ALAMI ADALAH SANGAT SERIUS. NAMUN, GEJALA ANDA ALAMI ADALAH SANGAT SERIUS. NAMUN, GEJALA
YANG BARU DAN KOMPLIKASI YANG TIDAK DISANGKA-YANG BARU DAN KOMPLIKASI YANG TIDAK DISANGKA-
SANGKA DAPAT TIMBUL DALAM BEBERAPA JAM HINGGA SANGKA DAPAT TIMBUL DALAM BEBERAPA JAM HINGGA
BEBERAPA HARI SETELAH CEDERA. 24 JAM PERTAMA BEBERAPA HARI SETELAH CEDERA. 24 JAM PERTAMA
ADALAH WAKTU YANG PALING GENTING DAN ANDA ADALAH WAKTU YANG PALING GENTING DAN ANDA
HARUS TETAP BERADA DALAM HARUS TETAP BERADA DALAM PPENGAWASAN KELUARGA ENGAWASAN KELUARGA
ATAU ORANG YANG DAPAT DIPERTANGGUNG-ATAU ORANG YANG DAPAT DIPERTANGGUNG-
JAWABKAN, PALING TIDAK DALAM PERIODE INI. JAWABKAN, PALING TIDAK DALAM PERIODE INI.
BILA ADA DARI TANDA-TANDA DIBAWAH INI TERJADI, BILA ADA DARI TANDA-TANDA DIBAWAH INI TERJADI,
SEGERA KEMBALI KE RUMAH-SAKIT:SEGERA KEMBALI KE RUMAH-SAKIT:
1. Mengantuk atau semakin sulit membangunkan pasien 1. Mengantuk atau semakin sulit membangunkan pasien
(Pasien harus dibangunkan setiap 2 jam selama masa tidur).(Pasien harus dibangunkan setiap 2 jam selama masa tidur).
2. Mual atau muntah.2. Mual atau muntah.
3. Kejang-kejang atau sawan.3. Kejang-kejang atau sawan.
4. Mengalirnya darah atau cairan dari hidung atau telinga.4. Mengalirnya darah atau cairan dari hidung atau telinga.
5. Nyeri kepala hebat.5. Nyeri kepala hebat.
6. Kelemahan atau kehilangan rasa dari tungkai atau lengan.6. Kelemahan atau kehilangan rasa dari tungkai atau lengan.
7. Bingung atau berkelakuan asing.7. Bingung atau berkelakuan asing.
8. 8. Satu pupil (bagian hitam dari mata) lebih lebar dari sisi Satu pupil (bagian hitam dari mata) lebih lebar dari sisi
lainnya; gerakan yang tidak biasa dari bola mata, lainnya; gerakan yang tidak biasa dari bola mata,
penglihatan ganda atau gangguan penglihatan lainnya.penglihatan ganda atau gangguan penglihatan lainnya.
9. Denyut nadi yang sangat lambat/sangat cepat, atau pola 9. Denyut nadi yang sangat lambat/sangat cepat, atau pola
pernafasan yg tidak biasa. pernafasan yg tidak biasa.
Jangan makan sedatif atau penghilang nyeri jenis apapun Jangan makan sedatif atau penghilang nyeri jenis apapun
yang lebih kuat dari parasetamol, paling tidak dalam 24 yang lebih kuat dari parasetamol, paling tidak dalam 24
jam pertama. Jangan gunakan obat-obat yang jam pertama. Jangan gunakan obat-obat yang
mengandung asetosal (aspirin). mengandung asetosal (aspirin).
Cedera KepalaCedera Kepala (traumatic brain injury)(traumatic brain injury)
Managemen di Unit Gawat DaruratManagemen di Unit Gawat Darurat
• Sama dgn CKRSama dgn CKR• GCS = 9-12 GCS = 9-12 ICU ICU• Head CT-scanHead CT-scan
CKB CKB Intubasi & Hiperventilasi Intubasi & Hiperventilasi
Cedera Kepala Sedang (CKS)Cedera Kepala Sedang (CKS)
MANAGEMENT OF MODERATE HEAD MANAGEMENT OF MODERATE HEAD INJURYINJURY
• INITIAL WORKUPINITIAL WORKUP– SAME AS FOR MILD INJURY,PLUS BASELINE SAME AS FOR MILD INJURY,PLUS BASELINE
BLOOD WORKBLOOD WORK– CT SCAN OF THE HEAD OBTAINED IN ALL CT SCAN OF THE HEAD OBTAINED IN ALL
CASESCASES– ADMISSION FOR OBSERVATIONAFTER ADMISSION FOR OBSERVATIONAFTER
ADMISSIONADMISSION• FREQUENT NEUROLOGICAL CHECKSFREQUENT NEUROLOGICAL CHECKS• FOLLOW-UP CT SCAN IF CONDITION FOLLOW-UP CT SCAN IF CONDITION
DETERIORATESDETERIORATES
MANAGEMENT OF MODERATE MANAGEMENT OF MODERATE (CONT)(CONT)
• IF PATIENT IF PATIENT IMPROVES (90%)IMPROVES (90%)
– DISCHARGE DISCHARGE WHEN WHEN APPROPRIATEAPPROPRIATE
– FOLLOW-UP IN FOLLOW-UP IN CLINICCLINIC
• IF PATIENT IF PATIENT DETERIORATE (10%)DETERIORATE (10%)– IF PATIENT STOPS IF PATIENT STOPS
FOLLOWING FOLLOWING SIMPLE SIMPLE COMMANDS, COMMANDS, REPEAT CT SCAN REPEAT CT SCAN AND MANAGE PER AND MANAGE PER SEVERE HEAD SEVERE HEAD INJURY INJURY PROTOCOL.PROTOCOL.
INITIAL MANAGEMENT OF SEVERE INITIAL MANAGEMENT OF SEVERE HEAD INJURYHEAD INJURY
• ASSESSMENT AND MANAGEMENTASSESSMENT AND MANAGEMENT– ABCABC– PRIMARY SURVEY AND AMPLE HISTORY PRIMARY SURVEY AND AMPLE HISTORY
(ALLERGIES, MEDICATIONS, PAST ILLNESS, (ALLERGIES, MEDICATIONS, PAST ILLNESS, LAST MEAL, EVENTS RELATED HEAD INJURY)LAST MEAL, EVENTS RELATED HEAD INJURY)
• NEUROLOGICAL REEVALUATION:NEUROLOGICAL REEVALUATION:• EYE OPENINGEYE OPENING• MOTOR RESPONSEMOTOR RESPONSE• VERBAL RESPONSEVERBAL RESPONSE• PUPILLARY LIGH REACTIONSPUPILLARY LIGH REACTIONS• DOLL’S EYEDOLL’S EYE
INITIAL MANAGEMENT OF SEVERE HEAD INITIAL MANAGEMENT OF SEVERE HEAD INJURY (CONT)INJURY (CONT)
• THERAPEUTIC AGENTSTHERAPEUTIC AGENTS– MANNITOLMANNITOL– ANTICONVULSANTANTICONVULSANT– MODERATE HIPERVENTILATIONMODERATE HIPERVENTILATION
INDICATION OF SURGERYINDICATION OF SURGERY
• EPIDURAL HEMORRHAGEEPIDURAL HEMORRHAGE• SUBDURAL HEMORRHAGESUBDURAL HEMORRHAGE• INTRACEREBRAL HEMORRHAGEINTRACEREBRAL HEMORRHAGE• DEPRESSED FRAKTUREDEPRESSED FRAKTURE
SECARA UMUM …SECARA UMUM …
• A, B, C’sA, B, C’s• Major early risk is hypotensionMajor early risk is hypotension
– Adequate fluid resuscitation to Adequate fluid resuscitation to restore normal BP does NOT restore normal BP does NOT worsen neurologic outcomeworsen neurologic outcome
– Avoid hypotonic fluidsAvoid hypotonic fluids• Emergent airway control forEmergent airway control for
– GCS 8 or lessGCS 8 or less– GSC 10 or less with abnormal head GSC 10 or less with abnormal head
CTCT– Rapid neurologic deteriorationRapid neurologic deterioration– If needed for other injuriesIf needed for other injuries
• Dilatasi pupil unilateral atau Dilatasi pupil unilateral atau bilateralbilateral
• Refleks cahaya asimetrisRefleks cahaya asimetris• Deserebrasi atau dekortikasiDeserebrasi atau dekortikasi• Deteriorasi neurologis Deteriorasi neurologis
progresifprogresif
Tanda-tanda klinis IC-HTNTanda-tanda klinis IC-HTN
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Head positionHead position– Head elevated 30 degrees and Head elevated 30 degrees and
midlinemidline• Sedation and pain controlSedation and pain control
– Analgesic + anxiolyticAnalgesic + anxiolytic• Fentanyl, morphine, or propofol Fentanyl, morphine, or propofol
plus a benzodiazepineplus a benzodiazepine• Continuous infusions or scheduled Continuous infusions or scheduled
doses to maintain sedationdoses to maintain sedation– Watch for and treat hypotensionWatch for and treat hypotension
• Seizure prophylaxisSeizure prophylaxis– Phenytoin or phosphenytoinPhenytoin or phosphenytoin
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Neuromuscular blockadeNeuromuscular blockade– Facilitates mechanical ventilation Facilitates mechanical ventilation
and control of pCOand control of pCO22
– Prevents shiveringPrevents shivering– Use if movement increases ICPUse if movement increases ICP
• Temperature controlTemperature control– A rise in temp of 1A rise in temp of 1oo C increases C increases
cerebral metabolic rate by 10%, cerebral metabolic rate by 10%, increasing ICP by several mm Hgincreasing ICP by several mm Hg
– Maintain temp < 37.5 Maintain temp < 37.5 oo C C• Scheduled acetaminophen, body Scheduled acetaminophen, body
exposure, cooling blanketexposure, cooling blanket
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Osmotherapy with mannitolOsmotherapy with mannitol– Decreases extracellular fluid in brainDecreases extracellular fluid in brain– Intermittent doses for ICP spikes or Intermittent doses for ICP spikes or
scheduled if elevated ICP is persistentscheduled if elevated ICP is persistent– Adverse effects:Adverse effects:
• Hypernatremia, hypokalemiaHypernatremia, hypokalemia• HyperosmolalityHyperosmolality• Hemodilution and drop in hematocritHemodilution and drop in hematocrit• HypotensionHypotension
– Follow serum osmolality and NaFollow serum osmolality and Na• Hold mannitol if serum osm > 320 Hold mannitol if serum osm > 320
mOsm/lmOsm/l
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Drainage of CSFDrainage of CSF– Possible if ventricular catheter is in Possible if ventricular catheter is in
placeplace– CSF drainage pressure usually set CSF drainage pressure usually set
at 20 cm Hat 20 cm H22OO
– CSF drains when ICP exceeds CSF drains when ICP exceeds drainage pressuredrainage pressure
– Ventricular catheters cannot be Ventricular catheters cannot be placed if cerebral edema has placed if cerebral edema has obliterated or significantly obliterated or significantly compressed ventriclescompressed ventricles
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Second tier therapies for intracranial Second tier therapies for intracranial hypertension refractory to sedation, hypertension refractory to sedation, muscle relaxation, osmotherapy, and muscle relaxation, osmotherapy, and moderate hypothermia:moderate hypothermia:– barbiturate “coma”barbiturate “coma”– induced hypertensioninduced hypertension– decompressive craniotomydecompressive craniotomy– hypothermiahypothermia
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Barbiturate “coma”Barbiturate “coma”– ICP control is the principal endpointICP control is the principal endpoint– EEG burst suppression is a useful guide to EEG burst suppression is a useful guide to
optimal barbiturate dosageoptimal barbiturate dosage• Pentobarbital 10mg/kg followed by Pentobarbital 10mg/kg followed by
infusion at 1 mg/kg/hr, titrated to infusion at 1 mg/kg/hr, titrated to effecteffect
• May give additional boluses during May give additional boluses during infusion for acute spikes in ICPinfusion for acute spikes in ICP
• Moderate doses cause sluggishly Moderate doses cause sluggishly reactive pupils while large doses may reactive pupils while large doses may cause mid position to 5 mm cause mid position to 5 mm nonreacting pupilsnonreacting pupils
• Watch for hypotensionWatch for hypotension
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• Induced hypertensionInduced hypertension– Inotropes to increase MAP, even beyond Inotropes to increase MAP, even beyond
normal for age, to achieve an optimal CPPnormal for age, to achieve an optimal CPP• DopamineDopamine• NorepineprineNorepineprine
– Rise in ICP in tandem with a rise in MAP Rise in ICP in tandem with a rise in MAP implies total loss of autoregulation and is a implies total loss of autoregulation and is a poor prognostic signpoor prognostic sign
• Decompressive craniotomyDecompressive craniotomy– Large portion of cranium removed to allow Large portion of cranium removed to allow
room for brain to swell and minimize room for brain to swell and minimize ischemiaischemia
– Dura must be opened as wellDura must be opened as well
MANAGEMENT OF INCREASED ICPMANAGEMENT OF INCREASED ICP
• HypothermiaHypothermia– Core body temp of 32Core body temp of 32oo to 33 to 33oo C C– Reduced cerebral metabolic Reduced cerebral metabolic
activity, reducing ICPactivity, reducing ICP– Also has cytoprotective effectsAlso has cytoprotective effects– Adverse effectsAdverse effects
• ArrythmiasArrythmias• CoagulopathiesCoagulopathies• HypokalemiaHypokalemia• Increased risk of infectionIncreased risk of infection
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• RespiratoryRespiratory– Maintain normocapniaMaintain normocapnia
• Hyperventilation only appropriate during early Hyperventilation only appropriate during early diagnosis and management or if herniation is diagnosis and management or if herniation is impendingimpending
– Maintain oxygenationMaintain oxygenation• pOpO2 2 > 100 is optimal> 100 is optimal
– PEEP to maintain alveolar recruitmentPEEP to maintain alveolar recruitment• ARDS, neurogenic pulmonary edema frequent ARDS, neurogenic pulmonary edema frequent
complicationscomplications• Hypoxemia has more deleterious effects on brain Hypoxemia has more deleterious effects on brain
than modest venous congestion caused by PEEPthan modest venous congestion caused by PEEP• PEEP of 5 to 10 cm HPEEP of 5 to 10 cm H22O not shown to have O not shown to have
detrimental effect on neurologic outcomedetrimental effect on neurologic outcome
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• CardiovascularCardiovascular– Maintain normal blood pressureMaintain normal blood pressure
• Hypotension significantly reduces CPPHypotension significantly reduces CPP• Inotropes if necessary to maintain normal Inotropes if necessary to maintain normal
BPBP– Induced hypertension if necessary Induced hypertension if necessary
• GastrointestinalGastrointestinal– Stress gastritis prophylaxis with HStress gastritis prophylaxis with H22 blocker blocker– Jejunal feeds to maintain healthy intestinal Jejunal feeds to maintain healthy intestinal
mucosa and prevent bacterial translocation mucosa and prevent bacterial translocation from gutfrom gut
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• Fluids, Electrolytes, NutritionFluids, Electrolytes, Nutrition– Goal is NORMOVOLEMIAGoal is NORMOVOLEMIA
• Total fluid intake should be @ 100% Total fluid intake should be @ 100% maintenancemaintenance
• Bolus as necessary to achieve normal CVPBolus as necessary to achieve normal CVP– Avoid hypotonic fluidsAvoid hypotonic fluids
• Lactated Ringer’s and 0.9% saline w/ 20 Lactated Ringer’s and 0.9% saline w/ 20 mEq KCl/l are good choices for maintenance mEq KCl/l are good choices for maintenance fluidsfluids
– Follow electrolytes closelyFollow electrolytes closely• Avoid hyponatremiaAvoid hyponatremia• Mannitol can cause electrolyte abnormalitiesMannitol can cause electrolyte abnormalities• Watch for SIADH, diabetes insipidus, Watch for SIADH, diabetes insipidus,
cerebral salt wastingcerebral salt wasting
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• Fluids, electrolytes, nutritionFluids, electrolytes, nutrition– Provide calories to meet metabolic demands of Provide calories to meet metabolic demands of
patientpatient• Increased metabolic demands during acute Increased metabolic demands during acute
phase of injuryphase of injury• Heavily sedated, relaxed, cooled patient has Heavily sedated, relaxed, cooled patient has
decreased metabolic demandsdecreased metabolic demands• Enteral feedings via nasojejunal catheter Enteral feedings via nasojejunal catheter
preferable to TPN if gut deemed to be preferable to TPN if gut deemed to be healthyhealthy
– Avoid hyperglycemiaAvoid hyperglycemia• Associated with poor neurologic outcomeAssociated with poor neurologic outcome• Watch serum glucose closely if dextrose Watch serum glucose closely if dextrose
containing fluids usedcontaining fluids used
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• RenalRenal– Place foley for strict I’s and O’sPlace foley for strict I’s and O’s
• HematologicHematologic– Coagulopathy common with head injuriesCoagulopathy common with head injuries
• Brain derived thromboplastin activator Brain derived thromboplastin activator substances releasedsubstances released
– Follow PT/PTT or DIC screens Follow PT/PTT or DIC screens – Blood component replacement if evidence Blood component replacement if evidence
of active bleeding or if surgical intervention of active bleeding or if surgical intervention anticipatedanticipated
– Maintain normal hematocrit to optimize Maintain normal hematocrit to optimize oxygen deliveryoxygen delivery
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• EndocrineEndocrine– DIABETES INSIPIDUSDIABETES INSIPIDUS
• Complete or partial failure of ADH Complete or partial failure of ADH secretion from shearing of pituitary secretion from shearing of pituitary stalkstalk
• Polyuria, hypernatremia, urine osm < Polyuria, hypernatremia, urine osm < plasma osmplasma osm
• Treatment:Treatment:Run maintenance fluids @ 100%Run maintenance fluids @ 100%Replace urine output cc for cc with Replace urine output cc for cc with dextrose-containing fluidsdextrose-containing fluidsContinuous vasopressin infusion or Continuous vasopressin infusion or DDAVP (subQ or intranasal) q 12 to 24 DDAVP (subQ or intranasal) q 12 to 24 hrshrs
MANAGEMENT OF OTHER SYSTEMSMANAGEMENT OF OTHER SYSTEMS
• EndocrineEndocrine– CEREBRAL SALT-WASTINGCEREBRAL SALT-WASTING
• ANP-like substance released from brain, ANP-like substance released from brain, inducing natriuresis and diuresisinducing natriuresis and diuresis
– SIADHSIADH• Elevated level of ADH inappropriate for Elevated level of ADH inappropriate for
prevailing osmotic or volume stimuliprevailing osmotic or volume stimuli• Hyponatremia, hypo-osmolality, urine Hyponatremia, hypo-osmolality, urine
osm > plasma osm, high urine Naosm > plasma osm, high urine Na• Treatment is water restrictionTreatment is water restriction
SUMMARYSUMMARY
• Identify and treat primary brain injuryIdentify and treat primary brain injury– Rule out neurosurgical emergencyRule out neurosurgical emergency
• Minimize secondary ischemic brain injury Minimize secondary ischemic brain injury by promoting cerebral perfusionby promoting cerebral perfusion– Maintain normovolemia and adequate BPMaintain normovolemia and adequate BP– Maintain normal electrolytes and Maintain normal electrolytes and
euglycemiaeuglycemia– Maintain normocapnia and adequate Maintain normocapnia and adequate
oxygenationoxygenation– Avoid factors that increase ICPAvoid factors that increase ICP– Treat intracranial hypertensionTreat intracranial hypertension
Summary of Recommended Summary of Recommended PracticesPractices
• Serial neurologic assessments and physical examinationSerial neurologic assessments and physical examination• Continuous cardio-respiratory, ICP, and CPP monitoring, Continuous cardio-respiratory, ICP, and CPP monitoring,
+/- cerebral metabolism monitoring adjuncts+/- cerebral metabolism monitoring adjuncts
• Maximize Oxygenation and VentilationMaximize Oxygenation and Ventilation
– Maximize oxygenation (cautious use of PEEP / keep Maximize oxygenation (cautious use of PEEP / keep
PEEP < 10 to prevent inhibited venous return / PEEP < 10 to prevent inhibited venous return /
individualize according to patient response)individualize according to patient response)
– NormoventilateNormoventilate
– Support circulation / maximize cerebral perfusion Support circulation / maximize cerebral perfusion
pressurepressure
– Maintain mean arterial blood pressure and maintain Maintain mean arterial blood pressure and maintain
CPP (goal > 60)CPP (goal > 60)
Summary of Recommended Summary of Recommended PracticesPractices• Decrease intracranial pressure Decrease intracranial pressure
– Evacuate mass occupying hemorrhages Evacuate mass occupying hemorrhages – Consider draining CSF with ventriculostomy when possibleConsider draining CSF with ventriculostomy when possible– Hyperosmolar therapy, +/- diuresis (cautious use to avoid Hyperosmolar therapy, +/- diuresis (cautious use to avoid
hypovolemia and decreased BP)hypovolemia and decreased BP)– Mid-line neck, elevated head of bead (some research Mid-line neck, elevated head of bead (some research
supports elevation not > 30 degrees)supports elevation not > 30 degrees)– Treat pain and agitation - consider pre-medication for Treat pain and agitation - consider pre-medication for
nursing activities, +/- neuromuscular blockade (only when nursing activities, +/- neuromuscular blockade (only when needed)needed)
– Careful monitoring of ICP during nursing care, cluster Careful monitoring of ICP during nursing care, cluster nursing activities and limit handling when possiblenursing activities and limit handling when possible
– Suction only as needed, limit passes, pre-oxygenate / +/- Suction only as needed, limit passes, pre-oxygenate / +/- pre-hyperventilate (PaCo2 not < 30) / use lidocaine IV or pre-hyperventilate (PaCo2 not < 30) / use lidocaine IV or IT when possibleIT when possible
– After careful preparation of visitors, allow calm contactAfter careful preparation of visitors, allow calm contact
Summary of Recommended Summary of Recommended PracticesPractices
• Decrease Cerebral Metabolic RateDecrease Cerebral Metabolic Rate
– Prevent seizures Prevent seizures
– Reserve pentobarbital for refractory Reserve pentobarbital for refractory conditionsconditions
– Avoid hyperthermia, +/- hypothermiaAvoid hyperthermia, +/- hypothermia
– Avoid hyperglycemia (early)Avoid hyperglycemia (early)
Late complications from head Late complications from head injuryinjury
Post-traumatic seizuresPost-traumatic seizures Communicating hydrocephalusCommunicating hydrocephalus Post-traumatic syndrome Post-traumatic syndrome
(or post-concussive syndrome)(or post-concussive syndrome) Hypogonadotropic hypogonadismHypogonadotropic hypogonadism Chronic traumatic encephalopathyChronic traumatic encephalopathy Alzheimer’s diseaseAlzheimer’s disease
Prediction of post-traumatic complaints after Prediction of post-traumatic complaints after mild traumatic brain injurymild traumatic brain injury
Conclusions: Conclusions: The presence of The presence of headache, headache, dizziness, or nauseadizziness, or nausea in the ER after MTBI in the ER after MTBI is strongly associated with the severity of is strongly associated with the severity of most PTC after six months. Identifying most PTC after six months. Identifying MTBI patients in the ER without headache, MTBI patients in the ER without headache, dizziness, nausea, or increased dizziness, nausea, or increased serum serum markermarker concentrations may be a concentrations may be a promising strategy for predicting a good promising strategy for predicting a good outcome.outcome. specific serum markers specific serum markers S-100B and neurone S-100B and neurone specific enolase (NSE)specific enolase (NSE)NSE and S-100B in serum and cerebrospinal fluid have NSE and S-100B in serum and cerebrospinal fluid have been reported to be markers of cell damage in the been reported to be markers of cell damage in the human central nervous systemhuman central nervous system
Condition with increased risk of post-Condition with increased risk of post-traumatic seizures after traumatic brain traumatic seizures after traumatic brain injuryinjury
EDH, SDH, ICHEDH, SDH, ICH # depressed terbuka dg cedera parenkim otak # depressed terbuka dg cedera parenkim otak Kejang dalam 24 jam pertamaKejang dalam 24 jam pertama GCS < 10GCS < 10 Cedera kepala terbukaCedera kepala terbuka Riwayat penggunaan alkoholRiwayat penggunaan alkohol Contusio cerebriContusio cerebri
Terima Kasih
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