trauma sistem saraf
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Trauma Sistem Saraf
Iwan Setiawan
Bagian ilmu Penyakit Saraf
Fakultas Kedokteran UMS
Klasifikasi cedera kepala
mekanisme severitas morfologi
Tertutup Penetrans
1. Ringan : GCS 13-152. Sedang : GCS 9-123. Berat : GCS <= 8
Fraktur tengkorakLesi intrakranial
a. Kalvaria a.1. Linear / stelata a.2.Depressed/ nondepressed
b. Basilar a .Fokal 1 Epidural 2 Subdural 3 Intraserebral
b .Difusa 1 Konkusi ringan 2 Konkusi klasik 3 Cedera aksonal difusa
(Saanin,2000)
Derajat kesadaran dengan Glasgow Coma scale
Kategori GCS Gambaran klinik CT Scan
Cedera Kranioserebral ringan
13-15 Pingsan ≤ 10 menit, defisit neurologik (-)
normal
Cedera Kranioserebral sedang
9-12 Pingsan >10 menit s/d 6 jam, defisit neurologik (+)
Normal / abnormal
Cedera Kranioserebral berat
3-8 Pingsan > 6 jam, defisit neurologik (+)
abnormal
Klasifikasi Lain:
A. Tanpa Defisit neurologis– Comotio Cerebri: pingsan sejenak, dengan atau tanpa
amnesia retrograd, tanpa kelainan neurologis
B. Dengan Kelainan Neurologis– Contusio Cerebri: Perdarahan permukaan otak, berupa
bintik perdarahan besar atau kecil, tanpa kerusakan duramater, dengan defisit neurologis yang reversibel
– Laseratio Cerebri: terputusnya / diskontinuitas jaringan otak, defisit neurologis berat, sembuh dengan gejala sisa.
– Epidural Hematom (EDH)– Subdural Hematom (SDH)– Intraserebral Hematom (ICH)
(Marjono, 2000)
Biomechanics of Traumatic Head Injury
Closed Head Injuries
Open Head Injuries
Shearing strainsthroughout thebrain
Subdural veinstorn as brainrotates forward
Swelling ofbrain stem
Damage to temporal lobes from rough bones at skull base
Compressionfracture
Types of Damage in a Closed Head InjuryTypes of Damage in a Closed Head Injury
Types of Damage in Brain Injury (Stamp, 2000)
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)
• GCS 13-15 : Mild Traumatic Brain Injury• GCS 9-12 : Moderate Traumatic Brain Injury• GCS <8 : Severe Traumatic Brain Injury
GCS Saat Masuk dan Outcome (Stein, 2000)
GCS at 24 hours Good Recovery or Vegetative or dead
moderate disability
11-15 91% 6%
8-10 59% 27%
5-7 28% 54%
3-4 13% 80%
Klasifikasi Severitas Cedera Kepala (York, 2000)
Severity level(% of headinjuries)
Characteristics
Minor headinjury (80%)
Transient loss of consciousnessGenerally followed by full recovery
Moderate headinjury (10%)
Impairment of consciousness.Recovery is more prolongedFocal deficits are more common.
Severe headinjury (10%)
Patient in coma for 24 hours or more.Mortality rate is about one-third.
Most will recover with some permanentdeficit
Lapisan-lapisan dalam pelindung otak
Epidural Hematoma
Pediatric Critical Care Textbook (1998) Lippincott Williams & Wilkins and Tutorial CT in Head Injury (Foo, 2001)
• Usually develop from injury to the middle
meningeal artery or one of its branches
• Usually temporoparietal in location
• Temporal bone fracture is often the cause
• The haematoma is confined, giving rise to its
characteristic biconvex shape
A case of 21 year old man with right temporal epidural hematoma with midline shift
Brain CT scan of 90-year-old man who slipped on a waxed floor
Commonly caused bydirect structural destruction
Subdural Hematoma
Pediatric Critical Care Textbook (1998) Lippincott Williams & Wilkins and Tutorial CT in Head Injury (Foo, 2001)
• Usually due to ruptured veins
• High density in acute phase, and becoming less
density by the time
•The blood may spread more widely with a crescentic
appearance and a more irregular inner margin.
The Mechanism
Acute subdural hematoma High-speed impact to the skull. Brain tissue will accelerate relative to a fixed dural structure, which in turn, tears blood vessels.
Chronic subdural hematomas Most cases begin as Subdural hygroma Dural border cells proliferate to produce a neomembraneFragile new vessels grow into the membrane.
Linear fracture results from low-energy blunt trauma over a wide surface area of the skull.
Depressed skull fractures result from a high-energydirect blow to a small surface area of the skull
Hemorrhagic contusion and diffuse axonal injury
Basal skull fracture• CSF Ottoehoea or Rhinorrhoea• Haematotympanum• Postauricular echimosis• Periorbital echimosis• Cranial nerve injury (I and VII)
(Greenberg, 2001)
Bracer, 1998
Pneumocephaluspresence of intracranial gas
Causes :• Skull defects• Infection of gas producing organism• Post invasive procedure• Barotrauma
PatognomosisMount Fuji Sign
Treatment of pneumocephalus• Conservative• Antibiotic treatment for gas producing organism• LCS fistula management if LCS leaks
• lowering ICP (bed rest, avoid staining, fluid restriction)• Surgical treatment
A case of 61 years old women with Gravitational rhinorrhoea with non traumatic extensive pneumocephalus(BMJ, 2002)
Pneumocephalus, due to entry of air from the sinuses. Develops a tension pneumocephalus due to a dural flap valve (Thamburaj, 2000)
Monroe- Kellie Principle
Copied from: Rogers (1996) Textbook of Pediatric Intensive Care p. 646
Brain Blood
CSF Mass
Bone
• 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
Komplikasi Cedera kranioserebral
• Sindrome Pasca-konkusio
• Epilepsi
• Sekuele kerusakan hemisfer
• Kelumpuhan saraf otak
• Gangguan mental dan neuropsikologis
POST TRAUMATIC SYNDROME
Somatic
Headaches Dizziness or light-headedness Visual disturbances: blurring is a comon
complain Diminished taste and smell Hearing difficulties: tinnitus, reduced auditory acuity Balance difficulties
POST TRAUMATIC SYNDROME
Cognitive impairment
Memory dysfunction Impaired concentration and attention Slowing of reaction time Slowing of information processing speed Impaired judgement
POST TRAUMATIC SYNDROME
Psychosocial
Irritability Anxiety Depression Personality change Fatique Sleep disturbance Decreased libido Decreased appetite
Trauma Medulla Spinalis
Lesi komplet (total) :– hilangnya seluruh modalitas sensorik di bawah tempat lesi– tertraplegi/ paraplegi– kontrol miksi dan defekasi menghilang– aktivitas refleks mula-mula menghilang kemudian meningkat
(hiperrefleksi)– gangguan termoregulasi jika di atas segmen Th 9-10– hipotensi ortostatik dapat terjadi pada fase akut pada lesi di
atas Th 6– gangguan fungsi gastrointestinal: distensi lambung dan usus
dan atonik yang bersifat sementara, gangguan respirasi pada lesi C1-C6
Trauma Medulla Spinalis
Lesi partial (sebagian) :
Lesi anterior : bilateral paresis dan hilangnya sensasi nyeri dan temperatur, dgn sensasi posisi, sentuhan, dan vibrasi relatif utuh, di sebalah kaudal dari lesi
Lesi unilateral (Brown Squard sindroma): Ipsilateral paresis, hilangnya sensasi propioseptik ipsilateral,Hilangnya sensasi nyeri dan temperatur kontralateral
Lesi sentral: Paresis berat setinggi lesi, Gangguan sensasi nyeri dan temperatur bersifat segmental dan dissosiatif
Trauma Medulla Spinalis
Lesi vertebral:– adanya deformitas– pembengkakan– nyeri setempat– keterbatasan gerakan spinal