trauma sistem saraf

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