Trauma Team Neurosurgery Hasan Sadikin

Bandung
 Kompetensi Dasar
Setelah mengikuti pelatihan ini peserta mampu
untuk memahami teknik dan penatalaksanaan cedera kepala.

KOMPETENSI KHUSUS
1. DAPAT MENJELASKAN PENGERTIAN CEDERA KEPALA
2. DAPAT MENGIDENTIFIKASIKAN KORBAN GAWAT DARURAT CEDERA KEPALA
3. DAPAT MENYEBUTKAN JENIS CEDERA KEPALA
4. DAPAT MENSIMULASIKAN TEKNIK PENATALAKSANAAN CEDERA KEPALA
 Head trauma: injury to the head,
which could cause structural or
functional damage to the brain.
 Indications:
 History of injury to the head, lacerations,
hematoma
 Visible wound on the head:, lacerations,
hematoma
 Abnormal radiological findings
 Clinical evidence of brain injury:
decrease of consciousness, amnesia,
neurological deficits, seizures
Brain Injury is a leading cause of
death and disability worldwide.
Injuries to the brain are among the most
likely to result in death and permanent
disability
 Head injuries are commonly presented to the
neurosurgeon, encompassing approximately 2%
of the population annually.
 10 % of these die prior reaching a hospital
 Of These
 80% mild
 10% moderate
 10% severe
 > 20% of head injured patients suffer varying
degrees of disability
 The head contents can be divided into the following:
1. Scalp.
2. Skull.
3. Meninges.
4. Brain.
5. Cerebrospinal fluid.
Scalp
1. S : Skin (epidermis, dermis)
2. C : Loose connective tissue
3. A: Epicranial aponeurosis
(galea aponeurotica)
4. L: Loose areolar tissue
5. P: Pericranium (periosteum)

Bleeding from scalp laceration can result in major blood loss, especially in children
 Composed of:
 Cranial Vault
 Cranial Base
 The floor of the cranial cavity is
divided into 3 parts:
- Anterior fossa → frontal lobe
- Middle fossa → temporal lobe
- Posterior fossa → brain stem
and cerebellum
Meninges
1. Dura mater
 Subdural space is a potential space, where
hemorrhage can occur
2. Arachnoid mater
 Cerebrospinal fluid circulate between the
arachnoid and pia matter in the subarachnoid
space
3. Pia mater
 Pia mater connects directly to brain
parenchyme
 Acceleration –deceleration injury
 Coup - Countercoup injury
 Rotational/shearing injury
Head injuries are classified according to:

1) Mechanism of injury
2) Severity of the injury
3) Morphology of the injury
 Blunt head injury
 High-velocity: motor vehicle
accident
 Low-velocity: falls, assault

 Penetrating head injury

 Gunshot wounds or other
penetrating wounds
 Type Stimulus Type of Response Points
Eyes Open Spontaneously 4
To verbal command 3
To pain 2
 Classified according to Glasgow No response 1
Coma Scale into: Best Motor To verbal command Obeys 6
1) Mild (GCS score 14-15) Response To painful stimulus Localized pain 5
2) Moderate (GCS score 9-13) Flexion-withdrawal 4
Flexion-abnormal 3
3) Severe (GCS score 3-8) Extension 2
No response 1
Best Verbal Oriented and converses 5
Response Disoriented and converses 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Skull • Vault •Open / closed
Fracture •Avulsed
•Linear
•Depressed
•Diastatic

•With/without CSF leakage

• Basilar
•With/without nerve palsy
Intracranial •Diffuse •Concussion
lesions •Contusion
•Diffuse axonal injury

•Epidural Hemorrhage
•Focal •Subdural Hemorrhage
•Intracerebral Hemorrhage
•Subarachnoid Hemorrhage
PREHOSPITAL

SIGN, 2009
 Anamnesa

Pemeriksaan umum untuk menyingkirkan cedera sistemik

Pemeriksaan neurologis terbatas

rontgen vertebra servikal

Pemeriksaan urin ( alkohol, zat toksik)

Pemeriksaan CT Scan kepala merupakan indikasi bila memenuhi kriteria kecurigaan perlunya
tindakan bedah saraf sangat tinggi
 Sakit kepala berat atau muntah2
 Riwayat penurunan kesadaran, rinorea, otorea, amnesia
 CT scan abnormal, fraktur skull
 Intoksikasi alkohol/ obat
 Cedera penyerta bermakna
 Tidak ada yang mengawasi di rumah
 Letak rumah jauh dari RS
 The significance of skull fracture should not be
underestimated since it takes considerable force to
fracture the skull.
 linear vault fracture increase the risk of an intracranial
hemorrhage by about 400 times in a conscious patient and
by 20 in comatose patient.
 Depressed skull fracture more than the thickness of the
skull require surgical elevation
 Open or compound skull fracture require early surgical
repair
 Basal skull fractures usually require CT
scan with bone window
 Clinical signs of basal skull fracture
 Periorbital ecchymosis (Raccoon eye)
 Local trauma or not?
 Retroauricular ecchymosis (Battle’s sign)
 CSF leakage (rhinorrhea, otorrhea)
 Halo Sign, litmus paper, β-transferrin
 7th nerve palsy
 Skull X-Ray is useful

•Linear
•Depressed
•Diastatic

•Basilar  cannot be seen

 CT scan is useful
 Bone window

•Linear
•Depressed
•Diastatic

•Basilar
 Linear fractures, diastatic fractures:
 High probability of intracranial lesion: epidural hemorrhage

 Depressed skull fractures:

 Less than 1 table (bone thickness)
 Elective surgical elevation
 More than 1 table (bone thickness)
 Open fracture: surgical debridement, craniectomy
 Closed fracture: surgical elevation, elective unless symptomatic

 Basilar skull fractures:

 Close observation, medical management
 Intracranial lesions can cause change in
intracranial pressure (ICP)
 Ruled by Monroe-Kelly doctrine
 Intracranial bleeding is a complication of
head injury, found in 25-45% of severe head
injuries, 3-12% of moderate head injuries,
and 1 in 500 mild head injury patients.
 Cushing Triad:
 High blood pressure
 Decreased pulse rate
 Abnormal respiratory type
 Transient and reversible LOC
 No distinguishable parenchymal injury
 Always accompanied by some degree of severity of posttraumatic amnesia
 The length of amnesia is a good measure of the severity of the injury
 Many patients with classic cerebral concussion have no sequalae other than
amnesia
 Some patients may have more long-lasting neurological deficits, e.g.
memory difficulties and depression
 Loss of consciousness >6 hours without intracranial mass
 Diffuse injury to axon, degeneration of white matter
 Major cause of unconsciousness and persistent
vegetative state after head trauma
 Result of traumatic shearing forces that occur when the
head is rapidly accelerated or decelerated
 Multiple small bleeds in the cerebral parenchyme
 Usually forms high-density area < 1 cm in diameter
 Due to direct impact with calvarium, most common at
bony protuberances (frontal poles, frontal base,
temporal poles, temporal base)
 10-20% of patient with head trauma and 17% of
previously conscious patient following head
trauma have EDH.
 Patient with epidural hematoma may present with
the classical “lucid interval” (20-50% of cases) or
“talk and die”.
1. Altered level of consciousness
2. Dilated pupil ipsilateral to the hematoma
3. Failure of the ipsilateral pupil to react to light.
4. Hemiparesis contralateral to the hematoma.
 Collection of blood between dura mater
and calvarium
 Commonly from torn dural vessel,
middle meningeal artery, bone fracture
 Sharp margins, biconvex shape, limited
by suture lines
 “Swirl sign”  shows ongoing bleeding
 Collection of blood between dura and arachnoid
membrane
 Crescent-shaped mass, crossing suture lines, does not
cross the falx, does not displace dural venous sinus
 Usually countercoup injury
 Clinical signs: lateralization on opposite side of trauma
 Occur most frequently from tearing of a bridging vein
between the cerebral cortex and a draining venous
sinus
 May also be caused by ICH, contusion. Contusion
present in 50% acute SDH cases
 May cover the entire surface of hemisphere
 Prognosis is much worse than epidural
 Classified by the amount of the time that has elapsed
from the time of the inciting event:
1. Acute SDH: <72 hr, appear hyperdense on CT
2. Subacute SDH: 3-20 days, appear iso- or hypodense
3. Chronic SDH: older than 20 days, appear hypodense
 Result from shearing or rapid
deceleration injuries
 Blood vessels burst, gathers
in parenchyme
 Traumatic ICH usually
superficial, rarely in deep
structures
 Delayed ICH: Injury to vessel
wall due to hypoxia, CO2
accumulation, acidic PH.
 Bleeding into the subarachnoid space, usually from contusion
 Usually over convexities, followed by fissure/sulci, or basal cistern
 2-fold increased risk of poorer outcome
Cerebral Edema
• Vasogenic Edema—disruption of the vascular endothelium
tight junction
• Cytotoxic Edema--resultant failure of the sodium-potassium
dependent pump.

Increased Intracranial Pressure

• Intracranial pressure/volume relationships are simply
expressed by the Monro-Kellie doctrine
ICP (mmHg) No of Patients Mortality

0-20 95 (47%) 19%

21-40 67 (33%) 28%

41-80 39 (20%) 79%

Total 201 (100%) 34%

40
From Miller JD, Br.J.Anaesthesia 57, 1985
 Types of brain herniation:
1. Uncal herniation
2. Central herniation
3. Cingulate herniation
4. Transcalvarial herniation
5. Upward herniation
6. Tonsillar herniation
 Increased water content of brain tissue
 Brain edema, increased cerebral blood
volume  ischemic brain damage
 Homogenous hypodensity of cortex
 Relative hyperdensity of cerebellum,
 Compression of sulcus and gyrus,
 Compression of cisterns, especially basal and
perimesencephalic,
 Compression of ventricles

 Worse outcome: mortality rate 22%-77%

 Pneumocephalus
 Accumulation of air in subdural space
 Due to communication with extracranial space:
dural tear, bone fracture
 Can cause tension pneumocephalus
 mt. Fuji sign
 Treated like a mass lesion: craniotomy
decompression with defect closure
INTENSIVE MANAGEMENT
1. Prompt ventilatory control
2. Immediate evacuation of major intracranial hematomas and contusion
3. Monitoring and control of ICP and CBF
1. Maintenance of normal systemic physiology--Maintain euvolemia (CVP 8-10 mm Hg)
Intracranial Pressure (ICP)
• Normal CPP > 50 mm Hg
• Autoregulatory mechanisms maintain
CBF at CPP’s down to 40 mm Hg CPP = MAP – ICP