HEAD TRAUMA

Adhitya Rahadi, M.D

INTRODUCTION
 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
 EPIDEMIOLOGY
 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
ANATOMY
 The head contents can be divided into the following:

1. Scalp.
2. Skull.
3. Meninges.
4. Brain.
5. Cerebrospinal fluid.
ANATOMY
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
ANATOMY

 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
ANATOMY
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
 PATHOPHYSIOLOGY
 Acceleration –deceleration injury
 Coup - Countercoup injury
 Rotational/shearing injury
CLASSIFICATION OF HEAD
TRAUMA
Head injuries are classified according to:

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

 Penetrating head injury

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

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
PENILAIAN GCS
 INDIKASI RAWAT INAP
 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
TATALAKSANA
UTAMA Blood

5B
Bowel
PRINSIP ATLS Bladder
Brain
Bone
Ringan Sedang Berat
Pilihan
Terapi
(14-15) (11-13) (9-10) <8

Head Up 300 (+) (+) (+) (+)

Neck Collar (-) (-)/(+) (+) (+)

O2

OGT/NGT (-) (-)/(+) (+) (+)

KATETER (-) (-)/(+) (+) (+)

URINE
HEAD TRAUMA
MORPHOLOGY
SKULL FRACTURES
 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
SKULL FRACTURES
 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 FRACTURE IMAGING
 Skull X-Ray is useful

Linear
Depressed
Diastatic

Basilar  cannot be
seen
 SKULL FRACTURE
IMAGING
 CT scan is useful
 Bone window

Linear
Depressed
Diastatic

Basilar
SKULL FRACTURE MANAGEMENT
 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
INTRACRANIAL LESIONS
 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
CEREBRAL
CONCUSSION
 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
 DIFFUSE AXONAL INJURY
 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
CEREBRAL CONTUSION
 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)
 EPIDURAL HEMATOMA
 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.
 EPIDURAL 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
SUBDURAL HEMATOMA
 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
SUBDURAL HEMATOMA
 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
 INTRACEREBRAL HEMATOMA
 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.
SUBARACHNOID HEMORRHAGE
 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
SECONDARY
BRAIN INJURY
 Cerebral Edema
• Vasogenic Edema—disruption of the vascular
endothelium tight junction
• Cytotoxic Edema--resultant failure of the sodium-
potassium dependent pump.

ncreased 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
BRAIN HERNIATION
 Types of brain herniation:

1. Uncal herniation
2. Central herniation
3. Cingulate herniation
4. Transcalvarial herniation
5. Upward herniation
6. Tonsillar herniation
ACUTE CEREBRAL SWELLING
 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%

OTHER PATHOLOGIES
 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
OTHER IMAGING MODALITIES
MANAGEMENT OF
HEAD TRAUMA
MANAGEMENT
CRANIOTOMY
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
Intracranial
Hg) Pressure (ICP)
• Normal CPP > 50 mm Hg
• Autoregulatory mechanisms maintain
CBF at CPP’s down to 40 mm Hg CPP = MAP – ICP
THANK
YOU..