Musculosceletal System 1

CRANIOCEREBRAL TRAUMA

dr. Fitriah Handayani, M.Kes, Sp.N

Medical Faculty
Tadulako University
2019
2
 DEFINITION
TraumaticBrain Injury (TBI)
disruption in the normal function of the brain that can be caused by a
bump, blow, or jolt to the head, or penetrating head injury

PRIMARY injury
• is the physiological or anatomical insult → associated structural changes resulting from
mechanical forces initially applied during injury

• The forces caused : tissue distortion, shearing, and vascular injury as well as destabilization of
cell membranes and frank membrane destruction.
 MECHANISM

• generation of free radicals

• Excitotoxicity
SECONDARY injury • ionic homeostasis disturbance
• disruptIon of the blood–brain barrier
• generation of nitric oxide
• Is systemic or local changes, which increase tissue
• lipid peroxidation
damage. Result directly form primary injury →
• mitochondrial dysfunction
discreet systemic or local phenomena
• energy failure
• Inflammation
• secondary hemorrhage
• axonal disruption
• apoptotic cell death
Ischemia → due to microvascular changes, systemic
• ischemia
hypotension or hypoxia, or elevated intracranial
pressure
Classification TBI by Mechanism 5

• injury caused by direct force to head, acceleration–

Closed/blunt force deceleration, or rotational forces. Common causes include
falls, assaults, and motor vehicle collisions.

• injury caused by overpressure waves generated from high-

grade explosives. A large amount of thermal, mechanical,
and electromagnetic energy is transferred to the brain.
• Energy come directly through cranium → transmitted
Blast Injury indirectly → through oscillating pressures in fluid-filled large
blood vessels → damage to the blood–brain barrier or gray–
white matter junction, → cerebral edema, axonal injury,
apoptosis, tissue degeneration

• injury induced by an object that penetrates the cranial vault.

Penetrating Injury Common causes include gunshot wounds, shrapnel, and
knife wounds.
 Clinical Classification of TBI 6

• GCS 13 to 15, the majority of patients with cranial trauma

fall in this group.
Mild TBI • Patients are awake, and may be confused but can
communicate and follow commands
• GCS 9 to 12, these patients are generally drowsy to
obtunded but not comatose.
Moderate TBI • They can open their eyes and localize painful stimuli.
They are at high risk of clinical deterioration and must be
monitored

• GCS 3 to 8, these patients are obtunded to comatose,

they do not follow commands and may exhibit
decerebrate or decorticate posturing.
Severe TBI • They have significant structural and metabolic brain
dysfunction and are at high risk of secondary brain injury
and deterioration.
7
8
9
10
 11

Mechanism of Brain Damage after TBI

EPIDURAL HEMATOMA
SUBDURAL HEMATOMA
 12

Craniocerebal

Epidural

Subdural
Epidural Hematoma
Subdural hematoma
ANATOMY 13
Introduction

• from Ancient Greek → ‘membrane’

MENINGES • Brain and spinal envelope with 3
layer : Dura, Arachnoid, and Pia
mater

D URA • EPIDURAL Space : potential space between the roof

of the skull (i.e., calvarium) and the superior surface of the

A RACHNOID
dura.
• SUBDURAL Space : potential space that potentially
P IA
exists between the meningeal layer of the dura and the
arachnoid mater
 Epidural Hematoma (EDH)
an extra-axial collection of blood within
the potential space between the outer
DEFINITION layer of the dura mater and the inner
table of the skull

• occurs in 2% of all head injuries, > 15% of all fatal head traumas.
• Males more than females.
• Incidence is higher among adolescents & young adults → mean
EPIDEMIOLOGY age are 20 - 30 years
• Rare after 50-60 years of age → during aging → dura mater
becomes more adherent to the overlying bone → ↓ chance of
hematoma developed
 16

incidence

• 66% temporoparietal region and middle meningeal

artery
• Anterio ethmoidal arteries maybe involved in forntal
injury
• Transverse or sigmoid sinus in occipital injuries
• Superioe sagittal sinus in vertex injury
• 5% in foassaposterior
 Pathogenesis EDH 17

• Most EDH result from arterial bleeding from a branch of

the middle meningeal artery.
Arterial Injury • The anterior meningeal artery or dural arteriovenous
(AV) fistula at the vertex may be involved.

• >10% of EDHs are due to venous bleeding following the

laceration of a dural venous sinus.
• In adults, up to 75% of EDHs occur in the temporal
Venous Injury region.
• In children, they occur with similar frequency in the
temporal, occipital, frontal, and posterior fossa regions.
 Subdural Hematoma (SDH)

is a collection of blood that

DEFINITION accumulates inside the skull but
outside the brain

• more prominent in older individuals → 80 cases per

100,000 person-years.
• Males have a higher incidence than females → 20% of
EPIDEMIOLOGY
subdural hematomas in males are bilateral
• infants & toddlers higher incidence compared other age
groups → incidence 40 per 100,000 person-years
 19

• sudden impacts shaking the skull → shifting of the brain within the skull (rattling
around like a tennis ball in a can) → tear the small blood vessels that bridge
between the skull and brain.
• Depending size & location vessels torn → , produce brisk bleeding with a rapid
patient collapse or much slower oozing with symptoms appearing many days
after the event.
• The events do not have to be direct blows to the head. About half of the chronic
SDH patients who report having fallen did so without hitting their heads.
Different Type SDH 20

Acute • usually appear within 72 hours of a traumatic event

Subacute • are ones found within 3-7 days of an injury

• may take weeks to months to appear

• commonly seen in the elderly population where brain shrinkage
stretches the blood vessels “bridging” between the skull and
Chronic brain, making them more vulnerable
• Brain shrinkage also creates more space within the skull,
making the effects of blood accumulation slower to appear.
21
Symptomps SDH 22

ACUTE
• Severe headaches CHRONIC
• Dizziness • Milder headache (80%)
• Changes in vision, speech, or mental • Behavior and personality changes
clarity • Confusion
• Seizures • Speech changes
• Nausea and vomiting • Limb weakness, numbness, or
• Weakness on one side of the body tingling
• Apathy, lethargy, or drowsiness •
Double vision
• Balance changes and difficulty
walking
• Memory loss
General management for severe TBI 23
24
Operative Treatment Indication 25

Epidural • Blood > 30mL

Hematoma • ≥ 5mm midline shift

Subdural • ≥ thick
Hematoma • ≥ 5mm midline shift

Relative operative CONTRAINDICATIONS :

• Age > 55 tahun
• Greater 4hours from time injury
• Postrescucitation GC 2, fixaed and dilated pupils
Operative Treatment 26

• drill a hole through the skull above the clot and wash it out
Burr Hole with copious irrigation. This is most efficient for removing
liquefied hematomas.
trephination
• This method is common for Chronic SDH’s

• required for a larger and firmer clot

• a larger section of the skull is removed, the clot is lifted out,
Craniotomy and the skull plate
• This is the most frequent method for Acute SDH’s

• removes a section of the skull, but with this method the bone
plate is left off for an extended period of time after clot
Craniectomy removal.
• This method is less commonly used, mostly in cases where
the underlying brain tissue has experienced major swelling.
27
28
29
30
31
 BRAIN CT 32

Diagram demonstrating types of intracranial

bleeds, across (A) axial and (B) coronal
views; EDH = epidural haematoma, SDH =
subdural haematoma, SAH = subarachnoid
haemorrhage, IPH = intraparenchymal
haemorrhage
 E
33

D
H
Typical acute EDH. A: Axial CT in the brain window shows hyperdense lentiform/biconvex
extra-axial hemorrhage (arrow). B: Corresponding image in the bone window shows overlying
fracture of the adjacent squamous temporal bone (black arrow). The source of bleeding is
likely from a tear of the adjacent middle meningeal artery. Note the EDH does not extend
beyond the dural attachments at the coronal and lambdoid sutures (white arrows).
 E
34

D
H
Acute frontal EDH. A: Axial CT in the brain window shows lentiform hemorrhage that
crosses midline, anterior to the falx (arrows). B: Slightly higher image in the bone
window shows diastatic fracture through the sagittal suture (arrow). The source of
bleeding is likely from a tear of the underlying sagittal dural venous sinus.
 S
35

D
H
Typical acute SDH. A: Axial CT in the brain window shows crescentic extra-axial
hemorrhage (arrows) that extends over right frontal and parietal
convexity. B: Corresponding image in bone window shows the location of the
coronal sutures (arrows). Note the SDH is not limited by the sutures.
 S
36

D
H
Acute SDH with decompressive craniectomy. A: Axial CT in a 6-year-old child who
was struck by a car shows relatively small, but predominantly hypodense, SDH (solid
arrow), with significant mass effect and midline shift (dotted arrow). B:She underwent
immediate decompressive craniectomy, with improved midline shift (dotted arrow)
S
37

D
H
Sedimentation in SDH. Axial CT images in an elderly patient on anticoagulation therapy who fell after
a syncopal episode, 2 days prior to admission. Bilateral SDHs are present, with sedimentation or
hematocrit effect, due to dependent layering of heavier hyperdense red blood cells. The first scan
shows a gradual gradation of hypodense serous component superiorly to hyperdense red blood cells
inferiorly. Over the course of 5 days, the dependent portion is larger and more dense, with more
sharply defined layer (arrows) as the clot develops.
38