CME Head Injury Slides
CME Head Injury Slides
CME Head Injury Slides
Head Injury
Table of contents
01 02
Approach to head Primary and
injury secondary survey
03 04
Definition
Blunt/penetrating injury to
the head and/or brain due to
external force with temporary
or permanent impairment in
brain function which may or
may not result in underlying
structural changes in the
Causes of head injury
Physiological changes
• Observed or self-reported loss of or
decreased level of consciousness
• Any loss of memory of events immediately
before or after the injury
• Any alteration in mental state or
neuropsychological abnormality at the time
of injury
• Objective neurological deficits (such as
weakness, loss of balance, change in vision,
praxis, paresis/paraplegia, sensory loss and
aphasia) that may or may not be transient.
Anatomical changes
* can be
influenced by
alcohol
intoxication,
sedative
medications,
hypoxia and
hypotension
Severity of brain injury
Mild Moderate Severe
GCS 13-15 9-12 ≤8
Duration of >30 mins
> 24
unconsciousne <30 mins and <24
hours
ss hours
Normal
Structural Normal or or
Normal
imaging abnormal abnorm
al
Classification of mild head injury
Diagnosis/ Investigations
- Complete and detailed history colletion and
thorough physical examination
- Bloods: FBC, Coagulation profile
- CT scan + repeated head CT + cervical imaging
- X- Ray (skull)
- MRI
- Electroencephalography (EEG)
- Positron emission tomography
Differential Diagnoses
• Primary anoxic, inflammatory, infectious, toxic or metabolic
encephalopathies, which are not complications of head
trauma
• Neoplasms
• Brain infarction (ischaemic stoke) and intracranial
haemorrhage (haemorrhagic stroke) without associated
trauma
• Alcohol intoxication, psychotropic drugs or substance
abuse
• Seizure
Special Considerations
• Anticoagulants should be immediately stopped and reversed
in patients with intracranial bleeding by using Vitamin K
(only for patients on Warfarin), fresh frozen plasma,
prothrombin complex concentrate or recombinant factor VIIa
as indicated and there should be consultation on this matter
among relevant specialists
• There is insufficient evidence on when to restrat antiplatelet
and anticoagulant in patients with head injury
• If there is urgent need for anticoagulant but risk of bleeding
is still considered as reasonably high, decision on when and
how to start anticoagulant should be decided by a
multidisciplinary team
Primary survey
02 and secondary
survey
PRIMARY SURVEY
Primary survey
ABCDE :
A - Airway
B - Breathing
C - Virculation
D - Disability
E - Exposure
Airway Assessment with
Cervical Spine Control
● Ascertain pathway
○ (1) Foreign Bodies, (2) Facial/Mandibular #, (3) Laryngeal/Tracheal #
● Assess for airway obstruction
○ Engage the patient in conversation – a patient who cannot respond verbally
is
○ (1) stridor, (2) retractions, (3) cyanosis
● Establish a patient airway
○ Jaw Thrust – displace tongue anteriorly from the pharyngeal inlet relieving
obstruction
○ Simple Suctioning / Clear Airway of Foreign Bodies
○ Nasopharyngeal airway / Oropharyngeal Airway
Tracheal Intubation
❏ Remove:
❏ Foreign body (use forceps)
❏ Salivation, blood, vomitus (Yankauer suction)
❏ At the same time look for gag reflex (no gag reflex brain stem injury from ponsà
poor prognosis
Assessment of breathing
● Expose the neck and chest: ensure immobilization of the head and neck
● Determine rate and depth of respiration
● Inspect and palpate the neck and chest for tracheal deviation, unilateral and
● bilateral chest movements, use of accessory muscles and any signs of injury (i.e. flail
● chest)
● Auscultate chest bilaterally: bases and apices
● If unequal breath sounds – percuss the chest for presence of dullness or hyper-
● resonance to determine hemothorax or pneumothorax
Life Threatening Conditions
Circulation with Haemorrhage
Control
Hypotension following injury must be considered to be hypovolemic in origin until proven
otherwise
Assessment of organ perfusion
A complete head to toe examination to inventory all injuries sustained in the trauma
after primary survey is completed
● AMPLE History (Allergies,medication,Past med,Last meal,Event/environment
related to injury)
● Complete head to toe examination
○ Respiratory System
○ Gastrointestinal System
○ Musculoskeletal system
○ Genitourinary System
Interpretation
03 of CT brain
INDICATIONS OF CT BRAIN
W 2000
L0
STEPS IN INTERPRETATION CT BRAIN
Extra-axial (Extracerebral)
◈ Extradural haematoma
◈ Subdural haematoma
◈ Subarachnoid hemorrhage
Intra-axial (Intracerebral)
◈ Intraparenchymal
haemorrhage
◈ Intraventricular haemorrhage
Extradural haematoma
⮚ Extradural haematoma / epidural haematoma – collection of blood that forms between the
inner surface of the skull and outer layer of the dura, which is called the endosteal layer.
⮚ EDHs are usually limited in their extent by the cranial sutures
⮚ Usually does not cross suture lines where the dura tightly adheres to the adjacent skull.
EXTRADURAL HAEMATOMA
◈ Biconvex, lenticular shape
◈ Does not cross suture lines, midline
shifted
◈ Hyperdense, sharply demarcated
Subdural haematoma
⮚ Subdural haematoma (SDH) - collection of blood accumulating in the subdural space, the
potential space between the dura and arachnoid mater of the meninges around the brain.
⮚ Bleeding beneath dura, following the shape of cerebral hemisphere, but restricted by falx
cerebri (does not cross midline)
SUBDURAL HAEMATOMA
◈ Crescentic shape along brain
surface
◈ Crosses suture lines
◈ Does not cross midline
◈ Hyperdense extra-axial
collection that spreads diffusely
over the affected hemisphere.
Chronic subdural haematoma
● Commonly in elderly
Mechanism:
• Sudden acceleration /
deceleration force will
result in the opposite
‘poles’ of the brain being
hit against the cranial vault
CT brain:
• Patchy hemorrhagic foci
mixed with low-density
oedema (salt-and-pepper
appearance)
• May need few hours to
show up in CT brain
DIFFUSE AXONAL INJURY
Diffuse axonal injury (DAI) – injury to axons
Mechanism:
• Sudden acceleration & deceleration of head
• Brain rapidly shifts inside the skull as injury
is occurring
• Tearing of axons & myelin sheaths (in white
matter)
CT brain:
• May be normal, or petechiael haemorrhage
in grey-white junction, corpus callosum,
upper brainstem
“CAN” : CISTERN
• Cisterns are collections of CSF, which
surround and protect the brain.
• Examine each for evidence of
effacement, asymmetry and the
presence of blood.
• Circum-mesencephalic —
surrounding the midbrain
• Suprasellar — around the circle
of Willis
• Quadrigeminal — located at the
top of the midbrain
• Sylvian — between temporal
and frontal lobes.
• Closure of the circummesencephalic cistern is one of the earliest signs
of increased intracranial pressure
• 80% of subarachnoid haemorrhages happen somewhere around the circle of
Willis / suprasellar cistern.
• One of the earliest places to see hydrocephalus is on the temporal tips of the
suprasellar cistern.
•Distal middle cerebral artery aneurysm (MCA)
• A SAH here may only fill up this cistern with blood.
•"Insular ribbon sign"
• The insular ribbon is the end organ of the middle cerebral artery - it is the
most distal brain perfused by the MCA.
• Loss of gray white matter here is the earliest sign of MCA ischemia.
“BE”: BRAIN
◈Intraventricular
haemorrhage (hyperdensity
within ventricular system)
◈Hydrocephalus
◈Ventricular effacement
“BAD”: BONE Skull fracture
Open
Vault Basillar
Open Closed
◈ Look for evidence of
fractures Closed
Mixed
Linear Skull Fracture
◈ Low-energy blunt trauma over a wide surface area of the
• - Runs through the entire thickness of the bone
skull.
• - It has little significance except when it runs
◈ Common type of fracture, especially in children younger through a vascular channel, venous sinus groove,
than 5 years. or a suture.
◈ Straight or curved fracture lines • - This may cause epidural haematoma, venous
◈ 75% of these fractures occur in the parietal bones, 15% in sinus thrombosis and occlusion
the occipital bones, and 5% in the frontal bone
Fracture Suture
Greater than 3mm width (widest at Less than 2mm in width (same width
the center and narrow at the end) throughout)
Usually runs in a straight line Does not run in a straight line (jagged)
Angular turns Curvaceous
linear parietal skull
fracture
Xray:
• Increased density where one border of the fracture fragment
overlies the adjacent bone
• Fragment lying deep to the skull vault
Depressed fracture (displaced toward the Depressed skull fractures are Depressed skull fracture with
brain) of the parietal bone over the frontoparietal region epidural haematoma
Post Op Findings
Reduced midline shift ,
no epidural haematoma
as it has been
evacuated, reduced
mass compression
Treatment and
04 management
Referral to nearest hospital
Consider referral of patients with mild head injury to nearest hospital
if:
● GCS of 15 but symptomatic (amnesia, headache, vomiting,
restlessness)
● Age ≥65 years old
● Treated with antiplatelets / anticoagulants
● GCS <15 and/or declining GCS score
● Alcohol intoxication & substance misuse
● Focal temporal blow
● Social issues
● Indicated for head CT
Management in ED
1.Primary survey according to ATLS guidelines:
a)Airway patency & cervical spine protection
b)Breathing – to detect any intrathoracic injury
c)Circulation & haemorrhage control
d)Disability – incl. GCS, pupil size, reaction to light
e)Exposure – incl. logroll
Even unconscious TBI patients may have increased blood pressure and ICP resulting
from this stress response.
Sedative agents can reduce metabolic stress on acutely injured brain tissue by
decreasing cerebral metabolism and consumption of oxygen in a dose-
• Analgesia / sedation
dependent manner that, in turn, decreases CBF and leads to a reduction in
• Anticonvulsants ICP.
• Intravenous fluids
Medications for early management
Post traumatic seizure (PTS) defined as a recurrent seizure disorder due to TBI.
1. Immediate seizure (<24 hours)
2. Early seizure (<7 days)
3. Late seizure (>7 days)