Head Trauma
Kampala Advanced Trauma Care Course
Outline
• Global context
• Epidemiology & Local epidemiology
• Main Principles of Treatment
• Anatomy/ Pathophysiology
• Management strategies/ Ideal treatment
• Adaptations for resource-limited settings/ context
appropriate treatment
Global context and epidemiology
• 5.6 million traumatic brain injuries per year worldwide
• Worldwide most commonly caused by MVCs and falls
• Highest prevalence in second and third decades of life
• Highest mortality rate found in persons aged 15-24
• Increased risk of TBI in: young, unmarried, men,
history of substance abuse, history of previous TBI
• 20% of TBIs occur in pediatric age group
Main Principles:
• Primary goal of treatment for patients with TBI is to
prevent secondary brain injury.
• Provide adequate oxygenation and maintain blood pressure at
level sufficient to perfuse the brain
• Obtaining a CT scan should NOT delay patient transfer
to a trauma center capable of immediate and definitive
neurosurgical intervention
• Consult neurosurgeon early
Initial Trauma
Assessment
Anatomy & Physiology
Kampala Advanced Trauma Care Course
Last Edited August 2016 by Maija Cheung MD & Michael DeWane MD
Anatomy
• Scalp
• Extensive blood supply can cause major blood loss if laceration
• Skull
• Fixed compartment – acceleration and deceleration injuries
• Meninges
• Cover the brain matter
• Enclose venous sinuses & bridging veins
• can tear and hemorrhage
• Enclose meningeal arteries
• can be injured with skull trauma
• Middle meningial artery most common
• Brain
• Sensitive to traumatic brain injury (TBI): a non-congenital
insult to the brain from an external mechanical force which
can lead to temporary or permanent impairment in cognitive
or psychomotor function
• Ventricular System
• Presence of blood in CSF may impair CSF reabsorption
resulting in increased intracranial pressure
• Intracranial Compartments
• Ipsilateral pupillary dilation associated with contralateral
hemiparesis is the classic sign of uncal herniation
Physiology:
• Intracranial Pressure (ICP)
• Elevations can reduce perfusion and cause ischemia
• Normal ICP is 10mm Hg, Pressure >20 mm Hg associated with
poor outcomes
• Cerebral Blood Flow
• TBI severe enough to cause coma may caused reduce cerebral
blood flow during first few hours after injury; this usually
increases over the next 2-3 days but in patients who are in comas
it stays reduced for days or weeks
• Cerebral perfusion pressure =mean arterial pressure –
intracranial pressure
• Enhance cerebral perfusion and blood flow by reducing ICP,
Physiology Continued:
Monro-Kellie Doctrine
• Total volume of intracranial contents must remain
constant because the skull is a rigid, non-expansile
container
• Blood and CSF may be compressed out of the container early
on providing a degree of buffering therefore EARLY after
injury, a mass such as a blood clot may enlarge whilethe
ICP remains normal however once the limit of
displacement of CSF has been reached, ICP rapidly
increases
Initial Trauma
Assessment
Traumatic Head Injuries
Assessment &CareInitial
Kampala Advanced Trauma Course
Last Edited August 2016 by Maija Cheung MD & Michael DeWane MD
Management
Head Injuries:
• Skull Fractures
• Diffuse Brain Injury
• Focal Brain Injuries
• Epidural Hematoma
• Subdural Hematoma
• Contusion and Intracerebral Hematoma
Skull Fractures
• Classified as
• Cranial vault or skull base
• Linear or stellate
• Open or closed
• Early surgical consult
• Basilar Skull Fracture Signs:
• Periorbital ecchymosis
• Retroauricular ecchymosis
• CSF leak from nose or ear
• 7th and 8th nerve paralysis (facial paralysis or hearing loss)
Diffuse Brain Injury:
• Range from mild concussion to severe ischemic injury
• Transient non-focal neurologic disturbance that often
includes loss of consciousness
• CT may initially appear normal or brain may appear
swollen
• High velocity impact or deceleration injury may show
multiple punctate hemorrhages throughout hemispheres
= diffuse axonal injury
Diffuse Axonal Injury (DAI):
• Widespread damage
• Result of shearing injuries that occur during rapid acceleration and
deceleration
• Usually associated with poor outcome
• Difficult to diagnose, disability not explained by subdural or
epidural hematoma may be due to DAI
• Grades:
• I = widespread axonal damage but no focal abormalities
• II = damage found in Grade I present in addition to focal abnormalities
especially in corpus callosum
• III = damage encompasses both Grades I & II injury plus rostral brainstem
injury and often tears in tissue
Post-Concussive Syndrome:
• Dizziness, nausea, restlessness often follow return of
consciousness
• May have transient memory loss
• Usually resolve over time; persistence or worsening of
syndromes or altered mental status should prompt urgent
re-evaluation for missed injury
• Effects of concussion are additive – each subsequent
concussion can worsen post-concussive symptoms and
lead to severe and lasting disability
Epidural Hematoma:
• Buildup of blood between dura and skull
• Most often in temporal region associated with tear in
middle meningial artery as a result from a skull fracture
• Typically biconvex or lenticular in shape
• 0.5% of patients with brain injuries, 9% of TBI patients
in comas
• Often characterized by loss of consciousness
followed by lucid interval then severe headache
with neurologic deterioration and altered mental
status
• Can raise intracranial pressure causing brain
herniation
• Confirm by CT scan
• Require urgent surgical evacuation
Subdural Hematoma:
• More common than epidural hematomas –
30% of patients with severe TBI
• Develop from shearing of bridging veins
• Symptoms slower onset than epidural
hematoma due to lower pressure of
bleeding veins
• Diagnose by CT scan
• Conform to contours of brain
• Associated with underlying parenchymal
injury
• May require urgent surgical
Contusions and Intracerebral
Hemorrhage:
• Present in 20-30% severe brain injuries
• Majority occur in frontal and temporal lobes
• May evolve over time to form hematoma or contusion with
mass effect
• Signs depend on location of brain contusion: weakness,
lack of motor coordination, aphasia, memory or cognitive
problems
• Diagnosed by CT Scan
• Repeat CT scan within 24 hours to evaluate for changes in
injury
Severity of Head Injury:
Glascow Coma
• Use Glascow Coma Score Scale
Eye Opening Spontaneously 4
• Motor + Eye + Verbal To Speech 3
To Pain 2
• Use best motor response to None 1
calculate score
Verbal Response Oriented 5
• Motor response is most reliable Confused 4
predictor of outcome Inappropriate Words 3
Incomprehensible 2
• Severe Brain Injury: GCS <8 Sounds
None
1
• Moderate Brain Injury: 9-12
Motor Response Obeys Commands 6
• Minor Brain Injury: 13-15 Localizes to Pain
Withdraws from Pain
5
4
Flexion to Pain 3
Extension to Pain 2
None 1
Maximum Score 15
Management of Minor Brain Injury
GCS 13-15
• History of disorientation, amnesia, transient loss of consciousness but
patient conscious and talking
• Primary & Secondary Survey
• Loss of consciousness, seizure activity, duration of amnesia
• Serial examinations with repeat GCS to monitor for change
• CT scan in all patients with:
• Suspected brain injury
• Suspected skull fracture
• >2 episodes of vomiting
• Older than 65 years of age
• Loss of consciousness >5 minutes
• Severe headaches
• Dangerous mechanism
• Focal neurological deficit
Minor Brain Injury Continued:
• Surgical consult early if abnormalities on CT scan
• If asymptomatic and fully awake and alert with no
neurologic abnormalities:
• Observe for several hours
• Re-examine - if stable can be discharged with instructions
regarding warning signs to seek further care
Management of Moderate Brain Injury
GCS 9-12
• Able to follow simple commands but usually confused or
somnolent and can have focal deficits such as hemiparesis
• 15% of patients seen in ED have moderate injury
• 10-20% of these deteriorate and lapse into coma
• Perform serial neurologic examinations!
• Obtain CT scan
• All patients with moderate brain injury should be admitted
to an ICU or unit capable of close monitoring and frequent
reassessment
• Follow up CT scan if initial CT is abnormal or if change in
neurologic status
Management of Severe Brain Injury
GCS <8
• 10% of patients treated in ED have severe brain injury
• Unable to follow simple commands, often require
cardiopulmonary stabilization
• Obtain CT scan as soon as possible
• ABC’s
• Stabilize and transfer to ICU or transfer to facility capable of
definitive neurosurgical care
• Early neurosurgical consult!
• May need additional therapeutic agents such as mannitol or
hypertonic saline
TBI Management:
• For all severity of TBI
• ABC’s
• Control bleeding from scalp lacerations
• Intubate if GCS <8 or inability to protect airway
• Cardiopulmonary stabilization
• Primary and Secondary Surveys - Don’t forget to do complete trauma
evaluation!
• Maintain normovolemia
• Monitor serum sodium levels
• Elevate head of bed 30 degrees
• Therapeutic agents in conjunction with surgical consult
• Mannitol, hypertonic saline, barbiturates, anticonvulsants
Initial Trauma
Assessment
Adaptations for Resource
Limited Setings
Kampala Advanced Trauma Care Course
Last Edited August 2016 by Maija Cheung MD & Michael DeWane MD
Diagnosis and Management Adaptations
The biggest challenge is the inability to obtain a CT
scan despite the patient’s condition necessitating one.
Skull x-rays can still very useful sources of information
and can help with:
• Diagnosis
• Decision making on surgical or non operative
treatment
Diagnoses from Skull X-ray:
1. Classification of head injury;
• Open head injury
• Fracture at base of skull
• Pneumocephalus
• Closed head injury
• Linear fracture,
• Depressed skull fracture
• Comminuted fracture
Remember, any skull fracture can have underlying brain
injury or an intracranial bleed!
Diagnoses from Skull X-rays Continued:
2. Midline shift
• In the anteroposterior view, the pineal body (always in the
midline) will have shifted either right or left to varying
degrees.
3. Penetrating injury with retained foreign body
4. Scalp hematoma without underlying fracture
Management Strategies:
• Any skull fracture should be considered as having an
underlying bleed until proven otherwise. Patients should
be closely monitored.
• A simple linear fracture in a neurologically intact patient
can be managed conservatively.
• A depressed skull fracture in a neurologically intact
patient can be managed conservatively.
• These fractures heal well and smooth over with time in children
• For adults, they may retain noticeable skull deformity.
Management Strategies Continued:
If you only have a skull x-ray, the following findings should
prompt urgent intervention:
• Skull fracture with any new neurological deficit
• Any fracture involving a sensitive area- Broca’s area, Wernicke’s area,
occipital region
• Any fracture with lateralising signs – anisocoria, unilateral weakness of
any limb
• A fall in GCS of greater than 2
• Focal convulsions
With the above findings, one should perform urgent
decompression with burr holes to evacuate any underlying clot.
Localize burr holes near fracture sites.
Management Strategies Continued:
Falling GCS in the absence of ventilator:
• The patient with head injury and a GCS of 8 or less or a
falling GCS to below 8 will need airway protection.
• If no access to a ventilator and the patient has respiratory
effort, a tracheostomy should be performed immediately to
secure the airway.
• These patients do well on the general ward or in the High
Dependency Unit. The nursing care for the tracheostomy is not
intense and such a procedure will save the patient.
THESE INTERVENTIONS SHOULD BE DONE TOGETHER
WITH THE OTHER ASPECTS OF MANAGEMENT OF HEAD
INJURY
Useful Resources
• [Link]
• Trauma Care Manual - Ian Greaves, Keith Porter, Jim
Ryan
• Trauma Management- Demetrios Demetriades, Juan A.
Asenio
Collaborators
• Maija Cheung, MD - Yale General Surgery Resident
• Michael DeWane, MD - Yale General Surgery Resident
• Naomi Kebba, MD – Surgeon, Uganda Heart Institute
• Michael Lipnick, MD - UCSF Anesthesiologist
• Doruk Ozgediz, MD - Yale Pediatric Surgeon
• Rodney Mugarura, MD – Orthopedidc Surgeon, Mulago
hospital
Last Edited February 2017 by Maija Cheung MD & Michael DeWane
MD
