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Case 1 : Diagnosis and

Management of Head Trauma


III – Section D Group 3
November 29, 2006

Sindiong, Robertito Paolo


Sio, Cherry Ann
Sison. Lincoln
So, Imee T
Solis, Ma. Rachelle
So- Reyes, Jamil Laurence
Sto. Domingo, Braulio II
Suller, Armida
GT, a 22 year old male, while walking along Gov.
Forbes St., was side swept by a speeding 10-
wheeler truck. He was seen by bystanders and
was immediately brought to STUH. At the
emergency room, vital signs were as follows: BP
110/70, PR 95/min, RR 20/min. A 5 cm laceration
was noted over the left temporal area, and
multiple abrasions and lacerations over the face
and extremities. He was noted to be confused,
with spontaneous eye opening, and localizes
upon painful stimuli. Pupils were 2mm, equally
reactive to light.
The surgical intern on duty immediately inserted
an IV line. A plain skull x- ray was then
requested, which revealed a linear fracture over
the left temporal area. On the way back, he was
noted to be less responsive. The left extremity
withdraws to pain, while the right was noted to
be in extended position. There was eye opening
on painful stimuli and no verbal output. Pupils:
3mm RTL, 5mm nonreactive left.
1. Discuss the classification of
head injury
Mild head injury - GCS 13 - 15
Moderate head injury – GCS 9 – 12
Severe head injury – GCS 3 – 8
Classification of head injury
Penetrating head injury – the dura is pierced
Compressive head injuries
– the skull is compressed between two
forces
- massive injury that usually results in
instantaneous death
Classification of head injury
Closed or Blunt head injuries
- Major problem in civilian life
- Head is suddenly accelerated or decelerated
as a result of a non-penetrating blow
- Dura remains intact
Concussion
• Temporary neuronal dysfunction after non-
penetrating trauma
• CT scan normal
• Memory difficulties common
• Brain in hypermetabolic state
• Second impact syndrome
– Brain more susceptible to trauma in 1st 1-2
weeks
Concussion
Colorado medical society system
• Grade 1 – head trauma patients
with confusion
• Grade 2 – patients with amnesia
• Grade 3 – patients who lose
consciousness
Contusion
• Bruise of the brain
• Breakdown of small vessels
• Bright on CT scan
• Small amounts of blood in injured
parenchyma
• Edema may develop causing mass
effect
Contusion
• Enlarge or develop into true
hematoma

• Contre coup injury


– Contusions in brain tissue opposite
site of impact
– Decelerations of brain against skull
Diffuse axonal injury
• Damage to axons due to rotational
acceleration and then deceleration
• Axons may completely be disrupted
and retract forming axon balls
• MRI – hemorrhage, usually in
corpus callosum and dorsolateral
midbrain
Penetrating injury
Subtypes
• Missile (bullets and fragmentation
devices)
• Nonmissile (knives and ice picks)
• X-ray and CT scan
• Cerebral angiography considered if
object passes near a major artery or
dural venous sinus
Penetrating injury
• Operative exploration necessary to
remove objects sticking out of the
cranium
• Debridement, irrigation,
hemostasis, and closure
• Small object w/in brain parenchyma
often left alone
Penetrating injury
• High-velocity weapons create
shockwave that destroys surrounding
tissue
• Patient treated w/ antibiotics
1. Differentiate primary brain
injury from secondary
brain injury.
Primary Brain Injury
• also Impact damage
• the initial injury to the brain as
a direct result of the trauma
• sudden and profound injury to
the brain that is considered to
be more or less complete at
the time of impact
• occurs at the time of the car
accident, gunshot wound, or
fall
• instantaneous onset
Primary Brain Injury
• from blow, acceleration, deceleration, or
rotation of the brain when it is slammed
back and forth on bony prominences inside
the skull
Primary Brain Injury
• Clinical effects:
– immediate
– maximal
– irreversible
– e.g. concussion,
contusion, acute
subdural
hematoma, diffuse
axonal injury
Secondary Brain Injury
• refers to the changes that evolve over a
period of time (from hours to days) after
the primary brain injury
• any subsequent injury to the brain after
the initial insult
• can result from systemic hypotension,
hypoxia, elevated ICP, or as the
biochemical result of a series of
physiologic changes initiated by the
original trauma
Secondary Brain Injury
• includes an entire cascade of cellular,
chemical, tissue, or blood vessel
changes
• contribute to further destruction of brain
tissue
• Complication of primary injury
Secondary Brain Injury
• Clinical effects:
– delayed
– progressive
– preventable
– e.g. dec cerebral perfusion,
inc ICP, cerebral edema,
hypoxemia, circulatory
shock
– hypoxia, ischemia, brain
swelling, infection,
hematoma
Brain edema
3. Explain and assign the
Glasgow Coma Scale
Glasgow Coma Scale

Glasgow coma scale Motor Response


 Conscious level 6 – follows
assessment commands
 Used to determine 5 – localizes
deterioration or 4 – withdraws
improvement in
patient’s condition 3 – decorticate
 Developed in 1974 2 – decerebrate
by Teasdale and 1 – no response
Jennett in Glasgow,
England
Glasgow Coma Scale
Eye Opening Verbal Response
4 – spontaneous 5 – oriented
3 – to voice 4 – confused
3 – inappropriate
2 – to pain
2 – incomprehensible
1 – no eye 1 – no sound
opening
In our patient’s case…
AT THE E.R. ON THE WAY
Motor: localizes pain BACK…
on painful stimuli (5) Motor: L withdraws to
Eye opening: pain, R extended (4)
spontaneous eye Eye opening: eye
opening (4) opening on painful
Verbal: confused (4) stimuli (2)
Verbal: no verbal
output (1)
Total: 13 (Moderate)

Total: 7 (Severe)
Total = M+V+E = 3-15
• Severity GCS Death/Vegetative
– Mild 14-15 5%
– Moderate 9-13 27%-54%
– Severe 3-8 54%-80%

***Should always have a high index of


suspicion for cervical spine injury and
other multiple injured organs
4. Discuss the presentation of
brain herniation syndromes in
the setting of trauma.
Monro - Kellie doctrine
• Total intracranial volume is fixed because of
the inelastic nature of the skull

Vi/c = V (brain) + V (CSF) + V (blood)

• ~ 1500 ml
– 85- 90% brain
– 10% intravascular cerebral blood volume
– <3% CSF
Compliance
• Based on the pressure volume index
within the intracranial vault
Compliance = change in volume
change in pressure
Intracranial compliance
Head injury

Cerebral edema

Increase relative volume of the brain

Pressure within the skull rises

Herniation
Intracranial compartment
• Divided into 3 compartments by 2 major
dural structures:
1. Tentorium cerebelli
– supra (cerebral hemispheres) and infratentorial
(brainstem and cerebellum) compartments

2. Falx cerebri
– divides the supratentorial compartment into left and
right hemispheres
Herniation
• Displacement of a portion of the brain from
its normal compartment into another one
• Terminal event: ischemia  infarction
• Types of herniation syndromes:
1. Uncal or transtentorial
2. Cingulated or subfalcine
3. Central transtentorial herniation
4. Tonsillar herniation
Uncal / Transtentorial
Herniation
• Most dramatic and most common herniation
syndrome
• Herniation of the inferomedial part of the
temporal lobe (uncus) into the tentorial notch
• Progressively impaired consciousness,
anisocoria (ipsilateral), hemiplegia &
hemiparesis (contralateral)
• Compress third cranial nerve
Cingulated / Subfalcine
Herniation
• Cingulate gyrus on the medial aspect of the
frontal lobe is displaced across the midline
under the free edge of the falx
• may compromise blood flow through the
anterior cerebral artery complexes
• Headache, weakness of the lower
extremities (contralateral), NO anisocoria
• Can occur in conjunction with transtentorial
herniations
Central Herniation
• Downward displacement of the
diencephalons and midbrain centrally thru
the tentorial incisura
• May cause significant upper brainstem
compression
• bilaterally small reactive pupils, Cheyne-
Stokes respirations, loss of vertical gaze,
bilateral arm dysesthesia, obtundation
Tonsillar herniation
• Results from acute expansion of posterior fossa
lesions
• cerebellar tonsils herniate thru the foramen
magnum into the upper spinal canal,
compressing the medulla and upper cervical
spinal cord
• cardiorespiratory arrest, hypertension, Cheyne-
Stokes respiration, neurogenic hyperventilation,
impaired consciousness, pposturing problems
• worst prognosis
Patient
• GCS of 7 (severe head injury)
• Linear fracture on L temporal area
• L = withdraws to pain, R = extended
(decerebrate)
• No verbal output
• Pupils  R = 3mm RTL, L = nonreactive
(anisocoric)
Uncal or Transtentorial
Herniation
Anisocoria
Uncal herniation

Ipsilateral compression of the oculomotor nerve

Dysfunction of the parasympathetic fibers

Unopposed sympathetic response


LIGHT

Ipsilateral dilated pupil


Contralateral hemiparesis /
hemiplegia
Uncal herniation

Compression of the ipsilateral


cerebral peduncle

Signals traveling through the cortical &


spinal tracts unable to decussate

Contralateral hemiparesis / hemiplegia


5. Differentiate cerebral
concussion, contussion, and
diffuse axonal injury
Concussion
• A concussion occurs when the head
hits or is hit by an object, or when the
brain is jarred against the skull, with
sufficient force to cause temporary loss
of function in the higher centers of the
brain
• Diffuse type of brain injury
Concussion
Concussion
• Symptoms of concussion include:
– headache
– disorientation as to time, date, or place
– confusion
– dizziness
– vacant stare or confused expression
– incoherent or incomprehensible speech
– incoordination or weakness
– amnesia for the events immediately preceding the blow
– nausea or vomiting
– double vision
– ringing in the ears
Contusion
• Condition in which direct parenchymal
injury of the brain has occurred through
transmission of kinetic energy of the
brain and bruising analogous to what is
seen in soft tissues
• Caused by the brain hitting the interior
of the skull
Contusion
• Coup contusion
– minimal injury underlying the point of
contact
• Countercoup contusion
– occur at the area of the brain opposite to
the blow
– may show extensive damage
• Histologically indistinguishable
Contusion

contact → tissue displacement → disruption of


vascular channels → hemorrhage → tissue injury and
edema
Contusion
• Signs and symptoms include
– Severe headache
– Dizziness
– Vomiting
– Increased size of one pupil or sudden
weakness in an arm or leg
– Restlessness, agitation or irritability
– Memory loss or forgetfulness
Contusion CT Scan
Diffuse Axonal Injury
• Results from high speed injury with
stretching or shearing of brain tissues
• Radiographically shows petechial
hemorrhages in white matter tracts
• Characterized by axonal separation
• Secondary biochemical cascades are
largely responsible for the damage to
axons
Diffuse Axonal Injury
Diffuse Axonal Injury
• The major cause of damage in DAI is
the tearing of axons
• Treatment is aimed at managing
swelling in the brain because torn axons
can not be repaired.
Diffuse Axonal Injury

Acceleration causes shearing injury, which refers to


damage inflicted as tissue slides over other tissue
6. Differentiate Acute Subdural
Hematoma and Acute Epidural
Hematoma
Acute Epidural Hematoma
 A collection of blood between the
cranium and dura
 Usually arterial in origin esp resulting
from laceration of the middle meningeal
artery associated with a fracture in the
squamous portion of the temporal bone
Acute epidural hematoma
Acute Epidural Hematoma
• Triphasic with a :
-mild head injury leading to a transient alteration of
consciousness followed by
-a “lucid interval” where patient regained
consciousness or is relatively symptom free, followed
by
-obtundation, focal deficit, ipsilateral pupillary
dilatation
• Consciousness is lost again when the expanding
epidural hematoma compress the brain to produce
focal deficit or inc ICP
Subdural hematoma
• Blood collections in the potential space
between the dura and the arachnoid
• Usually venous in origin
Subdural hematomas
• Subdural hematomas are most often
caused by head injury, when rapidly
changing velocities within the skull may
stretch and tear small bridging veins.
• subdural hemorrhages generally result
from shearing injuries due to rotational
or linear force
Subdural hematoma
3 Classifications of Subdural
Hematoma
• Acute Subdural Hematoma (1-2 days)
• Subacute Subdural Hematoma (3-21
days)
• Chronic subdural hematoma (>21 days)
Acute Subdural Hematoma
• Usually present as an evolving
intracranial mass
• Collection of blood is usually small in
amount but usually accompanied by
severe brain contusion leading to
severe brain edema
7. Discuss the management of
increased intracranial pressure in
head trauma.
Increased intracranial
pressure in head trauma
• Continuous recording of intracranial
pressure must be achieved.
• ICP monitors employs fiberoptic strain
gauges that can be inserted directly to the
cerebral cortex.
Increased intracranial
pressure in head trauma
• Pressure measurement through a lumbar
puncture is not done because it does not
reflect accurately the ICP and there is an
increased risk of cerebellar or temporal
lobe herniation.
Increased intracranial
pressure in head trauma
• The first step in lowering the high ICP is to
control the factors that are know to raise
the pressure such as hypoxia,
hypercarbia, hyperthermia, awkward head
positions, and high mean airway
pressures.
If ICP exceeds 15-20 mmHg:
• induce hypocarbia by controlled
ventilation (pCO2 at 28 to 33 mmHg)
• induce hyperosmolar dehydration (0.25
to 1.0g of 20% mannitol q 3-6hrs or
0.75 to 1 mg/kg of furosemide) to
maintain serum sodium above 138
meq/L
If ICP exceeds 15-20 mmHg:
• intravenous fluids with free water should
be avoided so as not to intensify cerebral
edema
• fluids such as 5% dextrose in water, 0.5%
saline, and 5% dextrose in 0.5% saline are
therefore avoided
• lactated Ringers solution is permissible
but normal saline, with or without added
dextrose is ideal
To avoid severe hypertension:
use the following:
• Diuretics
• beta-adrenergic blocking agents
• angiotensin converting enzyme
inhibitors (should be used rather than
agents that dilate the cerebral
vasculature)
To avoid severe hypotension:

• vasopressor agents such as


neosynephrine is used
8. Discuss the principles of
management of open skull
fracture, closed skull fracture,
basal skull fracture and CSF leak.
Open Skull Fracture
• Have either a skin laceration over the
fracture or the fracture runs through the
paranasal sinuses and the middle ear
structures, resulting in communication
between the external environment and the
cranial cavity
• Involve a fracture or penetration of the
bones of the skull
• May be clean or contaminated/dirty
Closed Skull Fracture
• Do not penetrate the bones of the skull.
• Occur from a hard blow or impact that jars the
brain within the skull. The rapid movement of
the brain within the skull can:
o Cause bruising, swelling, or tearing of
the brain tissue.
o Stretch, pull apart, or tear nerves or
blood vessels,causing bleeding within
or around the brain.
• Can be more difficult to identify because there
may not be visible signs of injury, such as
bleeding or deformity.
Both open and closed head injuries may cause:
• A concussion
• A brain bruise (contusion)
• Bleeding within or around the brain, a life-
threatening injury. Symptoms of this type of injury
may be the same as those of a concussion. More
serious symptoms usually develop within 24
hours after the injury. In rare cases, if the
bleeding is slow, symptoms take longer to
develop.
Imaging Studies
• Skull X-ray
- fracture at the vertex
• CT scan
- standard modality for aiding in the
diagnosis of skull fractures
• MRI
- for suspected ligamentous and
vascular injuries
Skull X-ray films - who
needs them?
• Impaired consciousness or neurological signs.
• History of loss of consciousness, amnesia, or fits.
• High speed injury or suspected penetrating injury.
• Scalp laceration to bone, large haematoma, or
suspected fracture on palpation.
• Persisting vomiting or headache.
• Loss of cerebrospinal fluid or blood from ear or nose.
• Difficulty in assessing the patient (children, drug or
alcohol intoxication).
The Society of British Neurological Surgeons. Guidelines for the initial management of head
injuries: recommendations form the Society of British Neurological Surgeons. Br J
Neurosurg 1998;12(4):349-52.
Indications for computed
tomography scanning
• Persistent coma after resuscitation.
• Deteriorating Glasgow coma score or
progressive neurological signs.
• Skull fracture if associated with (1)
impaired consciousness, (2) fits, (3)
neurological symptoms or signs.
• Open skull fractures (including fractured
base of skull).
The Society of British Neurological Surgeons. Guidelines for the initial management of
head injuries: recommendations form the Society of British Neurological Surgeons.
Br J Neurosurg 1998;12(4):349-52.
Treatment
Open fracture
 careful irrigation and debridement
 broad-spectrum antibiotics + tetanus toxoid
 wound exploration in the operating room under
direct vision to prevent loose pieces of bone
from damaging the underlying brain
 repair of dural sinus tear
 bony segments reassembled
 if depressed: prophylaxis for posttraumatic
seizures
Treatment
Closed fracture
 elevation depressed skull fractures if
the depressed segment is more than 5
mm below the inner table of adjacent
bone
 repair of venous sinus tear
 if depressed: prophylaxis for
posttraumatic seizures
Basal Skull Fracture
• a linear fracture involving the base of the
skull
• usually associated with a dural tear and
is found at specific points on the skull
base
• commonly involve the roof of the orbits,
the sphenoid bone, or portions of the
temporal bone
Basal Skull Fracture
Temporal fracture
• encountered in 75% of all skull base
fractures
• 3 subtypes:
1. Longitudinal fracture
2. Transverse fracture
3. Mixed
Basal Skull Fracture
Occipital condylar fracture
• results from a high-energy blunt trauma
with axial compression, lateral bending,
or rotational injury to the alar ligament
Basal Skull Fracture
Clinical Manifestations:
• Battle's sign - ecchymosis of the mastoid process of
the temporal bone (petrous temporal bone fractures)
• Raccoon eyes - periorbital ecchymosis i.e. "black
eyes" (anterior cranial fossa fractures)
• Cerebrospinal fluid rhinorrhea and/or rhinorrhea
• Cranial nerve palsy
• Bleeding from the nose and ears
Basal Skull Fracture
Basal Skull Fracture
• CT scan
• Conservative management
• No antibiotic prophylaxis needed
CSF Leak

• CSF leak is an escape


of the fluid that
surrounds the brain and
spinal cord, from the
cavities within the brain,
or from the central canal
in the spinal cord.
• Head injury: rhinorrhea
or otorrhea
Management
Preoperative investigations
• Coronal high definition CT scan
- fracture site
• CT cisternography
- precise location of the CSF leak
• CSF isotope infusion studies with platelet
insertion into the nasal cavities
Management
• Most traumatic CSF leaks resolve spontaneously;
the majority resolve within the first 24 to 48 hours.
• CSF rhinorrhea: Conservative management
consists of a 1- to 2-week trial of bed rest with the
patient in a head-up position.
• CSF otorrhea secondary to recent surgery or
trauma can often be treated conservatively with a
compressive dressing and bed rest with head
elevation.
• If conservative management fails: Surgical repair
Management
• If conservative management fails:
surgical repair
- rhinorrhea: intracranial or extracranial
approach
- otorrhea: subtemporal approach
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