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Dr. Ronny. Y, Sp.s

Traumatic Brain Injury (TBI) maybe divided into 2

categories, primary and secondary brain injury.
Primary injury is defined as the initial injury to
brain as a direct result of the trauma. This is the
initial structural injury caused by the impact on
the brain, and , like other forms of neural injury,
patients recover poorly.

Secondary brain injury is defined as any

subsequent injury to the brain after the initial
Secondary brain injury can result from
systemic hypotension, hypoxia, elevated ICP, or as
the biochemical result of a series of physiologic
changes initiated by the original trauma.

The treatment of the injury is directed at either

preventing or minimizing secondary brain injury.
Elevated ICP may result from the initial brain
trauma or from secondary injury to the brain.
In adults, normal ICP is considered 0-15 mmHg.
In young children, the upper limit of normal ICP is
lower, and this limit may be considered 10 mmHg.

Mild head injury are generally defined as those

associated with GCS core 13-15,
Moderate head injuries are those associated with a
GCS score 9-12.
A GCS score of 8 or less define a severe head injury.

Laboratory studies
After the patient has been stabilized and an
appropriate neurologic examination has been
conducted, the diagnostic evaluation may begin.
Patients with TBI do not require any additional
blood tests beyond the standard panel of tests
obtained in all trauma patients.
A urine toxicology screen and an assessment of
the blood alcohol level are important for any
patient who has an altered level of consciousness
because any central nervous system depressant
can impair consciousness.


Imaging studies

CT Scan
A CT Scan is the diagnostic study of choice in the
evaluation of TBI because it has a rapid
acquisition time, is universally available, is easy
to interpret, and is reliable

2. MRI

Initial clinical evaluation

The evaluation of the spine for potential injury is
critically important in patients with TBI because
approximately 10% of those with severe head
injury have a concomitant spine injury. Many of
these injuries are cervical spine injuries.

Neurologic assessment
The neurologic assessment begins with
ascertaining the GCS score. This is a screening
examination and does not substitute for a
thorough neurologic examination

In addition to determining the GCS score, the

neurologic assessment of patients with TBI should
include the following :
* Brainstem examination pupillary examination,
ocular movement, corneal reflex, gag reflex
* Motor examination
* Sensory examination
* Reflex

Pupillary examination
A careful pupillary examination is a critical part of
the evaluation of patients with TBI, especially in
patients with severe injuries

Closed head injury
Mild head injury
Patients who are discharged after mild head injury
should be given an instruction sheet for head injury
care. The sheet should explain that the person with
head injury should be awakened every 2 hours and
assessed neurologically. Caregivers should be
instructed to seek medical attention if patients
develop severe headaches, persistent nausea and
vomiting, seizures, confusion or unusual behavior, or
watery discharge from either the nose or the ear.

As many as 30% patients who experience a

concussion develop post concussive syndrome (PCS).
PCS consists of a persistence of any combination of
the following after a head injury : headache, nausea,
emesis, memory loss, dizzines, diplopia, blurred
vision, emotional lability or sleep disturbance.

Moderate and severe head injury

The treatment of moderate and severe head
injuries begins with initial cardiopulmonary
stabilization by ATLS guidelines. The initial
resuscitation of a patient with head injury is of
critical importance to prevent hypoxia and

Indications for surgery in patients with

head injuries :
Extra axial hematoma with midline shift greater
than 5 mm,
Intra axial hematoma with volume greater than
30 mL,
An open skull fracture,
A depressed skull fracture with more than 1 cm of
inward displacement.

In addition, any temporal or cerebellar hematoma

that is larger than 3 cm in diameter is considered a
high-risk hematoma because these regions of the
brain are smaller and do not tolerate additional
mass as well as the frontal, parietal, and occipital
lobes. These high risk temporal and cerebellar
hematomas are usually evacuated immediately.

If no surgical lesion is present on the CT scan image, or

following surgery if one is present, treatment of the
head injury begins.
The first phase of treatment is to
institute general measures.
Once appropriate fluid resuscitation has been completed
and the volume status is determined to be normal,
intravenous fluids are administered to maintain the
patient in a state of euvolemia or mild hypervolemia.

A previous tenet of head injury treatment was fluid

restriction, which was believed to limit the
development of cerebral edema and increased ICP.
Fluid restriction decreases intravascular volume
and, therefore, decreases cardiac output. A decrease
in cardiac output often results in decreased cerebral
flow, which results in decreased brain perfusion and
may cause an increase in cerebral edema and ICP.
Thus, fluid restriction is contraindicated in patients
with TBI.

Another supportive measure used to treat patients

with head injuries is elevation of the head. When
the head of the bed is elevated to 20-30, the
venous outflow from the brain is improved, thus
helping to reduce ICP.
If a patient is hypovolemic, elevation of the head
may cause a drop in cardiac output and CBF;
therefore, the head of the bed is not elevated in
hypovolemic patients.
In addition, the head should not be elevated :
(1) in patients in whom a spine injury is a possibility
(2) until an unstable spine has been stabilized.

Sedation is often necessary in patients with traumatic

injury. Some patients with moderate head injuries
have significant agitation and require sedation. In
addition, patients with multisystem trauma often have
painful systemic injuries that require pain medication,
and many intubated patients require sedation. Shortacting sedatives and analgesics should be used to
accomplish proper sedation without eliminating the
ability to perform periodic neurologic assessments.

The prevention of early posttraumatic

seizures does not improve the outcome following
TBI. Therefore, the prophylactic use of
anticonvulsants is not recommended for more than
7 days following TBI and is considered optional in
the first week following TBI.

Diuresis and brain edema

Diuretics are powerful in their ability to decrease brain

volume and, therefore, to decrease ICP. Mannitol, an
osmotic diuretic, is the most common diuretic used.
Mannitol draws water out from the brain into the
intravascular compartment. It has a rapid onset of
action and a duration of action of 2-8 hours. Mannitol is
usually administered as a bolus because it is much
more effective when given in intermittent boluses than
when used as a continuous infusion. The standard dose
ranges from 0.25-1 g/kg, administered every 4-6 hours.

The limit for mannitol is 4 g/kg/d. At daily doses higher

than this, mannitol can cause renal toxicity. Mannitol
should not be given if the patient's serum sodium level
is greater than 145 or serum osmolality is greater than
315 mOsm.
Other diuretics that sometimes are used in patients
with TBI include furosemide, glycerol, and urea.
Mannitol is preferred over furosemide because it tends
to cause less severe electrolyte imbalances than a loop

Other supportive treatments

Decreased serum protein (albumin) from

malnutrition causes a decreased serum osmolality
compared to the osmolality in the surrounding
tissues. This allows intravascular water to flow
along the increased osmotic gradient into the
tissues, increasing edema.
Hyperalimentation should be initiated as soon as
possible if the course is likely to be protracted.

Penetrating trauma

The treatment of penetrating brain injuries

involves 2 main aspects. The first is the treatment
of the TBI caused by a penetrating object.
Penetrating brain injuries, especially from highvelocity missiles, frequently result in severe ICP
elevations. This aspect of penetrating brain injury
treatment is identical to the treatment of closed
head injuries.

The second aspect of penetrating head injury

treatment involves debridement and removal of the
penetrating objects. Penetrating injuries require
careful debridement because these wounds are
frequently dirty.


Functional deficits resulting from TBI are common

and can be divided into 2 categories, as follows: systemic
complications and neurologic complications.
The systemic complications of TBI are typical of any
severe injury and depend on the types of intensive
treatments used.
The neurologic complications of TBI
include focal neurologic deficits, global neurologic
deficits, seizures, CSF fistulae, hydrocephalus, vascular
injuries, infections, and brain death.

The cranial nerves that are injured most commonly in

patients with TBI are cranial nerves I, IV, VII, and
Anosmia caused by traumatic injury to the first cranial
nerve occurs in 2-38% of patients with TBI. It is more
common in those with frontal fractures and in those
with posttraumatic rhinorrhea. Posttraumatic anosmia
improves slowly, and as many as one third of patients
do not show any improvement in olfaction.

Facial nerve injuries often occur with head injuries

in which the temporal bone is fractured.
Cochlear nerve injury (cranial nerve VIII) is also a
common occurrence in patients with head injury,
especially in patients with temporal bone fractures.


Hydrocephalus is a common late complication of

TBI. Posttraumatic hydrocephalus may present as
either ventriculomegaly with increased ICP or as
normal pressure hydrocephalus. In patients with
increased ICP secondary to posttraumatic
hydrocephalus, the typical signs of hydrocephalus
are often observed and include headaches, visual
disturbances, nausea/vomiting, and alterations in
the level of consciousness. Normal pressure
hydrocephalus usually manifests as memory
problems, gait ataxia, and urinary incontinence.


Posttraumatic seizures are very common in those

with a penetrating cerebral injury, and late
seizures occur in as many as half of these patients.

Cerebrospinal fistulae, either in the form of

rhinorrhea or otorrhea, may occur in as many as 510% of patients with TBI. They may present either
immediately or in a delayed fashion and are more
frequent in patients with basilar skull fractures.
Approximately 80% of acute cases of CSF
rhinorrhea resolve spontaneously within 1 week. A
17% risk of meningitis exists when CSF rhinorrhea
is present.

Prophylactic antibiotics have not been

demonstrated to decrease this meningitis risk,
although very few studies have examined this
issue. More than 95% of acute episodes of CSF
otorrhea resolve spontaneously within 1 week, and
CSF otorrhea is complicated by meningitis in fewer
than 4% of cases.

Delayed CSF fistulae may occur from 1 week after

the initial injury to years later. These delayed
fistulae are more difficult to treat and frequently
require surgical intervention.

Vascular injuries


Dr. Ronny. Y., Sp. S

Brain injury can be at the site of impact, but can

also be at the opposite side of the skull due to a
contrecoup effect (the impact to the head can cause
the brain to move within the skull, causing the
brain to impact the interior of the skull opposite
the head-impact).
If the impact causes the head to move, the injury may
be worsened, because the brain may ricochet inside
the skull causing additional impacts, or the brain
may stay relatively still (due to inertia) but be hit by
the moving skull (both are contrecoup injuries).

Specific problems after head injury can include :

Skull fracture
Lacerations to the scalp and resulting
hemorrhage of the skin
Traumatic subdural hematoma, a bleeding below
the dura mater which may develop slowly
Traumatic extradural, or epidural hematoma,
bleeding between the dura mater and the skull
Traumatic subarachnoid hemorrhage

Cerebral contusion, a bruise of the brain

Concussion, a temporary loss of function due to
Dementia pugilistica, or "punch-drunk
syndrome", caused by repetitive head injuries, for
example in boxing or other contact sports

Mild concussions are associated with sequelae.
However, a slightly greater injury is associated
with both anterograde and retrograde amnesia
(inability to remember events before or after the
injury). The amount of time that the amnesia is
present correlates with the severity of the injury.
In all cases the patients develop postconcussion
syndrome, which includes memory problems,
dizziness, tiredness, sickness and depression.

Epidural hematoma
Epidural hematoma (EDH) is a rapidly
accumulating hematoma between the dura mater
and the cranium. These patients have a history of
head trauma with loss of consciousness, then a lucid
period, followed by loss of consciousness. Clinical
onset occurs over minutes to hours. Many of these
injuries are associated with lacerations of the middle
meningeal artery. A"lenticular", or convex, lensshaped extracerebral hemorrhage will likely be
visible on a CT scan of the head.

Subdural hematoma
Subdural hematoma occurs when there is tearing
of the bridging vein between the cerebral cortex
and a draining venous sinus. At times they may
be caused by arterial lacerations on the brain
A crescent shaped hemorrhage compressing the
brain will be noted on CT of the head.
Surgical evacuation is the treatment.
Complications include uncal herniation, focal
neurologic deficits

Cerebral contusion
Cerebral contusion is bruising of the brain tissue.
The majority of contusions occur in the frontal
and temporal lobes. Complications may include
cerebral edema and transtentorial herniation.
The goal of treatment should be to treat the
increased intracranial pressure.

Diffuse axonal injury

Diffuse axonal injury, or DAI, usually occurs as
the result of an acceleration or deceleration
motion, not necessarily an impact. Axons are
stretched and damaged when parts of the brain
of differing density slide over one another.
Prognoses vary widely depending on the extent of

Patients with concussion may have a history of
seconds to minutes unconsciousness, then normal
arousal. Disturbance of vision and equilibrium
may also occur.
Common symptoms of head injury include coma,
confusion, drowsiness, personality change,
seizures, nausea and vomiting, headache and a
lucid interval, during which a patient appears
conscious only to deteriorate later.

Symptoms of skull fracture can include :

leaking cerebrospinal fluid (a clear fluid drainage
from nose, mouth or ear) may be and is strongly
indicative of basilar skull fracture and the
tearing of sheaths surrounding the brain, which
can lead to secondary brain infection.
visible deformity or depression in the head or
face; for example a sunken eye can indicate a
maxillar fracture

an eye that cannot move or is deviated to one side

can indicate that a broken facial bone is pinching
a nerve that innervates eye muscles
Basilar skull fractures, those that occur at the
base of the skull, are associated with Battle's
sign, a subcutaneous bleed over the mastoid,
hemotympanum, rhinorrhea and otorrhea.