HEAD TRAUMA

Definition
impairment

in brain function as a
result of mechanical force
can be temporary or permanent, and
may or may not result in underlying
structural changes in the brain
based on the Glasgow Coma Scale
(GCS), divides TBI into severe (GCS
score of 3 to 8), moderate (GCS
score of 9 to 13), and mild (GCS
score of 14 or 15)

Epidemiology
Mild

TBI makes up a majority of head

injuries in the U.S. (approximately 80%)
Moderate TBI accounts for approximately
10% of head injuries. Overall, 40% of
patients with moderate TBI have an
abnormal finding on CT scan and 8%
require neurosurgical intervention
In severe TBI mortality approaches 40%,
with most deaths occurring within the first
48 hours. Fewer than 10% of patients with
severe TBI make even a moderate
recovery.

Anatomy

The

scalp is composed of five layers: skin,

subcutaneous tissue, galea, areolar tissue,
and pericranium
The skull comprises the frontal, ethmoid,
sphenoid, and occipital bones and two
parietal and two temporal bones

Anatomy
The

cranium is an enclosed space with a fixed volume. Any changes

to the volume of the intracranial contents affect the ICP. Normal ICP
is <15 mm Hg and is determined by the volume of the three
intracranial compartments: the brain parenchyma (<1300 mL in the
adult), CSF (100 to 150 mL), and intravascular blood (100 to 150 mL)
Normal values for ICP vary with age. In adults and older children the
normal range is <10 to 15 mm Hg, in children the normal range is
from 3 to 7 mm Hg, and in infants normal ICP may range from 1.5 to
6.0 mm Hg.
Cerebral blood flow is generally maintained when the CPP is >60 mm
Hg. This level is considered the lower limit of autoregulation, below
which local control of cerebral blood flow cannot be adjusted to
maintain flow adequate for function
Rapid rises in ICP may lead to a phenomenon known as the Cushing
reflex (hypertension, bradycardia, and respiratory irregularity). This
triad is classic for an acute rise in ICP, but it is seen in only one third
of cases and is more common in children than in adults.

Pathopysiology
The

brain consumes 20% of the body's total oxygen

requirement and 15% of total cardiac output. The brain is
exquisitely sensitive to ischemia and low-oxygen states
Cerebral blood flow changes and adapts to the regional
needs of the tissue.. Under normal circumstances,
microvascular changes in blood volume, pH, PO 2, and PCO2
regulate local cerebral blood flow to maintain an equilibrium
between oxygen delivery and metabolism
CPP is calculated as the difference between the
mean arterial pressure (MAP) and the intracranial
pressure (ICP):
MAP ICP = CPP
Local cellular oxygen demands can be met and regional
cerebral blood flow maintained over a wide range of CPPs
(between 50 and 150 mm Hg in a normally functioning
system)

Pathophysiology

BIOMECHANIC
Direct

Injury.
struck by an object or its motion is
arrested by another object. The
resulting damage depends on the
consistency, mass, surface area, and
velocity of the object striking the head
Indirect Injury. In indirect brain injury,
the cranial contents are set into
motion by forces other than the direct
contact of the skull with another object

Cushings reflexes
Progressive

hypertension
associated with bradycardia and
diminished respiratory effort is a
specific response to acute,
potentially lethal increases in ICP

Uncal Herniation
The

most common clinically significant traumatic

herniation syndrome
Uncal herniation is often associated with traumatic
extra-axial hematomas in the lateral middle fossa or
the temporal lobe
The classic signs and symptoms are caused by
compression of the ipsilateral uncus of the temporal
lobe on the U-shaped edge of the tentorium cerebelli
as the brain is forced through the tentorial hiatus
As compression of the uncus begins, the third cranial
nerve (CN) is compressed; anisocoria, ptosis,
impaired extraocular movements, and a
sluggish pupillary light reflex develop on the
side ipsilateral to the expanding mass lesion

Central Transtentorial Herniation

The

central transtentorial herniation

syndrome is demonstrated by
rostrocaudal neurologic deterioration
caused by an expanding lesion at the
vertex or the frontal or occipital pole of
the brain.
The initial clinical manifestation may be
a subtle change in mental status or
decreased level of consciousness,
bilateral motor weakness, and
pinpoint pupils (2 mm)

Cerebellotonsillar
Herniation
occurs

when the cerebellar tonsils

herniate downward through the
foramen magnum
Pinpoint pupils are noted. Flaccid
quadriplegia is the most common
motor presentation because of
bilateral compression of the
corticospinal tracts
Mortality from cerebellar herniation
approaches 70%

Upward transtentorial herniation

occasionally

occurs as a result of an
expanding posterior fossa lesion.
Level of consciousness declines
rapidly
These patients may have pinpoint
pupils from compression of the
pons. Downward conjugate gaze
is accompanied by the absence
of vertical eye movements

Clinical Features
History

taking

Details regarding the mechanism of injury

should be solicited from witnesses or the
victim to determine whether the headinjured
patient is at high risk for intracranial injury.
The patients condition before trauma may
give clues to important, otherwise
unsuspected, comorbid factors such as
preexisting coagulopathy (e.g., hemophilia).
Past medical history, medications (particularly
anticoagulants), recent drug or alcohol use,
and complaints immediately before the
traumatic event should be determined

Clinical Features
GCS
Pupillary

examination
Motor examination : posturing
CN examination
In the severely head-injured patient, the CN
examination is often limited to the pupillary
responses (CN III), gag reflex (CNs IX and X), and
corneal reflex (CNs V and VII). Facial symmetry
(CN VII) can sometimes be assessed if the patient
grimaces with noxious stimuli. In patients who are
awake and cooperative, a formal CN examination
should be performed
Other

examination finding

Ancillary Lab test

Laboratory

Tests. The acute management of the severely headinjured

patient is directed by physical examination and diagnostic imaging.
Ancillary laboratory tests that may provide useful information in the
subsequent management of the patient include a urine toxicology screen,
blood alcohol level, complete blood count, electrolytes, glucose, and
coagulation studies.
Neuroimaging. In the acute phase the most useful imaging technique is a
noncontrast-enhanced head CT scan. This scan delineates acute intraaxial and extra-axial bleeding, subarachnoid blood, cerebral swelling,
ischemic infarction caused by hypoxia after trauma, evidence of
increased ICP, and pneumocephalus. The bone windows of the CT scan
can detect skull fractures (including basilar fractures); plain skull
radiographs are not necessary in patients who undergo CT scanning.
Magnetic resonance imaging (MRI) is better than CT in detecting posttraumatic ischemic infarctions, subacute nonhemorrhagic lesions and
contusions, axonal shear injury, and lesions in the brainstem or posterior
fossa. Monitoring and managing patients in the MRI suite can be very
difficult, especially patients with severe TBI who have other lifethreatening injuries. MRI is not recommended as the first-line imaging
modality for severe or moderate head injury.

Disposition
All

patients with severe head

trauma require an imaging
modality to determine the extent
and nature of the brain injury and
the necessity of neurosurgical
intervention. Neurosurgical
consultation should be obtained as
soon as possible to help direct the
patients subsequent
management.

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