Traumatic Brain Injuries

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Out lines :
 Traumatic Brain Injuries
 Mechanism of Injury
 Pathophysiology
 Classification of Brain Injuries
 Neurologic Assessment of Traumatic Brain Injury
 Nursing Assessment of the Patient with Traumatic
Brain Injury
 Diagnostic Procedures.
 Medical Management
 Nursing Management
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Traumatic Brain Injuries
 More than 1.7 million traumatic brain injuries (TBIs)
occur annually
 approximately 52,000 Americans die each year of TBI
with 275,000 hospitalized as a result of their injury .
 Children aged 0 to 4 years, older adolescents aged 15 to
19 years, and adults aged 65 years and older are most
likely to sustain a TBI .

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Mechanism of Injury
 TBIs occur when mechanical forces are transmitted to
brain tissue
 Mechanisms of injury include penetrating or blunt
trauma to the head
 Penetrating trauma can result from the penetration of
a foreign object such as a bullet, which causes direct
damage to cerebral tissue
 Blunt trauma can be the result of deceleration,
acceleration, or rotational forces.

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 Deceleration injury causes the brain to crash against
the skull after it has hit a hard surface such as the
dashboard of a car .
 Acceleration injury occurs when the brain has been
forcefully hit, such as with abaseball bat.

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Pathophysiology
 Primary Injury.
 occurs at the moment of impact as a result of
mechanical forces to the head
 The extent of and recovery from injury are related to
whether the primary injury was localized to an area or
whether it was diffuse (widespread) throughout the
brain .
 Primary injuries may include direct damage to the
parenchyma or as injury to the vessels that causes
hemorrhage, compressing nearby structures .
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 Examples of primary injuries include contusion,
laceration, shearing injuries, and hemorrhage .
 Primary injury may be mild, with little or no
neurologic damage, or severe, with major tissue
damage.

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 Secondary Injury.
 is the biochemical and cellular response to the initial
trauma that can exacerbate the primary injury and
cause loss of brain tissue not originally damaged .
 can be caused by ischemia, hypercapnia,hypotension,
cerebral edema, sustained hypertension, calcium
toxicity, or metabolic derangements .

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 Tissue Ischemia.
 occurs in areas of poor cerebral perfusion as a result of
hypotension or hypoxia .
 The cells in ischemic areas become edematous .
 Extreme vasodilation of the cerebral vasculature
occurs in an attempt to supply oxygen to the cerebral
tissue.
 This increase in blood volume increases intracranial
volume and raises intracranial pressure (ICP) .

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 Hypotension.
 Hypotension typically is not caused by brain injury
unless terminal medullary failure occurs .
 If a trauma patient is unconscious and hypotensive , a
detailed assessment of the chest , abdomen, and pelvis
is performed to rule out internal injuries.

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 Hypercapnia.
 caused by hypoventilation in an unconscious patient,
hypercapnia results in cerebral vasodilation, increased
cerebral blood volume, and raised ICP.
 Brain Edema.
 Cerebral edema occurs as a result of the changes in the
cellular environment caused by contusion, loss of
autoregulation, and increased permeability of the
blood– brain barrier.

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 Initial hypertension in the patient with severe TBI is
common.
 As a result of the loss of autoregulation, increased
blood pressure results in increased intracranial blood
volume and elevates ICP.
 Every effort must be made to control hypertension to
prevent the secondary injury caused by increased ICP .
 As pressure increases inside the closed skull vault,
cerebral perfusion decreases, which further
compromises the brain.
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Classification of Brain Injuries
 Skull Fracture.
 Skull fractures can be classified as open (dura is torn)
or closed (dura is not torn), or they can be classified as
those of the vault or those of the base.
 Assessment findings may include cerebrospinal fluid
(CSF) loss—described as rhinorrhea (from nose) or
otorrhea (from ear), Battle sign (ecchymosis overlying
the mastoid process behind the ear), “raccoon eyes”
(subconjunctival and periorbital ecchymosis), or palsy
of the seventh cranial nerve.

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 Concussion.
 A concussion is a brain injury accompanied by a brief
loss of neurologic function, especially loss of
consciousness.
 When loss of consciousness occurs, it may last for
seconds to an hour.
 The neurologic dysfunctions include confusion,
disorientation, and sometimes a period of antegrade or
retrograde amnesia .
 headache, dizziness, nausea, irritability, inability to
concentrate, impaired memory, and fatigue .
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 Contusion.
 usually is related to acceleration–deceleration injuries,
which result in hemorrhage into the superficial
parenchyma .
 Frontal or temporal lobe contusions are most common
and can be seen in a coup–contrecoup mechanism of
injury .
 A large contusion can produce a mass effect that can
cause a significant increase in ICP.
 Contusions are almost always associated with
subdural hematoma (SDH)
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 Because a contusion can progress over 3 to 5 days after
injury, secondary injury may occur .
 Larger contusions that produce considerable mass
effect require surgical intervention to prevent the
increased edema and elevations in ICP as the
contusion matures.

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 Cerebral Hematomas.
 Extravasation of blood creates a space occupying lesion
within the cranial vault that can lead to increased ICP.
 Epidural Hematoma.
 (EDH) is a collection of blood between the inner skull and
the outermost layer of the dura.
 most often associated with patients with skull fractures and
middle meningeal artery lacerations .
 The classic clinical manifestations of EDH include brief
loss of consciousness followed by a period of lucidity .
 Rapid deterioration in the level of consciousness should be
anticipated because arterial bleeding

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 A dilated and fixed pupil on the same side as the
impact area is a hallmark of EDH .
 Diagnosis of EDH is based on clinical symptoms and
evidence of a collection of epidural blood identified on
the CT scan.
 Treatment of EDH requires surgical intervention to
remove the blood and to cauterize the bleeding
vessels.

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 Subdural Hematoma.
 Is the accumulation of blood between the dura and
underlying arachnoid membrane, most often is related
to a rupture in the bridging veins between the cerebral
cortex and the dura .
 Acceleration–deceleration and rotational forces are the
major causes of SDH .
 The three types of SDH—acute, subacute, and
chronic—are based on the timeframe from injury to
clinical symptoms.
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 Acute Subdural Hematoma.
 Hematomas that occur after a severe blow to the head .
 Careful observation for deterioration of the level of
consciousness or lateralizing signs, such as inequality
of pupils or motor movements, is essential .
 Subacute Subdural Hematoma.
 are hematomas that develop symptomatically 2 days to
2 weeks after trauma.

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 Chronic Subdural Hematoma .
 is diagnosed when symptoms appear days or months
after injury.
 Clinical manifestations of chronic SDH are insidious.
 The patient may report a variety of symptoms such as
lethargy, absent-mindedness, headache, vomiting, stiff
neck, and photophobia and may show signs of
transient ischemic attack, seizures, pupillary changes,
or hemiparesis.

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 Intracerebral Hematoma .
 results when bleeding occurs within cerebral tissue.
 Traumatic causes of ICH include depressed skull
fractures, penetrating injuries (bullet, knife), or
sudden acceleration–deceleration motion.
 Medical management of ICH may include surgical or
nonsurgical management.
 It is thought that hemorrhages that do not cause
significant ICP problems should be treated without
surgery .

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 Missile Injuries.
 Missile injuries are caused by objects that penetrate the
skull to produce a significant focal damage but
little acceleration–deceleration or rotational injury.
 The injury may be depressed, penetrating, or perforating .
 A high-velocity missile (bullet) can produce shock waves
that are transmitted throughout the brain in addition to
the injury caused by the bullet.
 The outcome after missile injury is based on the degree of
penetration, the location of the injury, and the velocity of
the missile.

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 Diffuse Axonal Injury.
 is a term used to describe prolonged post-traumatic coma
that is not caused by a mass lesion .
 caused by acceleration–deceleration and rotational forces.
 DAI occurs as a result of damage to the axons or disruption
of axonal transmission of the neural impulses.
 The pathophysiology of DAI is related to the stretching and
tearing of axons as a result of movement of the brain inside
the cranium at the time of impact.

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 DAI may not be visible on CT or magnetic resonance
imaging (MRI).
 DAI can be classified as one of three grades based on
the extent of lesions: mild, moderate, or severe .
 Treatment of DAI includes support of vital functions
and maintenance of ICP within normal limits.
 The outcome after severe DAI is poor because of the
extensive dysfunction of cerebral pathways.

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Neurologic Assessment of TBI
 The cornerstone of the neurologic assessment is the
GCS, although it is not a complete neurologic
examination.
 Pupils and motor strength assessment must be
incorporated .
 TBIs are divided into three descriptive categories—
mild, moderate, or severe—on the basis of the
patient’s GCS score and duration of the unconscious
state.

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Degree of Injury
 Mild Brain Injury
 Mild TBI is described as a GCS score of 13 to 15, with a
loss of consciousness that lasts up to 15 minutes.
 Moderate Brain Injury
 Moderate TBI is described as a GCS score of 9 to 12,
with a loss of consciousness for up to 6 hours.
 They are at high risk for deterioration from increasing
cerebral edema and ICP .

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 Severe Brain Injury.
 Patients with a GCS score of 8 or less after
resuscitation or those who deteriorate to that level
within 48 hours of admission have a severe TBI.
 Patients with severe TBI often receive ventilatory
support along with ICP and hemodynamic monitoring

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Nursing Assessment of the Patient
with TBI
 As in all traumatic injuries, evaluation of the airway,
breathing, and circulation (ABCs) .
 Level of consciousness, motor movements, pupillary
response, respiratory function, and vital signs are all part
of a complete neurologic assessment of the patient with a
TBI .
 Level of consciousness can be elicited to assess
wakefulness.
 Determination of orientation to person, place, and time
assesses mental alertness .
 Pupils are assessed for size, shape, equality, and reactivity.

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Diagnostic Procedures
 The cornerstone of diagnostic procedures for
evaluation of TBI is the CT scan .
 Continuous monitoring of ICP enables rapid
intervention during these particularly vulnerable
times.

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Medical Management
 Surgical Management
 A craniotomy is performed to remove the EDH, SDH,
or large ICH .
 A decompressive craniectomy specifically for elevated
ICP. This procedure involves removal of the overlying
bone flap to allow the underlying brain tissue to
expand and swell .

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 Nonsurgical Management
 includes management of ICP, maintenance of
adequate cerebral perfusion pressure (CPP) and
oxygenation, and treatment of any complications (e.g.,
pneumonia, infection) .
 ICP monitoring may be required for patients with a
GCS score less than 8 and abnormal findings on a head
CT scan .

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Nursing Management
 Priority nursing goals include stabilization of vital signs,
prevention of further injury, and reduction of increased
ICP.
 hemodynamic management, pulmonary care, maintenance
of body temperature, and control of the environment, can
impact outcome after TBI.
 Hemodynamic and fluid management are vital.
 CPP should be maintained at a minimum of 60 mm Hg .
 Capnography (monitoring of exhaled carbon dioxide levels)
is suggested to prevent inadvertent hypocapnia or
hypercapnia

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 Aggressive pulmonary care must be instituted .
 Cerebral oxygen consumption is increased during
periods of increased body temperature, and therefore
euthermia (36° to 37° C) .
 In the early post injury phase, the patient’s
environment must be controlled.
 Stimuli that produce pain, agitation, or discomfort
can increase ICP .

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Spinal Cord Injuries
 Is a mechanical forces disrupt neurologic tissue and its
vascular supply to the spinal cord

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Spinal Cord Injuries
 Mechanism of Injury
 Hyperflexion
 Hyperextension
 Rotation
 Axial loading
 Penetrating injuries

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Mechanism of Injury
 Hyperflexion
 Most often seen in cervical area especially at the level of C5
C6.
 Because it is the most mobile portion of the
cervical spine.
 This type of injury most often is caused by
sudden decelaration motion.

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Mechanism of Injury
 It occurs from compression of the cord as a result of
fracture fragments or dislocation of the vertebral bodies.

 Instability of the spinal column occurs because of the

rupture or tearing of the posterior muscles and
ligaments.

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Mechanism of Injury
 Hyperextension
 It involves backward and downward motion of the head.
 With this injury the spinal cord is stretched and
distorted.
 Neurologic deficits associated with this injury are often
caused by contusion and ischemia of the cord without
significant bony involvement

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Mechanism of Injury
 Rotation
 Often occur in conjunction with a flexion or extension
injury.
 Severe rotation of the neck or body results in tearing of
the posterior ligaments and displacement of the spinal
cord.

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Mechanism of Injury
 Axial loading or Vertical Compression
 Occur from vertical force along the spinal cord.

 Compression injuries cause burst fractures of the

vertebral body that often send bony fragments into the
spinal canal or directly into the spinal cord.

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Mechanism of Injury
 Penetrating Injuries
 Penetrating injury to the spinal cord can be caused by a
bullet, knife, or any other object that penetrates the cord.
 These types of injury cause permanent damage by
anatomically transecting the spinal cord.

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Pathophysiology
 PRIMARY injury is the neurologic damage that occurs
at the moment of impact.

 SECONDARY injury can occur within minutes of

injury and can last for days to weeks.

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Pathophysiology
 Several events after Spinal Cord Injuries lead to Spinal
Cord Ischemia and loss of neurologic function.
 A cascade of events is initiated that includes systemic
and local vascular changes, electrolyte and
biochemical changes, neurotransmitter accumulation,
and local edema.

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 Functional injury of spinal cord
 Complete injury
 Tetraplegia
 Paraplegia
 Incomplete injury
 Brown-Séquard Syndrome
 Central Cord Syndrome
 Anterior Cord Syndrome
 Posterior Cord Syndrome

• Spinal Shock
• Neurogenic Shock

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Spinal Cord Injuries
 Complete Injury
 Results in a total loss of sensory and motor function
below the level of injury.
 Tetraplegia: The injury occurs from the C1 to T1
level. Residual muscle function depends on the
specific cervical segments involved.

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Spinal Cord Injuries
 Paraplegia: The injury occurs in the thoracolumbar
region (T2 to L1).
 Patients with injuries in this area may have full use of
the arms and may need a wheelchair, although some
may have limited ability to ambulate short distances
with crutches and orthoses.
 Thoracic L1 and L2 injuries produce paraplegia with
variable innervation to intercostal and abdominal
muscles.

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Spinal Cord Injuries
 Incomplete Injury
 Results in a mixed loss of voluntary motor activity and
sensation below the level of the lesion. It exists if any
function remains below the level of injury.
 Incomplete injuries can result in a variety of
syndromes, which are classified according to the
degree of motor and sensory loss below the level of
injury

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Spinal Cord Injuries
 Brown-Séquard Syndrome.
 Is associated with damage to only one side of the cord.
 This produces loss of voluntary motor movement on the
same side of injury. With loss of pain, temperature, and
sensation on the opposite side
 Functionally, the side of the body with the best motor
control has little or no sensation, whereas the side of the
body with sensation has little or no motor control.

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Spinal Cord Injuries
 Central Cord Syndrome
 Is associated with cervical hyperextension hyperflexion
injury and hematoma formation in the center of the
cervical cord.
 This injury produces a motor and sensory deficit more
pronounced in the upper extremities than in the lower
extremities.
 Various degrees of bowel and bladder dysfunction may
be present.

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Spinal Cord Injuries
 Anterior Cord Syndrome
 Is commonly caused by flexion injuries or acute herniation of
an intervertebral disk.
 Damaged with paralysis evident below the level of injury.
 The result is a loss of motor function and loss of the sensations.
 Below the level of injury, position sense and sensations of
pressure and vibrations remain intact.

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Spinal Cord Injuries
 Posterior Cord Syndrome.
 Is associated with cervical hyperextension injury with
damage to the posterior column. This results in the loss
of position sense, pressure, and vibration below the level
of injury.
 Motor function and sensation of pain and temperature
remain intact. These patients may not be able to
ambulate because the loss of position sense impairs
spontaneous movement.

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Spinal Cord Injuries
 Spinal Shock
 Is a condition that can occur shortly after traumatic
injury to the spinal cord.
 Spinal shock is the complete loss of all muscle tone and
normal reflex activity below the level of injury.
 Patients with spinal shock may appear completely
without function below the area of the injury, although
all of the area may not necessarily be destroyed.

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Spinal Cord Injuries
 Neurogenic Shock
 Known as a second shock state that can occur after
spinal cord injury above the T6 level.
 Sympathetic nerve fibers are disrupted and the
parasympathetic system becomes dominant.
 The classic signs of neurogenic shock are hypotension,
hypothermia, and bradycardia.

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Spinal Cord Injuries
 Assessment
 Airway
 Breathing
 Circulation
 Neurologic
 Diagnostic Procedures

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 Airway
 Evaluation of airway clearance.
 If an unresponsive person, oral airway is inserted while
the patient’s neck is maintained in a neutral position.
 Intubation before severe hypoxia can occur.

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 Breathing.
 Assessment of breathing patterns and gas exchange is
made after an airway has been secured.
 The level of injury dictates the degree of altered
breathing patterns and gas exchange.
 Because complete injuries above the C3 level result in
paralysis of the diaphragm, patients with these injuries
require ventilatory assistance.

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 Circulation
 Assessment of cardiac output and tissue perfusion is
imperative to detect life-threatening injuries and
promote recovery of injured spinal cord tissue.
 The patient with SCI is at high risk for developing
alterations in cardiovascular system .
 a variety of serious and potential physiologic
alterations, including dysrhythmias, cardiac arrest,
orthostatic hypotension, emboli, and thrombophlebitis.

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 Neurologic Assessment for Spinal Cord Injury.
 A detailed motor and sensory examination includes
the assessment of all 32 spinal nerves for evidence of
dysfunction.
 Carefully mapped pathways for the sensory portion of
the spinal nerves, called dermatomes, can assist in
localizing the functional sensory level of injury .

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 Diagnostic Procedures.
 X-RAY
 CT scan of all seven cervical vertebrae and the top of T1
must be obtained to rule out cervicothoracic junction
injury.
 Flexion and extension views can identify subtle ligament
injuries.
 Tomography, myelography, and MRI also may be used.

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Spinal Cord Injuries
 Medical Management
 Pharmacologic management
 Methylprednisolone
 Surgical management
 Laminectomy
 Spinal fusion
 Rodding
 Non-Surgical management
 Cervical injury
 Thoracolumbar injury
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 Surgical Management.
 Laminectomy :
The spinal cord is decompressed by removing bony
fragments or herniated disk material from the spinal
canal.

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 Spinal Fusion.
 Two to six vertebral disks are fused together to provide
stability and to prevent motion.
 The fusion is achieved by using bone parts or bone chips
taken from the iliac crest, or by using wire to achieve fusion,
or by using acrylic glue.
 Rodding
 Larger segments of the spinal column by means of a variety of
rodding procedures, such as the use of Harrington rods.
 The rods are attached by screws and glue to the posterior
elements of the spinal column. These types of procedures
most often are performed to stabilize the thoracolumbar area.

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Spinal Cord Injuries
 Nursing Management

 Maintain head and neck alignment until spinal x-rays are completed and rule out
a spinal injury or the spine is stabilized using an external fixation device like
cervical traction or tongs.
 Foley catheter
 Monitor the patient for respiratory status with vital signs.
 Assess the patient’s neurologic status including Glasgow Coma Scale.
 Prepare for administration of IVF if hypotension occurs.
 Prepare to administer vasopressors if IVF does not improve the patient’s BP.
 Prepare the patient for surgery if internal stabilization is needed.
 Monitor the patients I & O to detect fluid imbalances.
 ROM.
 Frequent position change .
 Provide emotional support for the patient and family. 75
 The goal is to prevent life-threatening complications
while maximizing the function of all organ systems.
 Nursing interventions are aimed at preventing
secondary damage to the spinal cord and managing the
complications of the neurologic deficit.
 Because almost all body systems are affected by SCI,
nursing management must include interventions that
optimize nutrition, elimination, skin integrity, and
mobility.
 Patients with SCIs have complex psychosocial needs
that require a great deal of emotional support from the
critical care nurse.

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