TBI&SCI

NORTHWESTERN UNIVERSITY,INC
Laoag City, Ilocos Norte
TRAUMATIC BRAIN INJURY
Traumatic Brain Injury or TBI occurs due to a violent blow or jolt to the head or an
object that penetrates brain tissue, such as a bullet or shattered piece of skull. According
to CDC, there are around 2.5 million TBIs each year in the US alone. Hence, TBI is a
major cause of preventable death and disability.
MECHANISMS OF INJURY
1. Penetrating Injury
A penetrating (open-head) injury involves an open wound to the head from a
foreign object (e.g., bullet). It is typically marked by focal damage that occurs along the
route the object has traveled in the brain that includes fractured/perforated skull, torn
meninges, and damage to the brain tissue (Hegde, 2006).
2. Non-penetrating/ Blunt Injury

a. Acceleration Injury
b. Deceleration Injury
c. Acceleration-deceleration injury
d. Rotation Injury
e. Compression injury
Acceleration-deceleration injury
CLASSIFICATION:
A. According to Severity
1. Mild
2. Moderate
3. Severe
1|Unit 2: Emergency Nursing

Criteria Mild Moderate Severe
Structural imaging Normal Normal or Normal or

abnormal abnormal
Loss of Consciousness (LOC) 0–30 min > 30 min and < > 24 hrs
24 hrs
Alteration of a moment up > 24 hours. Severity based on

consciousness/mental state to 24 hrs other criteria
(AOC)
Post-traumatic amnesia (PTA) 0-1 day > 1 and < 7 > 7 days
days
Glasgow Coma Scale (best 13-15 9-12 <9

available score in first 24
hours)
B. According to Pathologic features

1. Focal- injury that is concentrated in one region of the brain.
2. Diffuse- form a continuum of progressively severe brain damage caused by
increasing amounts of acceleration-deceleration injury to the brain. It is the most
common type of head injury.
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TYPES OF INJURIES:
a. Primary injury
- occurs at the time of impact and
results in focal or diffuse injury.
1. Scalp Lacerations
 Abrasion: the top layer of the scalp is scraped away; this is a minor injury that
may cause slight bleeding. The area is cleaned and possibly dressed, and no other
treatment is required.
 Contusion: the scalp is bruised with possible effusion of blood into the
subcutaneous layer without a break in the integrity of the skin; there is no
specific treatment.
 Laceration: the scalp is torn and may bleed profusely; suturing may be necessary.
on other signs and symptoms, a computed tomography (CT) scan

rather than a skull film may be ordered to rule out underlying skull or brain injury.
Scalp lacerations often require suturing and aseptic management.
2. Skull Fracture
The mechanism of skull injury is direct contact.
Classification:
1. Linear: a singular fracture line occurring to the skull, which could be displaced
or nondisplaced
2. Comminuted: the skull is splintered or shattered into pieces. It refers to a bone
that is broken in at least two places.
3. Depressed: a fracture of the skull in which a fragment is depressed; the scalp
and/or dura may or may not be torn. Where the fracture causes displacement
of the bone toward the brain.
Open depressed fracture: also known as compound skull
fracture; is an opening of the skull as a result of
comminuted depressed skull fractures and tearing of the
dura mater and the scalp
4. Basal skull fracture: A break of the bones at the base of
your skull.

A CT is used to diagnose a skull fracture. If a fracture is found on CT,

there is always the question of associated brain injury, and magnetic resonance
imaging (MRI) provides better resolution and clearer pictures at the fracture-
cerebral site.
Treatment of skull fractures depends on the type of fracture.
1. Linear skull fractures do not require special medical management other than
observation for underlying cerebral injury.
2. A depressed skull fracture with an open scalp, skull, and dura mater requires
surgery to débride, elevate, and remove bone fragments from the wound. If the
fragments are extensive, a craniectomy may be necessary. Surgical elevation
of depressed skull fractures may be necessary with greater than 8 to 10 mm
depression, neurological deficit, CSF leak, and presence or absence of open
depressed fracture
**Craniectomy- a surgery done to remove a part of your skull in order to relieve
pressure in that area when your brain swells
(a) (b)
© (d)
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3. Facial Fractures
 commonly coexist with TBI. Injuries may involve the soft tissue, the facial bones or
both. The facial bones include most of the paranasal sinuses and the primary receptor
organs for the senses
 Facial injuries can result in disfigurement, motor and sensory dysfunction, and deficits
in communication.
 CT scan is used to diagnose a facial fracture that can lead to injury of the eye.
 Some studies have shown that early craniofacial repair can be performed safely with
appropriate general surgical and neurosurgical support in selected patients, thus
avoiding costly delays and complications.
** Craniofacial repair- series of surgical procedures involving the skull and face.
Reconstructs damaged bone and tissue and improves the appearance of disfigured
areas of the face and head.
4. FOCAL CEREBRAL INJURIES

A. Cerebral Contusions
➢ bruising of the surface of the brain.
➢ The clinical effect of a contusion depends on its size and related cerebral
edema. Small, unilateral, frontal lesions may be asymptomatic, whereas larger
lesions may result in neurological deficits.
Classification:
• Fracture contusions occur at the sites of fractures and are particularly severe
in the frontal lobes when associated with fractures in the anterior fossa.
• Coup contusions are found directly under the areas of impact (contact).
• Contrecoup contusions, by contrast, are cerebral injuries at the opposite pole
of direct contact. A contrecoup injury is most often a contusion, but
occasionally it may be a laceration. Both coup and contrecoup injuries are
caused by the rapid acceleration- deceleration of the semisolid brain within
the rigid cranial vault.

B. Cerebral Lacerations
 A cerebral laceration refers to a traumatic tearing of the cerebral tissue. It is
related to high impact injuries and is treated in the same manner as a cerebral
contusion is managed.
C. Intracranial Hemorrhage/Hematomas
-Intracranial hemorrhage may be an
occult development in a patient who has
sustained a seemingly minor TBI in
which consciousness has been
maintained or quickly restored.
Traumatic intracranial hemorrhage

-presence may not be clinically apparent until sufficient blood accumulates to
cause signs and symptoms of a space-occupying lesion and mass effect.
-The interval between bleeding and the appearance of clinical symptoms may be
minutes or weeks, depending on the site and rate of bleeding.
1. Epidural Hematoma (EDH)

- also known as an extradural
hematoma
- refers to bleeding into the potential
space between the inner table of the
skull (inner periosteum) and the dura
mater.
- EDHs are commonly identified through
CT scan of the head (without contrast).
2. Subdural Hematoma (SDH)

- refers to bleeding between the dura mater and arachnoid layer.
- Most SDHs are caused by tearing of the bridging veins located over the
convexity of the brain. Other causes include tearing of small cortical arteries,
cerebral contusions, and acute bleeding into chronic.
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Three classes with approximate time intervals are recognized:

a. Acute: up to 48 hours. This consists of clotted blood that is hyperdense on CT.
- Common signs and symptoms associated with an acute SDH
 gradual or rapid deterioration of the LOC from drowsiness
 slow cerebration
 confusion to coma
 pupillary changes
 hemiparesis or hemiplegia.
b. Subacute: 2 days to about 2 weeks. The clot

now lyses, and blood products and fluid are
present. Clot will be seen isodense on CT
scan.
- Signs and symptoms correspond
closely to those of the acute SDH.
c. Chronic: longer than 2 weeks to several

months. The clot is a fluid mass and is
hypodense on CT.
- can develop from seemingly minor
TBIs. The SDH slowly enlarges, probably because of repeated small bleeding.
Symptoms:
 headache (progressing in severity)

 slow cerebration
 confusion
 drowsiness
 possibly seizure
 Papilledema
 sluggish ipsilateral pupillary response
 hemiparesis may later develop.
3. Traumatic Subarachnoid Hemorrhage (TSAH)

 is the accumulation of blood throughout the subarachnoid and is usually
caused by surface contusions. Onset of symptoms varies according to location
and the rate of bleeding.

Signs and Symptoms:

 headache
 reduced level of consciousness
 nuchal rigidity
 hemiplegia
 and/or ipsilateral papillary abnormalities.
4. Intracerebral Hematoma (ICH)
- ICH refers to bleeding into the brain parenchyma

resulting from contusions or blood vessel injury.
Approximately 16% of TBI cases are due to ICH.
- Manifestations include headache; altered mental status,
which can vary from confusion to a reduced level of
consciousness or coma.
5. Intraventricular Hematoma (IVH)

 IVH occurs secondary to traumatic subarachnoid hemorrhage or as an
extension from an ICH and could be suggestive of severe head injury.
Signs and symptoms:
 altered level of consciousness
 hemiparesis
 ipsilateral pupil dilatation
 intracranial hypertension
5. DIFFUSE CEREBRAL INJURIES: Concussions and Diffuse Axonal Injuries

- A cerebral concussion is defined as a transient, temporary, neurogenic dysfunction
caused by mechanical force on the brain.
- Acceleration-deceleration (with shearing stress on the reticular formation) is the
mechanism of injury usually due to a nonpenetrating injury such as a sudden blow to
the head.
A. CONCUSSIONS
- Concussions are classified as mild or classic, based on the degree of symptoms,
particularly those of unconsciousness and memory loss.
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a. Mild concussion - defined as temporary neurological dysfunction without loss of

consciousness or memory.
b. Moderate or classic concussion- includes temporary neurological dysfunction,
unconsciousness, and memory loss. Recovery of consciousness varies from
minutes to hours.
- The diagnosis of concussion is based on the patient’s history and neurological
examination.
 CT scan or MRI is usually unremarkable.
 Depending on the severity of the concussion, a short-stay admission may
be done to observe the patient’s neurological status. In other cases, a
patient may be discharged home under the supervision of a responsible
adult.
 The patient should also be cautioned in avoiding alcohol, illicit drugs,
and/or other substances such as narcotic analgesics or sedatives that may
mask any signs of neurological dysfunction. For any persistent and/or
worsening signs and symptoms, follow-up is imperative
B. Diffuse Axonal Injury

- DAI is a primary TBI associated with
acceleration-deceleration during which
shearing forces damage nerve fibers at the
moment of injury. Because of the
difference in acceleration gradient on
certain areas of the brain during primary
impact, shearing forces at the white– gray
junction, corpus callosum, brainstem, and
sometimes cerebellum produce diffuse
tearing of axons and small blood vessels.
- It is characterized by distinct gross and microscopic findings including axonal
swellings that are widely distributed in the cerebral hemispheric white matter, corpus
callosum, and upper brainstem; gross hemorrhagic lesions of the corpus callosum;
and gross hemorrhagic lesions involving one or both dorsolateral quadrants of the
rostral brainstem.

- A grading system based on the distribution of pathologic findings

DAI grade 1: there is histologic evidence of axonal damage in the
white matter of the cerebral hemispheres, corpus callosum, brainstem,
and less commonly cerebellum.
DAI grade 2: in addition to evidence of axonal injury, there are also
focal lesions of the corpus callosum.
DAI grade 3: in addition to findings of grades 1 and 2, there are lesions
of the dorsolateral quadrant of the rostral brainstem
- DAI is characterized clinically by functional cerebral failure, which may range
from confusion to coma and death. It is also classified clinically as:
Mild DAI: coma lasting 6 to 24 hours with the patient beginning to
follow commands by 24 hours. Outcome: death is uncommon, but
cognitive and neurological deficits are common; mild to moderate
memory impairment.
Moderate DAI: coma lasting longer than 24 hours, followed by
confusion and long lasting amnesia. Outcome: incomplete recovery in
those who survive.
Severe DAI: coma is prolonged and associated with prominent
brainstem signs. Outcome: death or severe disability.
- The clinical diagnosis of DAI is based on immediate onset of unconsciousness
in a patient who has significant cerebral trauma and no intracranial lesion
noted on CT scan. In some cases, an MRI may demonstrate small lesions not
evident on a CT.
-
b. Secondary injury
Secondary injury occurs as an indirect result of the insult. It results from
processes initiated by the initial trauma and typically evolves over time. These include
1. ischemia (insufficient blood flow);

2. hypoxia (insufficient oxygen in the brain);
3. hypo/hypertension (low/high blood pressure);
4. cerebral edema (swelling of the brain);
5. raised intracranial pressure (increased pressure within the skull), which can lead to
herniation (parts of the brain are displaced);
6. hypercapnia (excessive carbon dioxide levels in the blood);
7. meningitis (infection of the meningeal layers) and brain abscess;
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8. biochemical changes (changes in levels of neurotransmitters, sodium, potassium,

etc.);
9. epilepsy.
PREHOSPITAL MANAGEMENT: Initial management of TBI
A: Airway
B: Breathing
C: Circulation
D: Disability or neurological evaluation and stabilization
Airway
 Patent airway should be assessed and secured.
 Patients with severe head injury with a Glasgow Coma Scale score of 8 or less, those
with facial fractures, and/or those with other injuries that may compromise adequate
oxygenation and ventilation should be intubated and assisted ventilation should be
instituted.
 Cervical spine stabilization should always be done during field intubation due to the
increased risk of cervical spinal injury among any TBI and/or multitrauma patients.
Breathing
 Hypoxia, which is PO2 less than 60 mm Hg on arterial blood gas or oxygen saturation
of less than 90% measured via pulse oximeter, is associated with higher mortality.
Circulation
 According to one study, raising blood pressure in hypotensive, severe TBI patients
improves outcomes in proportion to the efficacy of the resuscitation.
 Early hypotension, defined as a single episode of systolic blood pressure of 90 mm
Hg or less, could significantly worsen the TBI patient’s outcome.
 Volume resuscitation is the primary method of attaining such blood pressure goal. In
cases where hypotension is refractory to fluid resuscitation, the use of vasopressors
may be initiated.
 Intravenous access should be established for fluid and/or drug administration. Isotonic
fluids such as 0.9% normal saline (NS) are highly recommended, although there is
growing evidence that the use of hypertonic saline for fluid resuscitation is more
beneficial because it also reduces intracranial pressure. The use of hypotonic
11 | U n i t 2 : E m e r g e n c y N u r s i n g
intravenous fluid in TBI patients is not recommended because it may cause and/or
exacerbate cerebral edema.
Disability
 All emergency medical personnel must be mindful of the disastrous consequences
associated with neck manipulation, which include cord transection, quadriplegia, and
death.
 GCS scoring should be calculated by trained emergency personnel prior to
administration of any sedative and paralytic agents. Pupils should also be assessed for
any abnormalities.
Specifically, severe TBI patients should be transported to a trauma center or

hospital with 24-hour CT scanning, 24-hour neurosurgery service, and a capability for
monitoring and managing intracranial hypertension.
EMERGENCY DEPARTMENT OR TRAUMA CENTER MANAGEMENT
• inserting arterial and central lines

• inserting an indwelling urinary catheter
• attaching monitoring equipment such as continuous electrocardiography
• conducting primary and secondary trauma surveys.
• The history and circumstances of injury and previous treatment are verified and
clarified.
MANAGEMENTS:
1. MANNITOL
- the osmotic diuretic of choice.
- It is indicated for intracranial hypertension.
- acts by drawing edematous brain tissue water into the intravascular area resulting in
reduced volume of the brain in a fixed skull, reducing the intracranial pressure.
- has neuroprotective properties. It decreases blood viscosity by diluting the blood and
deformability of the erythrocytes resulting in increased cerebral blood flow.
- Onset of action is within 15 to 30 minutes with peak in 60 minutes and duration of
action for 6 to 8 hours.
- An indwelling urinary catheter is necessary to monitor urinary output.
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- Blood pressure and electrolytes should be monitored carefully, because one danger
associated with mannitol-induced diuresis is hypotension and electrolyte imbalances
(hypokalemia and hyponatremia).
2. Hypertonic Saline
-The principal effect of hypertonic saline on ICP is possibly due to osmotic
mobilization of water across the intact blood–brain barrier, which reduces cerebral
water content.
3. Seizure Management
- Posttraumatic seizures (PTSs) are classified according to the time of
occurrence. Early PTSs occur within 7 days following injury, whereas late PTSs occur
after 7 days after injury. Studies have shown that prophylactic anticonvulsants are
effective in preventing early PTSs but are not useful for prevention of delayed PTSs.
4. Cardiovascular Management
- Optimal volume resuscitation and cardiac function with maximum tissue
perfusion should be a priority in TBI.
5. Respiratory Management
- Patients with severe TBI usually have reduced mental status and require
intubation and mechanical ventilation. Patent and secure airway should be maintained.
The SaO2 saturation, arterial blood gases, and the quality of respirations are major
clinical parameters for assessment. Hypoxemia should be avoided.
6. Temperature Control
- The goal is to maintain normothermia while preventing shivering.
Chlorpromazine (Thorazine) is used to control shivering
7. Electrolyte Management
- Electrolyte imbalances are common in TBI patients. The most common
electrolyte imbalance is hyponatremia often associated with SIADH or cerebral salt
wasting. Hyponatremia can exacerbate cerebral edema or cause seizures therefore, early
recognition of hyponatremia is important. Intravenous solutions with higher
concentrations of saline, extra salt added to the enteral feeding, and drug therapy
8. Endocrine Management
- Blood glucose levels should be maintained between 60 and 150 mg/dL to
prevent secondary brain injury
NURSING MANAGEMENT OF TRAUMATIC BRAIN INJURY
1. Proper positioning and elevation of the head of bed at 30 degrees.

2. Cervical collar and endotracheal tubes must be checked for tightness around the neck.
3. Use pharmacologic orders for sedation and analgesia as needed
4. Hemodynamic stability is another important patient goal.
5. Treatment is usually pharmacologic, and is guided by targeted physiologic values for
hemodynamic variables, such as cardiac output and MAP.
6. Maintaining a patent airway, the common pathway to the respiratory system, is another
top priority in TBI management.
7. Suction is needed to prevent an increase in carbon dioxide and subsequent hypercapnia,
which contributes to cerebral vasodilatation, cerebral edema, and increased ICP.
8. . Nursing management to prevent pneumonia should incorporate the following:
a. Maintain a patent airway.
b. Turn from side to side every 2 hours to prevent stasis of fluid in the lungs.
c. Do not position on the back, because this increases the possibility of
aspiration
d. Administer chest physiotherapy to loosen and drain pulmonary
secretions.
e. Use meticulous aseptic technique when delivering care. The intubated
or tracheotomized patient is at high risk for infection.
f. Be sure to clear secretions from the back of the throat when suctioning.
g. Elevate the head of the bed to 30 degrees.
SPINAL CORD INJURIES
Spinal Cord Injury (SCI) is a loss of body function that also involves the loss of
independence. The loss of function may be permanent or temporary, depending on the
type of injury.
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SCI is usually associated with what is commonly called a broken neck or broken
back. Generally speaking, SCI is damage to the spinal nerves, the body's central and
most important nerve bundle, as a result of trauma to the backbone.
An SCI is described by its level, type, and severity. The level of injury for a
person with SCI is the lowest point on the spinal cord below which sensory feeling and
motor movement diminish or disappear.
The closer the spinal injury is to the skull, the more extensive is the curtailment
of the body's ability to move and feel. If the lesion is low on the spine, say, in the sacral
area, it is likely that there will be a lack of feeling and movement in the thighs and lower
parts of the legs, the feet, most of the external genital organs, and the anal area. But the
person will be able to breathe freely and move his head, neck, arms, and hands. By
contrast, someone with a broken neck may be almost completely incapacitated, even to
the extent of requiring breathing assistance.
TYPES OF SCI:
 Complete injury is the situation when the injury is so severe that almost all feeling
(sensory function) and all ability to control movement (motor function) are lost below
the area of the SCI. Paraplegia or tetraplegia are results of complete spinal cord injuries.
Tetraplegia (formerly called quadriplegia) generally describes the condition of a person
with an SCI that is at a level anywhere from the C1 vertebra down to the T1. These
individuals can experience a loss of sensation, function, or movement in their head,
neck, shoulders, arms, hands, upper chest, pelvic organs, and legs.
Paraplegia is the general term describing the condition of people who have lost feeling in
or are not able to move the lower parts of their body. The body parts that may be affected
are the chest, stomach, hips, legs, and feet. The state of an individual with an SCI level
from the T2 vertebra to the S5 can usually be called paraplegic
 Incomplete injury occurs when there is some sensory or motor function below the
damaged area on the spine.
LEVELS OF SPINAL CORD INJURY
There are four sections of the spinal cord that impact the level of spinal cord injury:
cervical, thoracic, lumbar and sacral. Each section of the spine protects different groups
of nerves that control the body. The types and severity of spinal cord injuries can depend
on the section of the spine that is injured.
1. Cervical Spinal Cord Injuries

 Cervical spinal cord injuries affect the head and neck region above the shoulders.
It is the most severe level of spinal cord injury. If there is an injury in the cervical
area, it will result in tetraplegia, also known as quadriplegia, meaning there is
limited or absent feeling or movement below the shoulders/neck.
 C1-C4 INJURY- POTENTIAL INABILITY TO BREATH
2. Thoracic Spinal Cord Injuries

 Thoracic spinal cord injuries affect the upper chest, mid-back and abdominal
muscles. Arm and hand function is usually normal with this level of spinal cord
injury.
 T-1 through T-5 nerves affect muscles, upper chest, mid-back and abdominal
muscles. These nerves and muscles help control the rib cage, lungs, diaphragm
and muscles that help you breathe. Injuries usually affect the abdominal and lower
back muscles and the legs, typically resulting in paraplegia. Arm and hand
function is usually normal.
 T-6 through T-12 nerves affect abdominal and back muscles. These nerves and
muscles are important for balance and posture, and they help you cough or expel
foreign matter from your airway. Injury usually results in paraplegia. Little or no
voluntary control of bowel or bladder but can manage on their own with special
equipment.
3. Lumbar Spinal Cord Injuries

 Lumbar spinal cord injuries affect the hips and legs. Injuries generally result in
some loss of function in the hips and legs. People with injuries to the lumbar
spinal cord have little or no voluntary control of their bowel or bladder, but can
manage on their own with special equipment
 Individuals may need a wheelchair or walk with braces with this level of spinal
cord injury.
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4. Sacral Spinal Cord Injuries

 Sacral spinal cord injuries affect the hips, back of the thighs, buttocks and pelvic
organs. Injuries generally result in some loss of function in the hips and legs.
There may be little or no voluntary control of bowel or bladder organs, but people
with this injury can manage on their own with special equipment.
 Individuals are most likely able to walk with this level of spinal cord injury.
CLASSIFICATION OF INJURIES
1. PRIMARY INJURY- refers to the destructive forces that directly damage the neural
structures, such as the shear forces tearing an axon or the direct compressive force
occluding a blood vessel, resulting in ischemia.
2. SECONDARY INJURY- refers to a cascade of vascular, cellular, and biochemical

events that occur following the injury, which can worsen a concurrent primary injury.
ASSESSMENT AND DIAGNOSTIC TEST
• Detailed neurologic examination

• Diagnostic x-rays (lateral cervical spine x-rays)- can show vertebrae misalignment
and fractures within minutes of injury.
• CT scanning- can detect bone fractures, bleeding, and spinal stenosis (narrowing of
the spinal canal).
• MRI scan- can show brain and spinal trauma from injury, herniated discs (problems
with the cartilage located between the vertebrae), vascular (blood vessel) irregularities,
bleeding, inflammation that might compress the spine and spinal cord, and injury to
the ligaments that support the cervical spine.
• Continuous electrocardiographic monitoring may be indicated if a cord injury is
suspected since bradycardia (slow heart rate) and asystole (cardiac standstill) are
common in acute spinal injuries.
EMERGENCY MANAGEMENTS
• the patient must be immobilized on a spinal (back) board, with head and neck in a
neutral position, to prevent an incomplete injury. The patient must be referred to a
regional spinal injury or trauma center because of the multidisciplinary personnel and
support services required to counteract the destructive changes that occur in the first
few hours after injury.
• During treatment in the emergency and x-ray departments, the patient is kept on the transfer
board. The patient must always be maintained in an extended position.
• Once the extent of the injury has been determined, the patient may be placed on a rotating
bed or in a cervical collar.
• Later, if SCI and bone instability have been ruled out, the patient can be moved to a
conventional bed or the collar removed without harm. If a rotating bed is needed but not
available, the patient should be placed in a cervical collar and on a firm mattress with a bed
board under it.
Management of Spinal Cord Injuries (Acute Phase)

• The goals of management are to prevent further SCI and to observe for symptoms of
progressive neurologic deficits.
• The patient is resuscitated as necessary, and oxygenation and cardiovascular stability are
maintained.
1. PHARMACOLOGIC THERAPY
In some studies, the administration of high-dose corticosteroids, specifically
methylprednisolone, has been found to improve motor and sensory outcomes at 6 weeks, 6
months, and 1 year if given within 8 hours of injury. In other studies, little improvement
was found. Use of high dose methylprednisolone, a corticosteroid, is accepted as standard
therapy in many countries and remains an established clinical practice in most institutions
in the United States.
2. RESPIRATORY THERAPY
Oxygen is administered to maintain a high arterial PO2 because hypoxemia can create
or worsen a neurologic deficit of the spinal cord.
Spinal cord innervation to the phrenic nerve, which stimulates the diaphragm, is lost.
Diaphragmatic pacing attempts to stimulate the diaphragm to help the patient breathe.
3. SKELETAL FRACTURE REDUCTION AND TRACTION

Requires immobilization and reduction of dislocations (and stabilization of the vertebral
column. Cervical fractures are reduced and the cervical spine is aligned with some form of
skeletal traction, such as skeletal tongs or calipers, or with use of the halo device.
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 Gardner-Wells tongs require no predrilled holes in the

skull.
 Crutchfield and Vinke tongs are inserted through holes
made in the skull with a special drill under local
anesthesia.
- Traction is applied to the tongs by weights, the amount
depending on the size of the patient and the degree of fracture
displacement.
- The traction force is exerted along the longitudinal axis of the
vertebral bodies, with the patient’s neck in a neutral position.
- The traction is then gradually increased by adding more
weights. As the amount of traction is increased, the spaces
between the intervertebral disks widen and the vertebrae
may slip back into position.
- Reduction usually takes place after correct alignment has been restored. Once reduction
is achieved, as verified by cervical spine x-rays and neurologic examination, the
weights are gradually removed until the amount of weight needed to maintain the
alignment is identified.
- A metal frame connects the ring to the chest. Halo devices provide immobilization of
the cervical spine while allowing early ambulation.
- Thoracic and lumbar injuries are usually treated with surgical intervention followed by
immobilization with a fitted brace.
4. SURGICAL MANAGEMENT
a. Cervical spine surgery aims to realign the spine, decompress the neural tissue, and
stabilize the spine with internal fixation (screws, plates, cages)
b. Thoracolumbar spine surgery typically involves spinal decompression, discectomy,

spinal fixation, or spinal cord simulation.
c. Laminectomy is a procedure that removes a part or all of the vertebral bone (lamina) that
were squeezing the spinal cord and nerves.
SIGNS AND SYMPTOMS NURSING CARE

Respiratory: C4 or higher (phrenic nerve) 1. Assess for breathsounds, breathing
- total loss of respiratory function pattern, and chest wall movement.
2. Care of ETT/ tracheostomy.
: Lower C or T spine 3. Incentive spirometry
- hypoventilation or inadequate
respiration
- secretions, atelectasis, pneumonia
Cardiovascular: above T6- SNS 1. Avoid vagal stimulation. (eg. gag

dysfunction- unopposed vagal tone reflex, bearing down)
(VAGUS NERVE- major nerve of 2. Monitor vital signs.
Parasympathetic Nervous System will 3. Administer atropine (counteract the
be overstimulated.) effect of vagus nerve)
4. IV infusion.
S/Sx: decreased heart rate 5. Administer vasopressors.
Peripheral vasodilation 6. Blood transfusion.
- decreased BP
“NEUROGENIC SHOCK” GOAL: SBP= >90 mmHg
MAP= >65 mmHg
Urinary/ GI: 1. IFC insertion.

S/Sx: neurogenic bladder/ bowel 2. DRE/ rectal stimulation, enema,
Urinary retention/ stoof softeners, fibers, increased
constipation/paralytic ileus OFI.
stress ulcers 3. H2 blockers, PPI’s
dysphagia
decreased gastric emptying
NCM 118
Page 20 of 21
Thermoregulation:
- inability to sweat and shiver before 1. Control external temperature.
the level of injury 2. Check body temperature frequently.
Metabolic/Nutrition:
-risk for metabolic alkalosis 1. Monitor lab tests.
- Nutritional support 2. Feeding via NGT.
3. Administer TPN within 24 hours.
Pain:
- nociceptive pain ( muscles/ viscera) 1. Tylenol, Ibuprofen, OPIODS.
(**respiratory depression)
- neuropathic pain (nerves) 2. Gabapentin, Pregabalin

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NORTHWESTERN UNIVERSITY,INC

Laoag City, Ilocos Norte

TRAUMATIC BRAIN INJURY

2. Non-penetrating/ Blunt Injury

1|Unit 2: Emergency Nursing

Criteria Mild Moderate Severe

Structural imaging Normal Normal or Normal or

Alteration of a moment up > 24 hours. Severity based on

Glasgow Coma Scale (best 13-15 9-12 <9

B. According to Pathologic features

on other signs and symptoms, a computed tomography (CT) scan

3|Unit 2: Emergency Nursing

A CT is used to diagnose a skull fracture. If a fracture is found on CT,

4. FOCAL CEREBRAL INJURIES

5|Unit 2: Emergency Nursing

Traumatic intracranial hemorrhage

1. Epidural Hematoma (EDH)

2. Subdural Hematoma (SDH)

Three classes with approximate time intervals are recognized:

b. Subacute: 2 days to about 2 weeks. The clot

c. Chronic: longer than 2 weeks to several

 headache (progressing in severity)

3. Traumatic Subarachnoid Hemorrhage (TSAH)

7|Unit 2: Emergency Nursing

Signs and Symptoms:

4. Intracerebral Hematoma (ICH)

- ICH refers to bleeding into the brain parenchyma

5. Intraventricular Hematoma (IVH)

5. DIFFUSE CEREBRAL INJURIES: Concussions and Diffuse Axonal Injuries

a. Mild concussion - defined as temporary neurological dysfunction without loss of

B. Diffuse Axonal Injury

9|Unit 2: Emergency Nursing

- A grading system based on the distribution of pathologic findings

1. ischemia (insufficient blood flow);

8. biochemical changes (changes in levels of neurotransmitters, sodium, potassium,

PREHOSPITAL MANAGEMENT: Initial management of TBI

Specifically, severe TBI patients should be transported to a trauma center or

EMERGENCY DEPARTMENT OR TRAUMA CENTER MANAGEMENT

• inserting arterial and central lines

NURSING MANAGEMENT OF TRAUMATIC BRAIN INJURY

1. Proper positioning and elevation of the head of bed at 30 degrees.

SPINAL CORD INJURIES

LEVELS OF SPINAL CORD INJURY

1. Cervical Spinal Cord Injuries

2. Thoracic Spinal Cord Injuries

3. Lumbar Spinal Cord Injuries

4. Sacral Spinal Cord Injuries

2. SECONDARY INJURY- refers to a cascade of vascular, cellular, and biochemical

ASSESSMENT AND DIAGNOSTIC TEST

• Detailed neurologic examination

Management of Spinal Cord Injuries (Acute Phase)

3. SKELETAL FRACTURE REDUCTION AND TRACTION

 Gardner-Wells tongs require no predrilled holes in the

b. Thoracolumbar spine surgery typically involves spinal decompression, discectomy,

SIGNS AND SYMPTOMS NURSING CARE

Cardiovascular: above T6- SNS 1. Avoid vagal stimulation. (eg. gag

Urinary/ GI: 1. IFC insertion.

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