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HEAD TRAUMA
DEFINITION
Head trauma may be defines as any injury to the scalp, skull or brain.
ETIOLOGY
Motor vehicle accidents are the foremost cause of head injuries. Other causes are
assaults, falls and accidents.
MECHANISMS OF INJURY
a. Acceleration- occurs when the immobile head is struck by a moving object.
b. Deceleration- if the head is moving and hits an immobile object
c. Deformation- refers to injuries in which the force results in deformation and
disruption of the integrity of the impacted body part (e.g., skull fracture).
RISK FACTORS
The major factor contributing to the occurrence of head injury is alcohol
consumption. Primary prevention centers on the education of clients of all ages.
Secondary prevention is not an issue in head trauma because other health conditions do
not increase the incidence of head trauma. Tertiary prevention focuses on preventing or
minimizing the complications of head trauma.
PATHOPHYSIOLOGY
a. Linear Skull Fractures- thin lines radiographically and do not require treatment.
b. Depressed Skull Fractures- may be associated with bone fragments penetrating
into brain tissue.
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c. Basilar Skull fractures- occurs in bones over the base of the frontal and temporal
lobes. They are rarely seen radiographically.
d. Concussions- is a head trauma that may result in loss of consciousness for 5
minutes or less. There is no break in the skull or dura.
e. Contusions- cause more extensive damage. It damages the brain substance itself,
causing multiple areas of petichial and punctuate hemorrhage and bruised areas.
SIGNS AND SYMPTOMS
a. Subjective- Lethargy and indifference to surroundings
b. Objective- signs of increased ICP, lack of orientation to time and place,
paresthesia, labored respirations, (+) Babinski sign, coma and dilatation and
fixation of pupils
PHARMACOLOGIC MANAGEMENT
a. Antiseizure medication- such as phenytoin
b. Histamine antagonist- such as cimetidine are given to reduce the risk of stress
ulcer.
c. Mild analgesics and antibiotics may be prescribed.
d. Osmotic diuretics may be required to reduce ICP.
NURSING MANAGEMENT
a. Observe for s/s of increased ICP. Institute neural checks every 15 minutes for
several hours.
b. Maintain airway.
c. Perform neurological assessment. Use Glasgow Coma Scale
d. Institute seizure precautions, administer anticonvulsants if ordered.
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e. Provide care for the unconscious client
1. Observe for changes in vital signs.
2. Keep the clients head slightly elevated to reduce venous pressure w/in
cranial cavity.
3. Provide frequent oral hygiene.
4. Position the client to prevent pressure areas from forming decubiti.
5. Maintain adequate fluid balance.
6. Evaluate the clients LOC at frequent intervals.
7. Provide auditory and tactile stimulation.
f. Support natural defense mechanism. Encourage diet of nutrient-defense foods.
g. Evaluate clients response from time to time.
SPINAL CORD INJURY
DEFINITON
Injury to the spinal cord can range in severity from mild flexion-extension
whiplash injuries to complete transection of the cord with quadriplegia. Trauma to the
cord can occur at any level but most commonly occurs in the cervical and lower thoracic-
upper lumbar vertebrae.
ETIOLOGY
Trauma is the most common cause of spinal cord injury. Traumatic injury may be
due to automobile or motorcycle accidents, gunshot or knife wounds, falls, or sporting
mishaps.
RISK FACTORS
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The feeling of immortality often held by adolescents and young adults contributes
strongly to their risk for spinal cord injury. Primary prevention centers on public
education. Secondary prevention involves preventing further damage to an already
compromised spinal cord. Minimizing the complications of spinal cord injury is the goal
of tertiary prevention.
PATHOPHYSIOLOGY
Spinal cord injuries most often occur as a result of injury to the vertebrae. The
cord is injured due to various forces applied to the spine. The forces injure the p\spinal
cord by compressing, pulling, or tearing the tissues. The most common sites of injury are
at the C1 to C2, C4 to C6 and T11 to L2 vertebrae. These segments of the spine are the
most mobile and thereby injured more easily.
MECHANISM OF INJURY
a. Flexion-Rotation, Dislocation, or Fracture Dislocation- this form of injury
ruptures supporting ligaments, fractures the vertebrae, damages blood vessels and
leads to ischemia of the spinal cord
b. Hyperextension- this type of injury stretches the spinal cord against the ligament
flava and can lead to dorsal column contusion and posterior dislocation of the
vertebrae.
c. Compression- often caused by falls or jumps in which the individual lands on the
feet or buttocks. The force of impact fractures the vertebrae and they compress the
cord.
CLINICAL MANIFESTATIONS
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The initial clinical manifestations of acute spinal cord injury depend on the level and
extent of injury to the cord. Below the level of injury or lesion, there is loss of:
a. Voluntary movement
b. Sensation of pain, temperature, pressure and proprioception
c. Bowel and bladder function
d. Spinal and autonomic reflexes
DIAGNOSTIC ASSESSMENT
a. Cross-table lateral x-ray
b. CT Scan
c. Peritoneal lavage may be performed for acutely quadriplegic or paraplegic clients
with multiple injuries to rule out intra-abdominal hemorrhage.
PHARMACOLOGIC MANAGEMENT
a. Vasoactive agents (methylprednisolone) are commonly used to support blood
pressure immediately after injury.
b. Long-term pharmacologic management may include urinary anti-infectves,
anticoagulants, laxatives and antispasmotics.
NURSING MANAGEMENT
The most important questions regarding spinal cord injured clients are the ff:
a. Is the client hemodynamically stable? Are vasopressor required to maintain
adequate blood pressure? Is circulation adequate, as evidenced by palpable
peripheral pulses and appropriate skin, nailbed and mucous membrane color?
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b. Is respiration adequate? Are accessory muscles being used for respiration? Is the
client exhibiting diaphragmatic breathing or nostril flaring? Does the client
complain of shortness of breath?
c. Are pupil responses, corneal responses and eye movements normal? At what
spinal cord level is sensation diminished or lost? At what level is motor function
diminished or lost? Is there any voluntary movement? Are normal reflexes, e.g.,
deep tendon, bulbocavernosus and anal reflexes absent? Is the client incontinent?
Are there bowel sounds? Is the abdomen distended? Is the client edematous? Is
the skin intact?