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.

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.

1. Observe for changes in vital signs.

2. Keep the client’s 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 client’s LOC at frequent intervals.

7. Provide auditory and tactile stimulation.

f. Support natural defense mechanism. Encourage diet of nutrient-defense foods.

g. Evaluate client’s 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
 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
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?
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?