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HEAD AND BRAIN INJURIES

HEAD AND BRAIN

INJURIES

• injury to the skull or brain that is severe enough to interfere with normal
functioning
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HEAD AND BRAIN INJURIES

The most important consideration in any

head injury is whether or not the brain is
injured.

Closed (blunt) brain injury - occurs when the head accelerates and then rapidly
decelerates or collides with another object and brain tissue is damage but there
is no opening through the skull and dura
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Open brain injury

• occurs when an object penetrates the skull, enters the brain, and
damages the soft brain tissue in its path (penetrating injury); or
• when blunt trauma to the head is so severe that it opens the scalp, skull,
and dura to expose the brain
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TYPES OF HEAD INJURIES

1. Cerebral Concussion- temporary loss of neurologic function with no
apparent structural damage due to jarring of the brain within the skull. With
temporary loss of consciousness from a few seconds to a few minutes

Symptoms
– light: dizziness and spots before the eyes (“seeing stars”), or if
– Severe: complete loss of consciousness for a time
– bizarre irrational behavior-frontal
– temporary amnesia or disorientation- temporal
– postconcussion syndrome- headache, dizziness, lethargy, irritability,
and anxiety, difficulty with memory and disruption in work habits
Treatment
• observe patient for headache, dizziness, lethargy, irritability, and anxiety
(may be hospitalized overnight)
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• resume normal activities slowly

• family is instructed to observe for the following and notify the physician or
if (+):
✓ Difficulty in awakening
✓ Difficulty in speaking
✓ Confusion
✓ Severe headache
✓ Vomiting
✓ Weakness of one side of the body

2. Cerebral Contusion- a more severe bruising type of injury to the brain

may occur with subdural or extradural collections of blood
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Symptoms
• unconscious for more than a few seconds or minutes
• patient lies motionless, with a faint pulse, shallow respirations, and cool,
pale skin
• bowel and bladder incontinence
• may be aroused with effort but soon slips back into unconsciousness
• BP and temp- ↓ similar to that of shock
• pulse, respirations, temperature, and other body functions return to normal
gradually
• residual headache and vertigo are common, and impaired mental function
or seizures may occur as a result of irreparable cerebral damage
❖ full recovery can be delayed for months

3. Diffuse Axonal Injury - involves widespread damage to axons in the

cerebral hemispheres, corpus callosum, and brain stem seen in mild,
moderate, or severe head trauma and results in axonal swelling and
disconnection
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Symptoms
• Severe injury: the patient has no lucid intervals and experiences
immediate, coma, decorticate and decerebrate posturing and global
cerebral edema

(A) Decorticate posturing - involving adduction and flexion of the upper

extremities, internal rotation of the lower extremities, and plantar flexion of the
feet.
(B) Decerebrate posturing - involving extension and outward rotation of upper
extremities and plantar flexion of the feet.

4. Intracranial Hemorrhage - Hematomas (collections of blood) that

develop within the cranial vault and are the most serious brain injuries
• Epidural (above the dura)
– most serious type of hematoma; forms rapidly from arterial bleed
– forms between dura and skull from a tear in the meningeal artery
– extreme surgical emergency
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Symptoms:
• Brief loss of consciousness followed by lucid interval with client awake and
conversant
• LUCID intervals- rapid absorption of CSF and decreased intravascular
volume occur as compensatory mechanism to maintain normal ICP. But
when compensation fails due to small increase in clot, rapid elevation of
ICP➔ increasing restlessness, agitation, confusion
• progresses to coma
• Signs of herniation may appear: deterioration of consciousness, dilation
and fixation of pupils, paralysis of extremity then condition deteriorates
rapidly
INTRACRANIAL PRESSURE
• pressure exerted by the volume of the intracranial contents within

• Monro-Kellie hypothesis states that because of the limited space for

expansion within the skull, an increase in any one of the components
causes a change in the volume of the others
• Because brain tissue has limited space to change, compensation typically
is accomplished by displacing or shifting CSF, increasing the absorption of
CSF, or decreasing cerebral blood volume.
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Pathophysiology: Cerebral Response to Increase ICP

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INCREASED ICP
Clinical Manifestations:
• changes in LOC (early)
• slowed speech and delay in response to verbal suggestions
• abnormal respiratory and vasomotor responses (late)
• restlessness (without apparent cause), confusion, or increasing
drowsiness - has neurologic significance due to compression of the brain
2◦ to swelling from HMG or edema, hematoma or tumor)
• as ICP increases ➔ stuporous and reacts only to loud auditory or painful
stimuli
• * Indicates serious impairment of brain circulation and immediate
intervention is required.
• client slips into a comatose state
• decortication, decerebration, or flaccidity- abnormal motor responses
• profound coma- pupils dilated &fixed, respirations impaired, death is
usually inevitable

ASSESSMENT AND DIAGNOSTIC FINDINGS

1. Ventriculostomy- ventricular catheter monitoring device used for monitoring
ICP
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2. Subarachnoid bolt (or screw) - hollow device inserted through the skull and
dura mater into the cranial subarachnoid space, with the advantage of not
requiring a ventricular puncture.
• The subarachnoid screw is attached to a pressure transducer, and the
output is recorded on an oscilloscope.

3. Epidural monitor- uses a pneumatic flow sensor that functions on a

nonelectrical basis
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4. Fiberoptic monitor or transducer-tipped catheter - reflects pressure

changes, which are converted to electrical signals in an amplifier and displayed
on a digital monitor.
• The catheter can be inserted into the ventricle, subarachnoid space,
subdural space, or brain parenchyma or under a bone flap.
• If inserted into the ventricle, it can also be used as a CSF drainage device.
• Waves of high pressure and troughs of relatively normal pressure-
indicate changes in ICP.
• Waveforms are captured and recorded on an oscilloscope

5. Lumbar puncture- contraindicated in patients with increased ICP.

Sudden release of pressure can cause the brain to herniate.
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Subdural (below the dura)- collection of blood between the dura and the brain
• venous in origin and is due to the rupture of small vessels that bridge the
subdural space

Causes:
1. Trauma- most common cause
2. Coagulopathies
3. Rupture of an aneurysm

CLASSIFICATION:
1. Acute and Subacute Subdural Hematoma
a. ACUTE- associated with major head injury involving contusion or laceration
• Symptoms: develop over 24 to 48 hours.
✓ changes in the level of consciousness (LOC),
✓ pupillary signs
✓ hemiparesis
✓ Coma, increasing BP, decreasing HR, and slowing RR- indicate
rapidly expanding mass requiring immediate intervention
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b. SUBACUTE- the result of less severe contusions and head trauma.

• S/S usually appear between 48 hours and 2 weeks after the injury and
are similar to those of an acute subdural hematoma
2. Chronic Subdural Hematoma- develops from seemingly minor head injuries
which produce enough impact to shift the brain contents abnormally
• most frequently in the elderly secondary to brain atrophy
• onset of symptoms may be lengthy- 3 weeks to months
• bleeding is less profuse and (+) compression of the intracranial contents
• 2 to 4 days after- the blood within the brain changes in character in
becoming thicker and darker
• few weeks after - the clot breaks down with the color and consistency of
motor oil
• calcification or ossification of the clot takes place
• the brain adapts to the invasion, and signs and symptoms fluctuate
Symptoms
• severe headache, which tends to come and go
• alternating focal neurologic signs
• personality changes- patient may be labeled neurotic or psychotic
• mental deterioration
• focal seizures
C. INTRACEREBRAL HEMORRHAGE AND HEMATOMA
• bleeding into the substance of the brain
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Causes:
• head injuries - force is exerted to the head over a small area (stab injury)
• from systemic hypertension- causes degeneration and rupture of a vessel
• rupture of a saccular aneurysm
• vascular anomalies;
• bleeding disorders such as leukemia, hemophilia, aplastic anemia, and
thrombocytopenia
• complications of anticoagulant therapy
• The onset may be insidious, beginning with the development of neurologic
deficits followed by headache.

ASSESSMENT AND DIAGNOSTIC FINDINGS

• Physical and neurologic examinations- evaluate the extent of injury
• CT and MRI- primary neuroimaging diagnostic tools and are useful in
evaluating soft tissue injuries
• Positron emission tomography (PET scan) - method of scanning
examines brain function rather than structure

MEDICAL MANAGEMENT
1. Any individual with a head injury is presumed to have a cervical spine
injury until proven otherwise.
From the scene of the injury:
• Transport on a board
• Head and neck alignment with the axis of the body
• Cervical collar
2. All therapy is directed toward preserving brain homeostasis and
preventing secondary brain injury.
Common causes of secondary injury :
• cerebral edema
• hypotension
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• respiratory depression that may lead to hypoxemia and electrolyte

imbalance
• stabilization of cardiovascular and respiratory function - to maintain
adequate cerebral perfusion, control of hemorrhage and hypovolemia, and
maintenance of optimal blood gas values
3. TREATMENT OF INCREASED ICP - requires aggressive treatment.
• Principle of treatment: maintaining adequate cerebral oxygenation &
prevent secondary injury
1. Surgery
a. evacuation of blood clots
b. debridement
c. elevation of depressed fractures of the skull
d. suture of severe scalp lacerations
NC:
1. Close monitoring of ICP; monitoring devices for ICP or drain CSF inserted
during surgery or at bedside- aseptic technique
2. If (+) increase: maintain adequate oxygenation, elevate the head of the bed,
and maintain normal blood volume.
• The patient is cared for in ICU
Controlling ICP in Severely Brain-Injured Patients
• Elevate the head of bed 30 degrees
• Maintain the patient’s head and neck in neutral alignment (no twisting)
• Initiate measures to prevent the Valsalva maneuver
• Maintain normal body temperature
• Administer O2 to maintain PaO2 > 90 mm Hg
• Maintain fluid balance with normal saline solution
• Avoid noxious stimuli (eg, excessive suctioning, painful procedures)
• Administer sedation to reduce agitation
• Maintain cerebral perfusion pressure > 70 mm Hg
2. Supportive Measures
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• ventilatory support
• seizure prevention
• fluid and electrolyte maintenance
• nutritional support
• pain and anxiety management
• intubation and mechanically ventilation of comatose patients
• antiseizure agents (seizures can cause secondary brain damage from
hypoxia)
• benzodiazepines- to calm agitated patients without decreasing LOC and
increasing ICP
• Insertion of NG tube – reduced gastric motility and reverse peristalsis-
associated with head injury making regurgitation and aspiration common
in the first few hours
3. Brain Death
• assist in the clinical examination for determination of brain death and the
process of organ procurement
• Brain Death Act – This act states that death will be determined with
accepted medical standards and that death will indicate irreversible loss of
all brain function. The patient has no neurologic activity upon clinical
examination
• EEG and cerebral blood flow (CBF) studies- used to confirm brain death
• Most patients are potential organ donors- provide information to the family
and assist with decision making on organ donation

NURSING PROCESS
I. Assessment
1. Elicit information:
• nature of the injury
• patient’s condition immediately after the injury
2. Obtain immediate health history. This should include the following questions:
• When did the injury occur?
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• What caused the injury? A high-velocity missile? An object striking the

head? A fall?
• What was the direction and force of the blow?
3. Determine if there was loss of consciousness and its duration and whether
patient could be aroused.
– indicates a significant degree of brain damage, and since changes
that occur minutes to hours after the initial injury can reflect
recovery or indicate development of secondary brain damage, this
finding might be helpful.
• Rapid and thorough assessment:
– Response to tactile stimuli if unconscious
– Pupillary response to light
– Status of corneal and gag reflexes
– motor function
– Glasgow Coma Scale (GCS)

GLASGOW COMA SCALE

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• 3 (least responsive)
• 8 or < (generally accepted as indicating a severe head injury)
• 15 (most responsive)
- detailed neurologic and systems assessments
• made initially and at frequent intervals throughout the
acute phase of care
• includes eye opening and responsiveness, vital signs,
and motor response reflected in hand strength or
response to painful stimulus

NURSING DIAGNOSIS
• Ineffective airway clearance and impaired gas exchange related to brain
injury
• Ineffective cerebral tissue perfusion related to increased ICP and
decreased CPP
• Deficient fluid volume related to decreased LOC and hormonal dysfunction
• Imbalanced nutrition, less than body requirements, related to metabolic
changes, fluid restriction, and inadequate intake
• Risk for injury (self-directed and directed at others) related to seizures
disorientation, restlessness, or brain damage
• Risk for imbalanced (increased) body temperature related to damaged
temperature-regulating mechanism
• Potential for impaired skin integrity related to bed rest, hemiparesis,
hemiplegia, and immobility
• Disturbed thought processes (deficits in intellectual function,
communication, memory, information processing) related to brain injury
• Potential for disturbed sleep pattern related to brain injury and frequent
neurologic checks
• Potential for compromised family coping related to unresponsiveness of
patient, unpredictability of outcome, prolonged recovery period, and the
patient’s residual physical and emotional deficit
• Deficient knowledge about recovery and the rehabilitation process
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Major Complications
• Decreased cerebral perfusion
• Cerebral edema and herniation
• Impaired oxygenation and ventilation
• Impaired fluid, electrolyte, and nutritional balance
• Risk of post-traumatic seizures

PLANNING AND GOALS

• maintenance of a patent airway
• adequate CPP
• fluid and electrolyte balance
• adequate nutritional status
• prevention of secondary injury
• maintenance of normal body temperature
• maintenance of skin integrity
• improvement of cognitive function
• prevention of sleep deprivation
• effective family coping
• increased knowledge about the rehabilitation process
• absence of complications

NURSING INTERVENTIONS – extensive and diverse

A. MONITORING FOR DECLINING NEUROLOGIC FUNCTION
• Parameters assessed initially and as frequently as the patient’s condition
requires:
1. Level of Consciousness- most sensitive neurologic indication of deterioration
of the patient’s condition
• Glasgow Coma Scale
2. Vital Signs- to assess the intracranial status
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Signs of increasing ICP include:

• ↓ HR, ↑increasing SBP and widening pulse pressure
• ↑ RR , ↓ BP, further ↓ in HR- as brain compression increases
Note: This is an ominous development
• rapid rise in body temp >38°C (100.4°F) - unfavorable because metabolic
demands of brain increases and may indicate brain stem damage
Note: a poor prognostic sign
• Tachycardia and arterial hypotension- indicate bleeding is elsewhere
3. Motor Function
• observe spontaneous movements- to raise and lower the extremities,
and compare the strength and equality of the hand grasp and pedal push
at periodic intervals
• presence or absence of spontaneous movement of each extremity is
noted
• speech and eye signs are assessed
• if the patient has (-) spontaneous movement- responses to painful stimuli
are assessed by applying a central stimulus (pinching the pectoralis major
muscle) to determine the patient’s best response
• Abnormal responses (lack of motor response; extension responses) -
associated with a poorer prognosis
4. Other Neurologic Signs
• Assess size and equality of the pupils and their reaction to light
• (+) Hematoma- unilaterally dilated and poorly responding pupil with
subsequent pressure on the CNIII due to shifting of the brain
• If both pupils become fixed and dilated- overwhelming injury and intrinsic
damage to the upper brain stem and is a poor prognostic sign
Deficits:
• anosmia (lack of sense of smell)
• eye movement abnormalities
• aphasia
• memory deficits
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• post-traumatic seizures or epilepsy

• (+) residual organic psychological deficits (impulsiveness, emotional
lability, uninhibited, aggressive behaviors) - lack insight into their
emotional responses
MAINTAINING THE AIRWAY
• Unconscious- position that facilitates drainage of oral secretions
• Head of the bed elevated to 30̊◦ - decreases intracranial venous pressure
• Establish effective suctioning procedures (coughing and straining-
increase ICP)
• Guard against aspiration and respiratory insufficiency
• Closely monitor ABG values
• Monitor the patient who is receiving mechanical ventilation
• Monitor for pulmonary complications
B. MONITORING FLUID AND ELECTROLYTE BALANCE
• Monitor serum electrolyte levels especially if receiving osmotic diuretics,
those w/ SIADH and those with post-traumatic diabetes insipidus
• Serial studies of blood and urine electrolytes and osmolality- head injuries
may be accompanied by disorders of sodium regulation (Hyponatremia or
Hypernatremia are common)
• Increasing lethargy, confusion, and seizures may be due to electrolyte
imbalance
• Endocrine function is evaluated by monitoring serum electrolytes, blood
glucose values, and intake and output
• A record of daily weights
C. PROMOTING ADEQUATE NUTRITION- Head injury results in metabolic
changes that increase calorie consumption and nitrogen excretion.
• Early initiation of nutritional therapy- improves outcomes in head-injured
patient
• Parenteral nutrition via a central line
• Enteral feedings administered via a nasogastric or nasojejunal feeding
tube
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• If there is (+) CSF rhinorrhea- oral feeding tube should be inserted instead
of nasal tube
• Elevate the head of the bed and aspirate the enteral tube for evidence of
residual feeding before feedings
• Continuous drip infusion or pump
D. PREVENTING INJURY
• patient emerging from a coma - increasingly agitated toward the end of the
day
• Restlessness may be due to:
• Hypoxia
• Fever
• Pain
• Full bladder
• may indicate injury to the brain but may also be a sign that the patient is
regaining consciousness
Agitation may be due to:
• Discomfort from catheters
• Intravenous lines
• Restraints
• Repeated neurologic checks
• Alternatives to restraints must be used whenever possible
• Strategies to prevent injury include the following:
• Ensure adequate oxygenation & assess the bladder
• Use padded side rails or wrap the patient’s hands in mitts.
• Avoid using restraints.
• Avoid using opioids as a means of controlling restlessness ( can cause
respiration depression, constrict the pupils, and alter responsiveness)
• Minimize environmental stimuli - keeping the room quiet,
• Limiting visitors, speaking calmly, and providing frequent orientation
• Provide adequate lighting to prevent visual hallucinations
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• Minimize disruption of the patient’s sleep/wake cycles.

• Lubricate the skin with oil or emollient lotion to prevent irritation
• If incontinence (+), external catheter on a male patient
E. MAINTAINING BODY TEMPERATURE
• Hyperthermia can be due to damage to the hypothalamus, cerebral
irritation from hemorrhage, or infection.
• Monitor temperature every 4 hours.
• Febrile: acetaminophen and cooling blankets as prescribed
• (do not induce shivering- increases ICP)
• If infection is suspected- C&S and antibiotics
F. MAINTAINING SKIN INTEGRITY
• Identify potential areas of breakdown- avoid pressure ulcers
• Assess all body surfaces and document skin integrity at least every 8
hours
• Turn and reposition the patient every 2 hours
• Provide skin care every 4 hours
• Assist patient to get out of bed to a chair three times a day if physically
able