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Nursing Care of Patients with

Neurological Dysfunction
Elaine Harris, RN, MS, CCRN
Care of Adults with High Acuity
Needs

Goals of Nursing Assessment


Gather data about functioning of the nervous
system in an unbiased, orderly manner and
clearly record it
Follow data over time, looking for
correlations and trends
Analyze the data to develop a list of
potential or actual diagnoses
Determine effects of dysfunction on daily
living and ability to perform self-care

Mental Status Assessment


Tests to evaluate level of consciousness
and arousal, orientation to environment
and thought content
LOC is the most critical parameter and
evaluates function of the cerebral
hemisphere
Responsiveness is categorized according
to the patients arousal to external stimuli

Levels of Arousal
Awake---the patient may
sleep more than usual or
be confused when first
awakening
Lethargic---drowsy but
follows simple commands
when stimulated
Obtunded---arousable with
stimuli. Responds verbally
with just one or two words.
Follows simple commands
but otherwise drowsy

Stuporous---very hard to
arouse; inconsistently may
follow commands or speak a
single word with much
stimulation
Semi-Comatose---movements
are purposeful when
stimulated; does not follow
commands or speak
coherently
Comatose---may respond with
reflexive posturing but limited
spontaneous movement

Orientation to Environment
What is your name? Where are you now?
What is the month, year, date, time?
An increase in wrong answers indicates
increasing confusion and possible
deterioration
Increase in correct responses may
indicate improvement

Assessment of Cognitive Ability


Maximum score = 30.

20 or lower = neuro impairment

Assessment of Motor Function

Tests of strength and coordination


What elicits motor response? Words? Pain?
Evaluate the ability to follow commands
Ask patient to move extremity against gravity
Noxious stimuli = eliciting pain by pinching
trapezius muscle, pressure on supraorbital
ridge, sternal rub, or compressing nailbeds

Motor Assessment, continued


Localization means the patient tries to
remove the stimulus in an organized way
Withdrawal means the patient simply
pulls away from the noxious stimuli

Decerebrate Rigidity
Extension, adduction and hyperpronation
of the upper extremities. Extension of
lower extremities with plantar flexion of the
feet. May clinch teeth.
Denotes midbrain or pons injury

Decorticate Rigidity
Flexion of the arms, wrists, fingers
Adduction of upper extremities and
extension of legs. Cerebral hemisphere
injury

Assessment of Strength, Coordination


Pronator Drift
Ask patient to lift legs one at a time
straight off bed against your resistance
Weakness indicates damage to motor
neuron pathways

Motor Strength, Coordination, cont


Hemiparesis (weakness)
Hemiplegia (paralysis)
Remember the cerebellum is responsible
for smooth synchronization, balance, and
ordering of movement.

Assessment of Vital Signs


Temp, HR, BP are considered late findings
in neuro deterioration but respiratory
changes may be seen early
CNS fevers can be very high and are
resistant to antipyretic therapy
Hypotension must be avoided in the postinjury patient because it leads to
decreased cerebral perfusion

Assessment of Respirations
Shallow, rapid respirations can indicate a
problem with maintenance of the airway or
need for suctioning
Snoring or stridor can indicate partially
obstructed airways
Cheyne-Stokes Respirations---crescendodecrescendo alternating with periods of apnea
Hypoventilation must be avoided for
respiratory acidosis occurs.

Other Assessment Areas

Pupil changes (size and shape)


Cranial nerve function
Sensation (perception of being touched)
Proprioception (Which way am I moving your
finger?)
Stereognosis (ability to recognize objects by
touch)
Graphestesia (ability to recognize numbers or
letters traced lightly on the skin)

Signs of Increased Intracranial Pressure

Increased ICP, continued


Manifested by deterioration in all aspects of
neurological functioning
LOC decreases as ICP increases. May begin
with restlessness, confusion, combativeness
and decompensate quickly
Pupil reactions begin to diminish (pupil
ipsilateral to the injury will dilate first)
Motor function declines, may posture
Changes in VS come late

Cushings Triad
A cluster of changes that indicate very
high ICP and impending herniation:
Increased systolic BP (widening pulse
pressure)
Bradycardia (may go into the 30s)
Decreased, irregular respirations

Nursing Care During Diagnostic Studies


Computer Tomography (CT)
Measures density of tissues, blood and bone
Cerebral edema appears less dense and therefore
is lighter in color than normal
Always used quickly in trauma setting, seizures,
headaches, LOC, diagnosis of suspected strokes
Will show skull fractures, tissue swelling,
hematomas, tumors
Patient education: lie still, may have
claustrophobia

Diagnostics, cont
Magnetic Resonance Imaging (MRI)
More detailed images that look like anatomy
Does NOT show bony anomalies as well as
CT
Can interfere with pacemakers, and patients
with surgical clips and prostetic implants
made of ferrous materials cant be scanned
Ventilators, monitors may be problematic

Diagnostics, cont
Cerebral Angiography
Gold standard for evaluating vascular problems
Can reveal large and small aneurysms and AV
malformations
Radiographic catheter is passed through
femoral artery to each of the arterial vessels
bringing blood to the brain and spinal cord
Radiopaque contrast is injected and rapid
images are taken

Diagnostics, cont
Cerebral blood flow studies
Radioisotope is injected IV and the brain is
scanned to determine which areas show
accumulation
Can determine cerebral vasospasms and
brain death (no blood flow)

Head Injuries
Injury to scalp, skull, or brain
Most serious is closed head injury with
traumatic brain injury (TBI))

Head Injury, continued


MVC and falls are the most common causes
Firearms, assaults, sports-related injuries,
recreational injuries, and war-related injuries
High potential for poor outcomes
GCS on arrival at the hospital is a strong
predictor of survival, with GCS below 8
indicating only a 30-70% chance of survival

Skull Fractures
Basilar skull fractures occur when the
base of the skull is injured
Battles Sign (post auricular ecchymosis)
and periorbital ecchymosis (Racoon
eyes) may be seen and indicate a tear in
the dura with leakage of CSF

Skull Fracture, cont


Rhinorrhea (CSF leaking from nose) or Otorrhea
(CSF leaking from ear) confirm torn dura
Risk of meningitis is great
Test fluid to see if it is CSF: glucose test strip
will be positive if it is CSF.
If there is bloody drainage, do halo test: let
drainage drip on a 4X4. Blood will coalesce in
the center and a yellow-ish ring encircles the
blood

Skull Fractures, cont

Concussion
A diffuse injury to the head. May or may
not lose consciousness
Often a brief disruption of LOC and
amnesia regarding the event. Headache,
lethargy can persist up to 2 months

Cerebral Contusion
Bruising of the brain tissue within a focal
area
May contain an area of hemorrhage,
infarction, necrosis and edema
Coup-Contrecoup Injury: brain moves
inside skull due to high energy or high
impact. 2 sources of injury

Epidural Hematoma
Bleeding between the dura and inner surface of
the brain
A neuro emergency! Usually a linear fracture
crossing a major artery in the dura, causing a
tear
Venous epidurals develop slowly, arterial bleeds
quickly
Hemorrhage in epidural space raises ICP
Classic: initial period of unconsciousness at
the scene with a brief lucid interval followed
by decreased LOC

Subdural Hematoma
Bleeding between the dura mater and arachnoid
layer of meninges
Veins that drain from the surface of the brain into
the sagittal sinus are the source for most
subdurals
Acute subdural hematomas develop within 24-48
hours of injury; decreasing LOC and headache
Size of hematoma determines clinical
presentation (Drowsy? Confused? Unconscious?)

Subdural, cont
The ipsilateral pupil dilates and becomes
fixed if ICP is significantly elevated
Chronic, sub-acute hematomas can occur
2-14 days after injury and are common in
older adults (brain atrophy = more space)
Be aware of intoxicated people who come
to ER.they may be acting strange from
ETOH or may have a subdural hematoma

Subdural Hematoma, cont

Emergency Nursing Care for Head


Injuries
Assure patent airway
Assume cervical
spine injury ALWAYS
Immediate CT
Oxygen via nonrebreather or
intubation
IV access with 2 large
bore catheters

Employ all measures


to reduce ICP
(elevate head of bed
30 degrees)
Control external
bleeding with
pressure dressing but
NO firm pressure until
depressed skull
fracture ruled out

Emergency, cont
NO NG TUBE and NO
NT suction in case dura
is torn or sinuses
fractured
Explain need for
frequent VS and neuro
checks
VS every few minutes,
oxygen sats, monitor,
GCS, pupil assessment

Treat N&V promptly


Determine CSF
leak.place loose
pad under nose/ear
Be calm, gentle, firm
if patient is combative
Protect self
Prepare for surgery
(crainiotomy)

Nursing Diagnoses for Head Injuries


Risk for ineffective cerebral tissue
perfusion RT interruption of cerebral blood
flow
Hyperthermia RT increased metabolism,
infection, loss of cerebral integrative
function due to hypothalamic injury
Acute pain

Nursing Goals for Head Injuries

Maintain adequate cerebral oxygenation


Remain normothermic
Achieve pain control
Be free of infection
Attain maximal cognitive, motor, sensory
function

Health Promotion to Prevent Head


Injuries

Seat belts (backseat, too)


Child safety seats
Helmits for motorcycles and bikes
Protective headwear for lumberjacks,
construction workers, miners, horseback riders,
snowboarders

Talk to groups of teenagers!

Increased Intracranial Pressure


Normal ICP is 5-15 mmHg
Increased ICP is life-threatening and results
from an increase in any of the three
components within the skull (brain, blood, CSF)
Increased ICP will decrease cerebral perfusion
pressure and can cause brain ischemia or
infarction
Edema distorts brain tissue, further increasing
ICP

Increased ICP, cont


Goal: To maintain cerebral blood flow
Sustained increases in ICP result in brain
stem compression and herniation of the
brain from the skull into the spinal canal.
This is fatal

Clinical Manifestations of Increased ICP


Change in LOC
Change in vital signs (Cushings Triad)
Cranial Nerve III compression (ipsilateral
pupil change)
Decreased motor function (contralateral to
injury)
Headache
Vomiting

Monitoring ICP

Monitoring ICP
Gold standard is ventriculostomy. Catheter is placed into
the lateral ventricle and attached to an external
transducer
Measures pressure inside ventricle and facilitates
removal of CSF if the ICP gets too high (normally 20-30
ml of CSF is produced every hour)
Transducer is leveled at the TRAGUS of the ear. Must
re-zero transduced any time patients position is changed
Three-way stop-cock opens to allow CSF to drain once
pressure reaches a certain level
ICP should NOT exceed 15 mmHg

Cerebral Perfusion Pressure Calculation


This can only be done if the patient has an
ICP monitor
CPP = MAP ICP
Normal CPP is 60-100. Less than 50 is
associated with ischemia and tissue death
Less than 30 is incompatible with life
Reminder: MAP = (systolic BP diastolic BP)
divided by 3, plus diastolic BP

Monitoring Brain Oxygen Levels


LICOX Brain Tissue Oxygenation Catheter is
placed in healthy, viable white matter of the brain
Normal brain oxygen level (PbtO2) = 20-40.
Lower than 20 = ischemia
This catheter also measures brain temp (cooler
brain temp produces healthier outcomes)

Nursing Management of the Patient


with Increased Intracranial Pressure

ICP Management
Maintain adequate cerebral
perfusion (keep BP up)
Maintain oxygenation (keep
pO2 = 100, pCO2 = 30-35)
Frequent VS, GCS
Mannitol (Osmitrol)
expands blood volume,
dilutes hematocrit and
blood viscosity AND pulls
fluid from cerebral tissue
into blood vessels

Barbiturates (Pentobarb)
reduces cerebral metabolism
causing decreases in ICP
and reduction in cerebral
edema. Drug induced coma
Nutrition within 3 days
Elevate HOB 30 degrees but
be sure there is no neck
flexion
Suction only if necessary,
then only 2 passes with
hyperoxygenation between

ICP management, cont


Quickly treat pain and
anxiety
Keep room dark and quiet
(noise increases rate of
metabolism and raises
ICP)
Monitor combinations of
sedatives, paralytics,
analgesics
PROPOFOL (Diprivan)
often used due to short
half-life

NORCURON (paralytic)
allows complete respiratory
control
I&O, electrolytes
Turn slowly, gently
Avoid hip flexion (increases
intraabdominal pressure
which increases ICP)
Protect from self-injury
Pad side rails
Talk, touch even if in coma

Stroke
Occurs when there is 3rd leading cause of
ischemia to part of the
death behind heart
brain OR hemorrhage
disease and cancer
into the brain
Ischemic strokes
Results in death of
(partial or complete
occlusion of an artery)
brain cells
account for nearly
About 25% of people
80% of strokes
with strokes are
Plaque build-up in
younger than 65
cerebral blood vessels

Hemorrhagic Stroke
(Intracerebral Hemorrhage)
Bleeding within the
brain caused by
rupture of a vessel
Poor prognosis---50% of people did in
first 48 hours
HYPERTENSION is
the most important
cause of intracerebral
hemorrhage

Other causes are


vascular
malformations
(congenital),
coagulation disorders,
anti-coagulant or
thrombolytic therapy,
trauma, ruptured
cerebral aneurysm

Hemorrhagic Stroke, cont


Commonly occurs
during activitysudden
onset of symptoms with
rapid progression over
minutes
Worst headache Ive
ever had, then N&V,
decreasing LOC,
weakness, deviation of
eyes, dilated pupils,
posturing

Subarachnoid
Hemorrhage--intracranial bleeding
into the cerebrospinal
fluid-filled space
between the
arachnoid and pia
mater membranes

Subarachnoid Hemorrhage, cont

Usually caused by rupture of an aneurysm


40% die immediately with no warning
Can happen at any age
Cocaine causes sharp increases in BP
Blood is an irritant to cerebral blood vessels and
causes spasms!
Same signs/symptoms as with a thrombolic stroke
(contralateral side)
Can cause bleeding into ventricle = hydrocephalus

Diagnosis of Cerebral Bleeding


Non-contrast CT is done STAT for any sign of
stroke
If an ischemic stroke, tPA (or streptokinase)
may be given
MRI will later show the extent of brain injury
Angiogram shows malformation of vessels
and can show the exact site of the
subarachnoid hemorrhage
Lumber puncture shows blood in CSF

Nursing Care for Patients with Cerebral


Bleeding

Anticoagulants of any kind are contraindicated


Manage hypertension
Seizure precautions
Prepare for immediate surgery is there is an aneurysm
Manage elevated ICP
Calcium channel blocker Nimodipine---decreases
vasospasm of cerebral arteries. Restricts influx of
calcium ions into cells by reducing the number of open
calcium channels. **HOLD if HR below 60 or BP
below 90/

Surgical Repair of Aneurysms


Can surgically clip the weakened area of
the artery
Coiling is most commonly done---insert a
metal coil into lumen of aneurysm via
interventional neuroradiology. Coils
prevent blood pulsation within the
aneurysm and eventually a thrombus forms
within the aneurysm and it becomes sealed
off

Clipping and Coiling Aneurysms

Spinal Cord Injury (SCI)


Young adult men 16-30 are at greatest risk
Causes: MVC = 42%; falls = 27%;
violence = 15%; sports injuries = 7%
Spinal cord is wrapped in tough layers of
dura and is rarely torn or transected by
direct trauma (unless GSW or stab).
Most often cord compression is made by
bone displacement

Mechanisms of Injury

Flexion or hyperextension
Flexion-rotation
Extension-rotation
Compression

Post-Injury Edema
Edema occurs by 24 hours after the initial
injury
Harmful because of lack of space for
tissue expansion, so more cord
compression occurs
Edema occurs above and below the injury
Extent of injury and prognosis for recovery
cannot be determined for at least 72 hours

Neurogenic Shock
Loss of vasomotor tone caused by the injury
Hypotension and bradycardia occur
Loss of sympathetic nervous system
innervation causes peripheral vasodilation,
venous pooling and decreased cardiac output
Most often occurs with cervical or high
thoracic injury (T-6 or higher)
Warm, dry skin BELOW the level of injury

Level of Injury
Cervical, thoracic, or lumbar
Cervical and lumbar injuries are most common
because these levels of the spine have the
greatest flexibility and movement
Cervical spine injury will cause paralysis of all 4
extremities (tetraplegia)
If low in the cervical spine, the arms are rarely
completely paralyzed
Thoracic or lumbar injuries cause paraplegia (loss
of sensation and paralysis of the legs)

Degree of Injury
Complete cord involvement results in total loss of
sensory and motor function below the level of injury
Incomplete involvement results in a mixed loss of
voluntary motor activity and sensation (some tracts
are intact)
Brown-Sequard Syndrome: damage to of the
cord. Loss of motor function and vasomotor
paralysis on the ipsilateral side. The contralateral
side has loss of pain and temp sensation. Most
common with penetrating trauma

Nursing CareRespiratory
Degree of involvement corresponds to level
of injury
C-4 or above causes total loss of respiratory
muscle function, so mechanical ventilation is
reuired
Lower cervical and thoracic injuries paralyze
abdominal muscles and intercostal muscles
(poor cough, atelectasis and pneumonia)
**Airway always first priority of care!

Cardiovascular Care
Any injury above T-6 influences
sympathetic nervous system regulation
Bradycardia is common as well as
peripheral vasodilation
Cardiac monitoring, Atropine to increase
heart rate if symptomatic
IV fluids, vasopressors (Dopamine) to
support BP

Urinary Care
Neurogenic bladder and urinary retention are
common
Bladder is atonic due to lack of nerve
innovation. It becomes overdistended
Foley, strict I&O in early stage
Once acute phase is over, remove indwelling
catheter and do intermittent cath to maintain
bladder tone
Condom cath if urine can be released

GI System Care

Injuries T-5 or higher cause hypomotility


Paralytic ileus and gastric distention are common
NG is placed early to relieve distention
Reglan may help encourage gastric emptying
Prevent stress ulcers (H2 blockers, proton pump inhibitors
Neurogenic bowel if injury is to T-12 or above: bowel is
areflexic and anal sphincter tone is absent
Bowel program: high fiber diet, adequate fluids, Dulcolax
suppository followed 30 minutes later with digital rectal
stimulation to cause bowel elimination
Stool softeners every day

Skin Care
Prevent skin breakdown with frequent
position change (LOGROLL!)
Weight gain or weight loss can contribute
to breakdown
Visual and tactile exam of skin every 12
hours

Thermoregulation
Poikilothermism---ability to maintain
normal body temperature
Interruption of the sympathetic nervous
system prevents peripheral temp sensations
from reaching hypothalamus
Inability to shiver or sweat below the level of
injury
Maintain heat/cool with warming or cooling
blankets, appropriate clothing

Deep Venous Thrombosis Prevention


Very common in first 3 months to get a DVT
People will not have pain or tenderness in
the legs
Pulmonary embolus is the leading cause of
death after initial injury
DVT prevention with Lovenox, sequential
compression devices, position changes,
ROM

Sexuality
Knowledge of the level and completeness
of the injury is needed to understand male
patients potential for orgasm, erection,
and fertility
Women with SCI remain fertile and can
have successful pregnancies

High Dose Steroids After Injury?


This is still protocol, but has been
questioned lately
Was thought to decrease edema in the
cord and improve function
Stay tuned to the EBP regarding this
important issue

Autonomic Dysreflexia
Patients with injuries T-6 or higher may
develop Autonomic Dysreflexia
A massive uncompensated CV reaction
mediated by the sympathetic nervous
system
Occurs in response to VISCERAL
STIMULATION

Autonomic Dysreflexia, cont


Receptors below the level of injury are stimulated
They respond with reflex arterial vasoconstriction
BUT the parasympathetic nervous system is
unable to directly counteract these responses via
the spinal cord
Baro-receptors in the carotid sinus and the aorta
sense hypertension and stimulate the
parasympathetic nervous system to decrease
heart rate
BP critically high, heart rate critically low

Symptoms of Autonomic Dysreflexia

BP 300/
Throbbing headache
Marked diaphoresis ABOVE the level of lesion
Bradycardia (30-40/minute)
Piloerection (erection of body hairs)
Flushed skin above the level of injury
Blurred vision, nasal congestion, anxiety, nausea
Can lead to status epilepticus, stroke, MI, death
Most common precipitating cause is a distended
bladder or rectum

Nursing Care for Autonomic Dysreflexia


Always measure BP immediately if patient has a
headache
Elevate head of bed 45 degrees or sit patient up
Notify MD
Search for cause (bladder? Rectum?)
Insert cath or do rectal stimulation with Lidocaine jelly to
prevent stimulation
If cath already in place, check for kinks or plugs
Remove skin stimuli, such as constricted clothing or tight
shoes
Vasodilators to lower BP

Grief and Depression

Grief and Depression


People with spinal cord injuries may feel overwhelming
loss
Loss of control over everyday life activities and must
depend on others for daily care
May believe they are useless and burdens to their families
Grief is a difficult, life-long process
Goal is for adjustment to occur.the ability to go on with
living with certain limitations
Families need grief care as well to avoid guilt and
misplaced sympathy
Support groups are very important

Brain Death

Brain Death
Irreversible end of all brain activity including the
brainstem
Due to total necrosis of cerebral neurons
following loss of oxygenation
A medical diagnosis and a legal term for patients
whose hearts continue to beat and who are
maintained on mechanical ventilation in the ICU
Occurs when the cerebral cortex stops
functioning or is irreversibly destroyed

Brain Death Criteria

Coma and unresponsiveness


Absence of brainstem reflexes
Apnea
***This means no response to anything, including
deep pain, cranial nerves, response to carbon
dioxide levels
Diagnosis made by physician
Cerebral perfusion studies and flat EEG may help
families come to terms with brain death, but not
required

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