NEUROLOGICAL
ALTERATIONS
NUR 203
Module C
Terms
• Define Terms associated with neurological
alterations:
– Headaches• Tension, migraines, cluster
– Tumors – benign, cancerous
– Infections-meningitis, encephalitis
– Head injury – contusions, concussions,
fractures, intracranial hemorrhage
Terms (cont)
• Transient ischemic attacks
• Cerebrovascular accidents
– Thrombotic
– Hemorrhagic
– Embolic
• Spinal Cord dysfunctions
– Spinal cord injuries
– Herniated disc
Terms
• Spinal Cord dysfunctions
– Spinal Shock
• Paralysis
– Quadriplegic (tetraplegia)
– Paraplegic
• Autonomic Dysreflexia
• Spasticity
• Neurogenic bladder/bowel
Terms
• Spinal Cord dysfunctions
– Respiratory
– Sexual
– Infection
• Neuromuscular dysfunction
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Multiple Sclerosis
Parkinson’s
Guillian-Barre
Amyotrophic Lateral Sclerosis
Neuromuscular Dysfunctions
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Myasthenia Gravis
Trigeminal Neuralgia
Bell’s Palsy
Muscular Dystrophy
Cerebral Palsy
Neural tube defects
VASCULAR HEADACHES
• Tension Headache
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Results from muscle contraction
Tight, band-like discomfort that is unrelenting
Pain builds slowly in severity
Triggered by fatigue and stress
Diagnosis confirmed when they occur more
than 15 days a month
• Treatment:
– Stress reduction techniques (bio-feedback,
psychotherapy and other methods of stress
reduction). Also, correction of poor posture.
Cluster Headaches
(sometimes classified as a form of
migraine)
• Cyclical pattern of periorbital pain lasting
form 4 – 8 weeks and usually occurring in
the spring or fall
– Headache lasts from 15 minutes to hours and
may occur several times a day and may awaken
from sleep. Unilateral in nature.
• Pain is described as deep, boring, intense
pain of such severity that the patient has
trouble staying still.
• May develop Horner’s syndrome
– Constricted pupils
– Unilateral lacrimation
– Rhinorrhea
• Triggered by consumption of alcohol
• Treated with 100% oxygen via mask
• Intranasal Lidocaine may be used
Migraine Headache
– Typically a “true vascular headache”
– Pain results from vasospasm and ischemia of
intracranial vessels.
– Unilateral pain, but may alternate sides
– Throbbing, pulsatile pain
– Photophobia, phonophobia, anorexia, nausea,
vomiting and focal neurogenic signs may be
present
– Aura may precede the event –scintillating
scotoma (flashing lights), euphoria, fatigue,
yawning, and/or craving for sweets
– Can be triggered by relief of intense stress,
missing meals, or tyramine rich foods
– Patient tries to find relief in a quiet, dark
environment
– Treatment: avoid precipitating factors
– Meds: propranolol, amitriptyline, valporate,
verapamil, phenelzine and methysergide taken
daily
• If medical treatment is sought at the time of
the event:
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Ergotamine
Dihydroergotamine
Sumatriptan
Chlorpromazine
Prochlorperazine
• Patient teaching for migraines:
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Identify triggers
Avoid alcohol
Avoid tyramine rich foods
Avoid low blood sugars
Reduce stress
INFECTIOUS /
INFLAMMATORY
DISORDERS
MENINGITIS
• Inflammation of the meninges of the brain
and spinal cord
– Bacterial
– Aseptic (other infective agents—usually viral)
CLINICAL MANIFESTATIONS
• Classic symptoms:
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Nuchal rigidity
Brudzinski’s sign
Kernig’s sign
Photophobia
• Other: fever, tachycardia, h/a, prostration, chills,
nausea, vomiting
• May be irritable at first with progression to
confusion, stupor, and semiconsciousness
• Seizures may occur
• Petechial or hemorrhagic rash may develop
• CSF is cloudy with bacterial
BRUDZINSKI’S SIGN
KERNIG’S SIGN
DIAGNOSIS
• Lumbar puncture:
– Bacterial: increased protein, decreased glucose,
cloudy, increased leukocytes
– Viral: increased protein, normal glucose, clear,
increased lymphocytes
• May culture other areas: blood, wounds,
sinuses, etc.
TREATMENT
• Isolate until results of CSF analysis are
obtained.
– Bacterial is very contagious
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ABX
Anticonvulsants
Fluid and electrolyte replacement
Monitor for increased ICP
Provide quiet environment
Analgesics may be avoided if they have CNS
depressant actions—will mask CNS changes
ENCEPHALITIS
• Inflammation of the parenchyma of the
brain and spinal cord. Usually caused by a
virus.
– Arbovirus encephalitis (transmitted by ticks and
mosquitoes)
– Herpes simplex virus encephalitis may occur as
a complication of measles, chickenpox, or
mumps.
CLINICAL MANIFESTATIONS
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Fever
Headache
Seizures
Nuchal rigidity
Altered LOC
Disorientation
Agitation
Restlessness or lethargy
Drowsiness
Photophobia
N/V
BRAIN ABSCESS
• A collection of either encapsulated or free
pus within brain tissue arising from a
primary focus elsewhere (ear, mastoid
process, sinuses, heart, distal bones, lungs,
bacteremia, etc).
MANIFESTATIONS
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Headache
Lethargy
Drowsiness
Confusion
Depressed mental status
Symptoms of infection
– Fever
– Chills
Traumatic Brain Injuries
• Over 2 million traumatic brain injuries occur each
year with approximately 500,000 injuries severe
enough to cause hospitalization.
• Approximately 50% of all trauma deaths
associated with head injury
• More than 60% of all vehicular trauma deaths are
a result of heat injury
Traumatic Brain Injury -Mechanism
of Injury
• Penetrating trauma
• Blunt trauma
– Acceleration
– Deceleration
– Rotational forces
Traumatic brain Injury – Patho
• Primary injury
• Secondary injury
• Goals of care include efforts to reduce morbidity &
mortality from primary & secondary injuries
Traumatic Brain Injury –
Patho. – Primary Injury
• Occurs at moment of impact
• May be mild or severe
• Types of primary injuries:
– Contusion, laceration, shearing injuries, and hemorrhage
Traumatic Brain Injury –
Patho. – Secondary Injury
• The biochemical & cellular response to the initial
trauma
– Can exacerbate the primary injury & cause loss of brain
tissue not originally damaged
• Ischemia is the primary culprit in secondary brain
injury
Traumatic Brain Injury - Patho –
Secondary Injury (cont.)
• Hypercapnia is a powerful vasodilator
– Results in cerebral vasodilatation & increased cerebral
blood volume & ICP
• Significant hypotension causes inadequate perfusion
to neural tissue
– *Not typical to be hypotensive with TBI
– If hypotensive, need to rule out internal injuries
Traumatic Brain Injury - Patho –
Secondary Injury (cont.)
• Cerebral edema
• Initial hypertension with severe TBI is common
• Must control HTN to prevent secondary injury
caused by increased ICP
• Effects of increases in intracranial pressure may be
varied.
BRAIN INJURY –
CEREBRAL HEMATOMAS
• Extravasation of blood produces a spaceoccupying lesion on the brain and leads to
increased ICP
• Epidural & subdural
– Extraparenchymal (outside of brain tissue)
• Produce injury by pressure effect and displacement
of intracranial contents.
Epidural Hematoma
• A collection of blood between the inner table of the
skull & the outermost layer of the dura
• Most often associated with:
– Skull fractures
– Middle meningeal artery laceration
Epidural Hematoma
• Incidence relatively low
• Can occur as a result of low-impact injuries (falls)
or high-impact injuries (MVAs)
• Occurs from trauma to the skull & meninges rather
than from the acceleration-deceleration forces seen
in other types of head trauma
Epidural Hematoma (cont.)
• Clinical manifestations:
– Brief loss of consciousness followed by period of lucidity
– This lucid period is followed by a rapid deterioration in
LOC
– Dilated, fixed pupil on the same side as the impact area is
a hallmark of EDH
– May c/o severe, localized H/A & may be sleepy
Epidural Hematoma (cont.)
• Diagnosis:
– Based on clinical symptoms &
– evidence of a collection of epidural blood identified on
CT scan
• Treatment:
– Involves surgical intervention to remove the blood and to
cauterize the bleeding vessels
Subdural Hematoma
• The accumulation of blood between the dura and
underlying arachnoid membrane.
• Most often is related to a rupture in the bridging
veins between the brain and the dura.
• Acceleration-deceleration & rotational forces are
the major causes.
• Often associated with cerebral contusions &
intracerebral hemorrhage
Subdural Hematoma (cont.)
• Three types:
– Acute,
– subacute, and
– chronic
• Based on the time frame from injury to clinical
symptoms:
Subdural Hematoma - ACUTE
• Hematoma that occurs after a severe blow to the
head.
• Clinical presentation determined by
– the severity of injury to the underlying brain at the time
of impact &
– the rate of blood accumulation in the subdural space.
Subdural Hematoma – ACUTE
• Observe for deterioration in level of
consciousness or lateralizing signs,
– such as inequality of pupils or motor movements.
• Deterioration may be rapid
• Surgical intervention may include
– craniectomy,
– craniotomy, or
– burr hole evacuation
Subdural Hematoma -SUBACUTE
• Develop symptomatically 2 days to 2 weeks after
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trauma.
Expansion of the hematoma occurs at a rate slower
than that in acute SDH.
Takes longer for symptoms to become obvious.
Clinical deterioration with subacute SDH usually is
slower than that with acute SDH
Surgical intervention, when appropriate, is the same
Subdural Hematoma – CHRONIC
• This term is used when symptoms appear days or
months after injury.
• Most patients usually are elderly or in late middle
age.
• Patients at risk include:
– Patients with coordination/balance disturbances,
– Elderly,
– Those receiving anticoagulation therapy
Subdural Hematoma –CHRONIC
• Clinical manifestations are insidious
• Patient may report a variety of symptoms:
– Lethargy, absent-mindedness, headache, vomiting, stiff
neck, and photophobia, and show signs of TIA, seizures,
pupillary changes, or hemiparesis
• Often not seen as initial diagnosis
• CT scan can confirm diagnosis of SDH
Subdural Hematoma – CHRONIC
• If surgical intervention required, evacuation of the
chronic SDH may occur by:
– Craniotomy, burr holes, or catheter drainage
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Outcome variable
Return of neurologic status variable
Recovery slow
Recurrence frequent
Subarachnoid Hemorrhage (SAH)
• Described as bleeding into the subarachnoid space
• Usually caused by rupture of a cerebral aneurysm or
arteriovenous malformation (AVM).
• Accounts for 6% to 7% of all strokes
– Non-traumatic SAH affects more than 30,000 people in
US each year
– Incidence > in women & increases with age
Subarachnoid Hemorrhage
(cont.)
• Overall mortality rate is 25% with most patients
dying on first day after injury.
• Approximately 2 million people in the US are
believed to have an unruptured cerebral aneurysm,
the congenital anomaly responsible for most cases of
SAH.
Subarachnoid hemorrhage (cont.)
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•
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Known risk factors include:
**Hypertension,
Smoking,
Alcohol use, and
Stimulant use
SAH – Patho
• Pathophysiology of two most common causes is
distinctly different:
– Cerebral Aneurysm
– Arteriovenous (AV)Malformation
SAH – CEREBRAL ANEURYSM
• As individual with a congenital cerebral aneurysm
matures,
– BP rises &
– more stress placed on vessel wall
• Saccular or berry-like & most occur at the
bifurcation of blood vessels
SAH – CEREBRAL ANEURYSM
• Vessel wall becomes thin & ruptures,
– Sending arterial blood at a high pressure into the
subarachnoid space.
• In other situations, the unruptured aneurysm
expands and
– places pressure on surrounding structures.
SAH – ARTERIOVENOUS
MALFORMATION
• Pathologic features related to the size & location of
the malformation.
• One or more cerebral arteries, known as “feeders”
feed an AVM
• Feeder arteries enlarge and increase the volume of
blood shunted through the malformation.
• Large, dilated, tortuous draining veins develop
SAH –ARTERIOVENOUS
MALFORMATION
• The enlarged veins rupture easily
• Cerebral atrophy is sometimes also present.
– It is the result of chronic ischemia because of the
shunting of blood through the AVM and away from
normal cerebral circulation
SAH – ASSESSMENT
• Characteristically has an abrupt onset of pain,
described as the “worst headache of my life.”
• Brief loss of consciousness, nausea, vomiting,
focal neurologic deficits, and a stiff neck may
accompany the headache.
• The SAH may result in coma or death.
SAH – ASSESSMENT
• May have “warning leaks” which go undetected.
• Symptoms of unruptured AVM may be found in the
history
– Headaches with dizziness or
– Syncope or
– Fleeting neurologic deficits
SAH - DIAGNOSIS
• Based on:
– Clinical presentation,
– CT scan,
• **Noncontrast CT is the cornerstone of definitive SAH
diagnosis
– Lumbar puncture
SAH – DIAGNOSIS (cont.)
• CT
– In 92% of cases, CT can demonstrate a clot in the
subarachnoid space, if performed within 24 hours of the
onset of the hemorrhage
• Lumbar puncture if initial CT negative
– CSF after SAH bloody in appearance with a RBC >
1000/mm3.
SAH – Cerebral Angiography
• Cerebral angiography necessary once SAH has been
documented
– To identify exact cause of the SAH
• If a cerebral aneurysm rupture is the cause,
– angiography essential for identifying exact location of
aneurysm in prep. for surgery.
• If AVM rupture the cause,
– angiography necessary to identify the feeding arteries &
draining veins
SAH – Medical Management
• Is a medical emergency!
• Preservation of neurologic function is the goal
• Initial treatment must always support vital
functions
• Early diagnosis is essential
• Ventriculostomy is performed to control ICP if
the patient’s LOC is depressed.
SAH – Medical Management
• Factors attributing to deaths:
• 19% - related to direct effects of the initial
hemorrhage
• 22% - rebleeding
• 23% - cerebral vasospasm
• 23% – non-neurologic medical complications
SAH – Re-bleeding
• The occurrence of a second SAH in an unsecured
aneurysm
• With conservative therapy, 20 – 30% likelihood of
re-bleeding in first month, with highest occurrence
on first day after initial bleed
• Mortality with aneurysmal re-bleeding is 48% to
78%
SAH – Rebleeding
CONS. MEASURES FOR PREV
• BP control:
– Maintain SBP no greater than 150 mm Hg
(individualized based on previous values):
– Nitroprusside, metoprolol, Hydralazine
– *Rebleeding more associated with variations in BP
• Prophylactic anticonvulsant therapy
SAH – Rebleeding –
Surgical Aneurysm Clipping
• Definitive treatment is surgical clipping
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w/complete obliteration of aneurysm.
Timing is key issue
Usually within first 48 hours of rupture
Eliminates risk of rebleeding
Allows more aggressive therapy post-op
Allows for flushing out excess blood & clots to
reduce risk of vasospasm
SAH – Rebleeding –
Surgical Aneurysm Clipping
• Classification of Subarachnoid Hemorrhage
• Early surgery recommended for patients with Grade
I or Grade II SAH & some patients with Grade III
• Careful consideration of patient’s clinical situation
is necessary in determining if candidate for surgery
& optimal time
SAH - Rebleeding
• Surgical procedure involves a craniotomy
• Requires skill of an experienced neurosurgeon
• Complications
SAH – Rebleeding
Surgical AVM Excision
• Decision for surgical excision depends on the
location & size of the AVM
• Surgical excision of large AVMs includes risk of
reperfusion bleeding
• Postop – low BP maintained to prevent further
reperfusion bleeding
• In large AVMs, 2 – 4 stages of surgery may be
required over 6 to 12 months
SAH – Rebleeding Embolization
• Used to secure a cerebral aneurysm or AVM that is
surgically inaccessible because of size, location, or
medical instability of the patient.
• Several techniques available – All use a
percutaneous transfemoral approach in a manner
similar to an angiogram
SAH – Rebleeding
Pharmacologic Therapy
• In the Past,
– antifibrinolytic agents were suggested (aminocaproic
acid)
• TODAY,
– Antifibrinolytic agents are NOT recommended for
routine use in SAH
SAH –
CEREBRAL VASOSPASM
• Presence or absence of cerebral vasospasm
significantly affects the outcome of aneurysmal
SAH
• Estimated that 50% of all SAH patients develop
vasospasm
– 32% resulting in symptomatic vasospasm &
– 15% - 20% result in ischemic stroke or death
SAH –
CEREBRAL VASOSPASM
• Onset usually 3 – 5 days after initial bleed & can
last for 3 to 4 weeks.
• Treatment:
– Induced hypertensive, hypervolemic, hemodilution
therapy
– Oral nimodipine; and
– Transluminal cerebral angioplasty
TRANSIENT ISCHEMIC
ATTACKS (TIA)
• Sudden, brief episodes of neurologic
dysfunction caused by temporary, focal
cerebral ischemia
• Lasts less than 24 hours, often as little as 5
– 20 minutes
• Warning sign of impending CVA
CLINICAL MANIFESTATIONS
• Carotid artery occlusion: weakness or
numbness in an arm or leg, aphasia, and
visual field cuts
• Vertebrobasilar circulation: vertigo,
diplopia, dysphagia, dysarthria, and ataxia
DIAGNOSIS
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Carotid bruit
CT
Doppler
Cerebral angiogram
ECG (looking for A fib if site of emboli
formation
• TEE (looking for site of emboli formation)
TREATMENT
• Antihypertensives
• Antiplatelet drugs
• Surgery
CEREBROVASCULAR ACCIDENT
(CVA OR STROKE)
• Neurological deficits occur as a result of
decreased blood flow to a localized area of the
brain.
• Risk factors:
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Hypertension
Diabetes Mellitus
CV disease, a-fib
Hyperlipidemia
Cigarette smoking, alcohol consumption, cocaine use
Obesity
ISCHEMIC CVA
• Occurs when blood supply to a part of the
brain is interrupted or occluded. Causes:
– Spasm: caused by irritation
– Thrombosis: platelets adhere to irregular
plaque surfaces
– Embolism: traveling clot which becomes
lodged in a narrow lumen
HEMORRHAGIC CVA
• Occurs in only 10 % of cases, usually
women
• Results from rupture of a cerebral blood
vessel that results in bleeding into the brain
tissue or the subarachnoid space
CLINICAL MANIFESTATIONS
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H/A
Vomiting
Seizures
AMS
Fever
ECG changes
Manifestations related to area of injury
• Motor deficits:
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Hemiplegia
Hemiparesis
Flaccidity
Spasticity
Rigidity
Dysphagia
• Elimination disorders
– Bowel
– bladder
• Sensory perceptual deficits
– Hemianopia
– Agnosia
– Apraxia
• Language disorders
– Aphasia
– Dysarthria
• Cognitive and behavioral changes
• Intellectual: memory and judgment changes
• Right sided CVA
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Impulsive
Over estimate their abilities
Have decreased attention span
Left sided weakness
• Left sided CVA
– Slow, cautious, and disorganized
– Right sided weakness
• Spatial perceptual defects: denial of illness
or non functioning body parts; erroneous
perception of self; agnosia; apraxia
DIAGNOSIS
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CT
MRI
Doppler ultrasound
Cerebral angiogram
Lumbar puncture if not contraindicated
TREATMENT
• Acute phase (first 12 – 72 hours):
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If not hemorrhagic: anticoagulant
Thrombolytics, if not hemorrhagic
Calcium channel blockers
Hyperosmolar solutions
Diuretics
Anticonvulsants
Decadron
Antipyretics
NURSING DIAGNOSIS
• ALTERED CEREBRAL TISSUE PERFUSION
– Monitor respiratory and airway patency
• Suction only as needed
• Lateral low Fowler’s position ( HOB 30 to 
cerebral edema, head in neutral position –
improves venous drainage)
• If risk for hemorrhage or IICP, no coughing,
deep breathing
• If no risk of hemorrhage, cough and deep breathe
• Oxygen as ordered
• Monitor Neurologic Status
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LOC
Pupilary response
Movement, strength of extremities
Babinski
Decorticate/decerebrate posturing
Changes in LOC
• Monitor CV status
– Assess for fluid overload (rales, SOB, dyspnea)
– Fluid restriction (if CO is low, increase fluid
based on ADH and aldosterone levels)
– Prevent thrombosis of lower extremities (ROM,
antiembolic hose, pneumatic compression
sleeves
• Monitor Neuro status
– Monitor temp (risk for hyperthermia
– Monitor for seizures (place on precautions)
• Impaired mobility:
– Prevent contractures
• Passive/active ROM
• TQ2H
• Prone position 15 – 30 minutes several times
daily
• Monitor for thrombophlebitis
• Self Care deficit
– Encourage use of unaffected side
– Teach to dress affected side first
• Sensory perceptual
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Keep environment clutter free
Well lighted environment
Bed in low position
Wheels locked
Side rails up
Keep needed objects of the unaffected side
• Elimination
Bladder
– Offer bedpan/urinal every 2 hours
– Encourage bladder training
– Teach Kegel exercises
– Use positive reinforcement
Bowel
– Encourage fluids (2000 cc/day unless CI)
– High fiber diet
– Stool softeners
– Establish bowel evacuation routine
• Swallowing
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Sit upright when eating and for 30 minutes after
Make sure neck is slightly flexed
Pureed or soft diet initially
Place food/drink on unaffected side
When finished eating, assess mouth for absence
of food
– Maintain suction at bedside
– Minimize distractions so they can concentrate
PROGNOSIS
• Assessment
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Neurologic
Urinary
Orthopedic
Bowel
Acute Spinal Cord Injury
• Diagnosis begins with:
– a detailed history of events surrounding incident,
– precise evaluation of sensory & motor function, &
– radiographic studies of the spine
• Majority occurs in males between 16 & 30
Mechanism of injury
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Hyperflexion
Hyperextension
Rotation
Axial loading
Penetrating injuries
Mechanism of injury
• Hyperflexion
– Most often seen cervical area at level of C5 to C6.
– Sudden deceleration motions
• Hyperextension
– Involve backward & downward motion of the head
– Often seen in rear-end collisions or diving accidents
Mechanism of Injury
• Rotation
• Often occur in conjunction with a flexion or
extension injury
• Axial loading
– Vertical compression
– Falls & lands on feet
• Penetrating injuries
– Bullet, knife, etc.
– Cause permanent damage by anatomical transection
SCI – Patho
• Result of a mechanical force that disrupts
neurologic tissue or its vascular supply or both.
• Injury process includes both primary & secondary
injury mechanism
SCI – Patho
• Primary injury
– The neurologic damage that occurs at moment of impact
• Secondary Injury
– The complex biochemical processes affecting cellular
function
– Can occur within minutes of injury and can last for days
to weeks
SCI – Patho
• Several events after a spinal cord injury lead to
spinal cord ischemia & loss of neurologic function
• Leads to:
– Ischemia,
– elevated intracellular calcium
– Inflammatory changes
• Current research focused on inhibiting secondary
processes & preserving functional neurons.
SCI
• Functional Injury of the spinal Cord
– The degree of disruption of normal spinal cord function
– Depends on what specific sensory & motor structures
within the cord are damaged
• Classified as:
– Complete or Incomplete
SCI
• Complete Injury
– Results in a total loss of sensory & motor function
below the level of injury
• Incomplete Injury
– Results in a mixed loss of voluntary motor activity &
sensation below the level of the lesion
SCI - Complete Injury
• Quadriplegia
– Injury occurs from the C1 to T1 level
– Also known as Tetraplegia
• Paraplegia
– Injury occurs in the thoracolumbar region (T2 to L1)
– May have full use of arms
SCI – Incomplete Injury
• Brown-Sequard Syndrome
– Damage to one side of the cord
– Loss of voluntary motor movement on same side as
injury, with loss of pain, temperature & sensation on
opposite side
• Central Cord Syndrome
– Motor & sensory deficit more pronounced in upper
extremities than in lower.
SCI – Incomplete Injury
• Anterior Cord Syndrome
– Loss of motor function, as well as loss of sensations of
pain & temperature below level of injury
– Below injury, position sense & sensations of pressure &
vibrations remain intact.
• Posterior cord Syndrome
– Loss of position sense, pressure & vibration below the
level of the injury.
– Motor function & sensation of pain & temperature
remain intact
Spinal Shock
• The complete loss of all normal reflex activity
below the level of injury.
• Manifestations include:
– Bradycardia & hypotension
• Intensity is influenced by level of injury &
• duration of this shock state can persist for up to 1
month after surgery
• *Be careful with positioning
Assessment for SCI
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•
•
•
•
Airway
Breathing
Circulation
Neurologic
Diagnostic Procedures
AUTONOMIC DYSREFLEXIA
• A life threatening complication that may occur
with SCI.
• Caused by a massive sympathetic response to a
noxious stimuli such as:
– Full bladder, line insertions, fecal impaction
• Results in:
– Bradycardia, hypertension, facial flushing, and
headache
AUTONOMIC DYSREFLEXIA
• Treatment aimed at alleviating noxious stimuli
• If symptoms persist, anti-hypertensive agents can
be administered to reduce blood pressure
• Prevention is imperative and can be accomplished
through use of a good B & B program
AUTONOMIC DYSREFLEXIA
• Clinical algorithm for treatment of autonomic
dysreflexia
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Positioning
Constrictive devices
Look for cause
BP
Catheter/Bowel
Medical Management
• Primary treatment is to preserve remaining
neurologic function
• Interventions Divided into:
– Pharmacologic
– Surgical
– nonsurgical
Medical Management
• Pharmacologic Management
• Methylprednisolone
– Bolus followed by continuous infusion for at least 24
hrs & preferably 48 hrs.
• Prevents post-traumatic spinal cord ischemia
• Improves energy metabolism
• Restores extracellular calcium
• Improves nerve impulse conduction
Surgical Management
• Laminectomy
• Spinal fusion
• Rodding
Non-surgical Management
• Cervical Injury
– Gardner-Wells and Crutchfield tongs
– Halo Vest
• Thoracolumbar
Nursing Management
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CV
Astute assessment of fluid volume
Inotropic or vasopressor support
Hypotension/hypertension
Bradycardia
DVT
Loss of thermoregulation (poikilothermy)
Nursing Management
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•
•
•
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•
•
CV
Astute assessment of fluid volume
Inotropic or vasopressor support
Hypotension/hypertension
Bradycardia
DVT
Loss of thermoregulation (poikilothermy)
Nursing Management
• Pulmonary complications are most common cause
•
•
•
•
of mortality
Observe rate, rhythm, pattern
ABGs
Watch for paralysis/weakness of respiratory muscles
airway
Nursing management
• Musculosketal
– ROM, PT, OT
– Splints
• Integumentary
• Elimination
Rehabilitation & Maximizing
Psychosocial Adaptation
• Provide dedicated emotional support
• “four D syndrome”
– Dependency, depression, drug addiction, and, if married,
divorce.
• Further support given by:
– Social workers, occupational therapists, psychiatric
clinical nurse specialists, pastors, physical therapists,
long-term rehab, support groups.
Disc Herniation
• An intervertebral disc is a pad composed of three
parts that rests between the centers of two
adjacent vertebrae.
• Discs provide cushions for spinal movement.
• Strenuous activity or degeneration of the disc or
vertebrae can allow the disc to move from its
normal location.
Disc Herniation –(cont.)
• Displacement of intervertebral disc material may
be referred to as:
–
–
–
–
Prolapse,
herniation,
rupture, or
extrusion
Disc Herniation (cont.)
• Ruptured intervertebral discs may occur at any
level of the spine.
• Lumbar discs are more likely to rupture than
cervical discs because of the:
– Force of gravity;
– continual movement in this region; and
– improper movements of the spine, as with lifting or
turning
Description
• Thoracic disc disorders are the least common
• More than half of patients give a hx of a previous
back injury.
• Heavy physical labor, strenuous exercise, & weak
abdominal and back muscles increase risk
• Repeated stress progressively weakens the disc,
resulting in bulging and herniation
Clinical Manifestations
• Lower back pain that radiates down the sciatic nerve
into the posterior thigh.
• Typically begins in the buttocks & extends down the
back of the thigh and leg to the ankle.
• Can also lead to groin pain
• Muscle spasms & hyperesthesia (numbness &
tingling) in areas of distribution of affected nerve
roots
Clinical Manifestations (cont.)
• Pain exacerbated by
– straining (coughing, sneezing, defecation, bending,
lifting, & straight-leg raising) or
– prolonged sitting &
• Is relieved by
– side-lying with the knees flexed.
Clinical Manifestations (cont.)
• Any movement of lower extremities that stretches
the nerve causes pain & involuntary resistance
• Straight-leg raising on the affected side is limited
• Complete extension of the leg is not possible when
the thigh is flexed on the abdomen.
• May have depression of deep tendon reflexes
Diagnostic Findings
• X-Ray Studies
– May show spinal degenerative changes
– Usually do not show a ruptured disc
• Magnetic resonance imaging (MRI)
– May show extrusion of disc material into the spinal
canal and impingement of a spinal nerve root
Diagnostic Findings
• Discography
– Injection of a water-soluble imaging material into the
nucleus pulposus
– Used to determine internal changes in the disc.
• Electromyography of the peripheral nerves
– To localize the site of the ruptured disc
Outcome Management
• Goals include:
– Reducing pain & spasms
– Improving mobility
– Repairing any structural problems in the spine or discs
Control Pain & Spasms
• Pain usually managed with
–
–
–
–
–
Non-steroidal anti-inflammatory drugs (NSAIDS),
muscle relaxants, and at times,
narcotics
Ice may be used for the first 48 hrs
After that heat may be used
Control Pain & Spasms- Positioning
• Semi-sitting position (in a recliner chair)
– More comfortable, reduces back strain
– promotes forward lumbar spine flexion
• Supine with pillows under the legs
• Lateral with thin pillow between knees with
painful leg flexed
• AVOID:
– prone position
– sleeping w/thick pillows under the head
Control Pain & Spasms
• Physical Therapists
– may be able to relieve pain & spasm with stretching
exercises & ultrasonic heat treatments
• Spinal manipulation
– Use of the hands on the spine to stretch, mobilize, or
manipulate the spine
• Work space or equipment modifications may be
necessary
• Progressive muscle relaxation exercises
• For severe lumbar disc problems with leg pain
– 2 to 4 days of bed rest on a firm mattress
Improve Mobility
• Most clients do not require bed rest
– > 4 days of BR can be debilitating & slow recovery
• Client taught use of proper body mechanics
• If have to sit, should change positions often
• Aerobic activities prescribed to help avoid
debilitation
• Walking, stationary bicycling, & back strengthening
– Begin within first 2 weeks after injury (perform for 20 to
30 minutes, 2 or 3 times per week)
Improve Mobility
• Work activities individualized
• Back brace or corset may be prescribed
– Usually not recommended once clinical manifestations
are relieved
• Exercise to strengthen the back and abdominal
muscles
– helps prevent further problems if the exercises are done
daily throughout life
Surgical Management
• Surgery indicated in clients with spinal disc
problems when
– Sciatica is severe & disabling
– Manifestations of sciatica persist without improvement or
worsen, and
– Physiologic evidence of specific nerve root dysfunction
• Also used to stabilize spinal fractures
Surgical Management (cont.)
• Chemonucleolysis
– Chymopapain - a proteolytic enzyme isolated from
papaya latex - is used as a meat tenderizer.
– Injected into the disc, it digests the protein in the disc &
shrinks it.
– Contraindicated in people with multiple allergies & in
people allergic to papaya.
– Immediate & delayed (after 15 days) allergic responses
– Use abandoned by most practitioners
Percutaneous Disectomy
• Herniated disc material can be excised with a
trocar to remove the center of the disc.
• The laser also is used to destroy the damaged
disc.
Microdisectomy
• The use of microsurgical instruments to remove the
herniated fragment of disc.
• Results in less trauma to the surgical site compared
with stand surgery & more tissue integrity is
preserved.
Decompressive Laminectomy
• Term laminectomy is confusing & is used loosely.
• Laminectomy
– Describes complete removal of the bone between the
spinous process & the facet;
– This is seldom necessary.
• Laminotomy
– More correct term for what is usually done
– Describes the creation of a hole in the lamina.
Decompressive Laminectomy (cont.)
• Surgical removal of the posterior arch, of a
vertebra, exposing the spinal cord.
• This procedure gives access to the spinal canal for
– Removing a spinal cord tumor
– Removing portions of the facets
– Decompressing bone infringement on the spinal cord
Decompressive Laminectomy (cont.)
• Foraminotomy
– Sometimes is performed to enlarge the intervertebral
foramen if it is narrowed & osteophytic processes
(overgrowth of bone) entrap the nerve root & impinge on
neural structures
Spinal Fusion/Arthrodesis
• Spinal fusion
– Describes the placement of bone grafts (bone chips)
between vertebrae
– New bone that grows fuses the two vertebrae &
immobilizes them to reduce the pain.
– Usually no more than 5 vertebrae are fused
• Fusing more than five vertebrae causes considerable loss of
movement in the spine
Spinal Fusion/Arthrodesis (cont.)
• Bone graft may be obtained from a bone bank or the
anterior-superior iliac crest.
• During healing, the graft gradually grows into the
vertebrae & forms a bone union
• This bone union causes permanent stiffness in the
area.
Spinal Fusion/Arthrodesis
• Lumbar Fusion
– Stiffness hardly noticed in the lumbar area after a while
• Cervical Fusion
– Stiffness usually noticeable in the cervical area
• The client cannot be guaranteed that back pain will
be relieved permanently or that further surgery will
not be required.
Spinal Fusion with Instrumentation
• Metal rods may be used to straighten & fuse the
spine in disorders such as scoliosis or multiple
vertebral fractures.
• Other devices also can be used to provide
additional support while the bones heal in a fused
manner
Complications
• General potential complications after spinal disc
surgery at any level include:
–
–
–
–
Infection and inflammation,
injury to nerve roots,
dural tears, and
hematoma
Complications (cont.)
• Non-union of the surgical area also is a risk
– Is associated with smoking
• Some surgeons assess serum nicotine levels prior to surgery to
reduce risk of non-union &
• validate statements of smoking cessation
Prognosis
• Patients with severe and disabling leg pain:
– Lumbar disectomy often relieves manifestations of pain
faster than continued medical management
• Patients w/o leg pain,
– little difference in medical vs surgical relief of
symptoms
• Client preference plays a big role in the technique
chosen
Preoperative Nursing Care
• Explain post op limitations, positioning, etc.
• If fusion is to be done:
– Encourage clients who smoke to stop.
– Clients need to be evaluated for autologeous blood
donation.
• 2 – 3 units should be donated, the last one at least 1 week
before the surgery
– Inform client of bone graft site & the additional pain
associated it.
Post Op
• Assess:
– Dressings, drains
– Level of pain & response to analgesia
– Neurologic function – compare to baseline
Post Op
• BR for post fusion -Risk for DVT
– Compression devices
– Observe for & report S/S
• Assess Wound Site:
– Bulging or clear drainage
• May indicate cerebrospinal fluid leakage
– Anterior approach
• Usual care for abdominal surgery is required
Positioning
• After lumbar fusion
– Bed is generally kept flat
• Log-rolling
– Usually beginning about 4 hrs after surgery, then q 2 –
4 hrs thereafter
– Ensure safety
– Common to have spasms & pain w/turning
• Analgesics & anti-spasmodics
Post–Op – Urinary Retention
• Common after spinal surgery –
– because of pain & spasms &
– as a side effect of narcotics.
• Assess for retention –
– Cath prn as ordered
Post Op – Paralytic Ileus
• Most common bowel problem after laminectomy & spinal
fusion
– Due to lack of peristalsis from a sudden loss of parasympathetic
function innervating the bowels &
– manipulation of the intestines in anterior approaches
• Assessment findings
– N & V,
– hard abdomen,
– absence of bowel sounds
Paralytic Ileus - Intervention
• NGT to low intermittent suction
• NPO
• Assess at least q 4 hrs
HERNIATION SYNDROMES
• **TO PREVENT HERNIATION:
– The goal of neurologic evaluation, ICP monitoring, and
treatment of increased ICP
Herniation Syndromes
• Herniation results in shifting of tissue
• Places pressure on cerebral vessels & vital function
centers of the brain.
• If unchecked, herniation rapidly causes death as a
result of the cessation of cerebral blood flow &
respirations
HERNIATION SYNDROMES –
(cont.)
• Supratentorial Herniation
–
–
–
–
Uncal
Central, or Transtentorial
Cingulate
Transcalvarial
• Infratentorial Herniation
– Upward transtentorial herniation
– Downward cerebellar herniation
Herniation Syndromes –
UNCAL
• Most often noted herniation syndrome
• Unilateral, expanding mass, usually of the
temporal lobe, increases ICP, causing lateral
displacement of the tip of the temporal lobe.
• Clinical S/S:
– Ipsilateral pupil dilation, decreased LOC, respiratory
pattern changes/arrest, contralateral hemiplegia
(decorticate/decerebrate)
Herniation Syndromes CENTRAL
• Often preceded by uncal and cingulate herniation
• Expanding mass lesion of the midline, frontal,
parietal, or occipital lobes
• S/S
– Similar to Uncal in late stages
Herniation Syndromes –
CINGULATE
• Occurs often
• Not in itself life-threatening, but if the expanding
mass lesion is not controlled, uncal or central
herniation will follow.
Herniation Syndromes –
Transcalvarial
• The extrusion of cerebral tissue through the
cranium
• In the presence of severe cerebral edema,
transcalvarial herniation occurs through an opening
from a skull fx or craniotomy site
Herniation Syndromes –
Upward Transtentorial Herniation
• Deterioration progresses rapidly
• Compression of 3rd cranial nerve & diencephalon
occurs
• Blockage of central aqueduct
• Distortion of 3rd ventricle obstruct CSF flow
Herniation Syndromes –
Downward Cerebellar Herniation
• Compression & displacement of the medulla
oblongata occur
• Rapidly results in respiratory & cardiac arrest
CHRONIC DISORDERS
AMYOTROPHIC LATERAL
SCLEROSIS (ALS)
• Also known as Lou Gehrig’s Disease
• A progressive degenerative neurologic disease
characterized by weakness and wasting of the
involved muscles, without any accompanying
sensory or cognitive changes.
• Unknown cause
• Affects men more than women, usually between
the ages of 40 – 60.
CLINICAL MANIFESTATIONS
• Musculoskeletal:
–
–
–
–
–
–
–
weakness and fatigue
“heaviness” of the legs
fasciculations (focal muscle twitching)
Uncoordinated movements
Loss of motor control in the hands
Spasticity
Paresis
– Hyperreflexia
– Atrophy
– Problems with articulation
• Respiratory
– Dyspnea
– Difficulty clearing the airway
• Nutrition
– Difficulty chewing
– Dysphagia
• Emotion
– Loss of control, liability
• Cognitive
– Intellect is not affected
– Remains alert and mentally intact throughout
the course of the disease
• Death is usually resultant from pneumonia
• Diagnosis is made with an EMG
TREATMENT
• Supportive
• Riluzole (Rilutek): drug which extends the
life by a few months
• Respiratory compromise usually results
within 2 – 5 years of diagnosis
INTERVENTIONS
• Mobility
–
–
–
–
–
–
ROM
Stretching exercises
Splints
Ankle boots
Wheelchair
Frequent rest periods to decrease fatigue
• Nutrition
–
–
–
–
–
–
–
–
Suction at bedside
Rest before meals
Upright to eat and 30 minutes after
Semisolid food
Frequent meals
Soft cervical collar to keep head upright
Enteral feedings
Syringe with short, small bore tubing (placed
on anterior aspect of tongue, used for giving
liquids)
• Breathing
–
–
–
–
–
–
–
Mechanical ventilation as necessary
Elevate HOB
TQ2H
Oxygen
Breathing exercises
Incentive spirometry
Suctioning as needed
• Communication
– Speech therapy
– Hand held computers
– Pointer held with teeth and use of a picture
board
– Word charts
– Eye blinks
MULTIPLE SCLEROSIS
•
•
•
•
•
•
Chronic, progressive disorder of the CNS.
Weakness
Remission
Progression
Glial scar tissue (hard, sclerotic plaque)
Loss of function
CLINICAL MANIFESTATIONS
• musculoskeletal
–
–
–
–
–
–
–
–
Fatigue (most common and often most disabling)
Limb weakness ( loss of muscle strength)
Ataxia
Intention tremors
Spasticity
Muscular atrophy
Dragging of the foot
Foot drop
• Urinary
–
–
–
–
–
Hesitancy
Frequency
Retention
Recurrent UTI’s
Incontinence
• Gastrointestinal
–
–
–
–
–
Difficulty chewing
Dysphagia
Diminished or absent sphincter control
Bowel incontinence
Constipation
• Respiratory
– Diminished cough reflex
– Respiratory infections
• Sensory
–
–
–
–
–
–
–
–
–
–
–
Blurred vision
Optic neuritis
Diplopia
Nystagmus
Eye pain
Visual field defects
Vertigo/ loss of balance and coordination
Nausea
Numbness
Parasthesias (numbness or tingling)
Diminished sense of temperature/ desensitized touch
sensation
• Neurologic
–
–
–
–
–
–
Emotional lability/ mood changes/ depression
Forgetfulness
Apathy
Irritability
Impaired judgment
Dysarthria (speech problems)
• Diagnosis
–
–
–
–
History
CSF evaluation
MRI
Optic/Auditory testing (shows slowed nerve
conduction)
TREATMENT
•
•
•
•
•
Corticosteroids
Interferon
Plasmapheresis
Surgery
Diet therapy
INTERVENTIONS
• Respiratory
– CDB Q 2 – 4 H
– Elevate HOB 90o to eat
• Immobility
– PT for walking and hydrotherapy
• Gastrointestinal
– Stool softeners
– Encourage activity
– Maintain fluid intake
• Skin
–
–
–
–
Assess every shift
TQ2H
Keep linen clean and dry
Massage around bony prominences
• Vision
– Assess acuity
– SR elevated, bed in low position, wheels locked
– Eye patch with diplopia
• Urinary
–
–
–
–
Administer appropriate meds
Intermittent catheterization
Assess for infection
Increase fluids to 3000 cc/day if allowed
• Teaching
– Factors which cause exacerbation
• Hyperthermia
• Stress
• Infection
• pregnancy
MUSCULAR DYSTROPHY
• A group of genetic disorders involving gradual
degeneration of muscle fibers
• Progressive weakness and skeletal muscle
wasting, accompanied by disability and
deformity
• Types:
1. Pseudohypertrophic MD (Duchene MD)
2. Facioscapulohumeral MD (LandouzyDejerine)
CLINICAL MANIFESTATIONS
• Evidence of muscle weakness usually
appears at 3-4 yrs
• May have history of delayed motor
development, especially walking
• First symptom may be : difficulties in
running, riding a bike
• Develop characteristic rising from squatting
or sitting position on floor (Gower’s sign)
TREATMENT
• Supportive measures
–
–
–
–
Physical therapy
Orthopedic procedures
Use of braces for spine and lower extremities
Breathing exercises
MYASTHENIA GRAVIS
• A chronic, progressive autoimmune disease
characterized by fatigue and severe muscle
weakness of the skeletal muscles, that
worsens with exercise and improves with
rest
• Manifestations result from a loss of Ach
receptors in the postsynaptic neurons of the
neuromuscular junction
CLINICAL MANIFESTATIONS
• Primary feature: increasing weakness with
•
•
•
•
•
sustained muscle contraction
Ptosis (drooping of upper eyelid)
Diplopia (double vision)
Facial weakness (snarls when smiling)
Dysphagia
dysarthria
• Weakness and fatigue
• Decreased function of hands, arms, legs,
•
•
•
•
•
•
and neck muscles
Weakening of intercostals
Decreased diaphragmatic movement
Breathlessness and dyspnea
Poor gas exchange
Inability to chew and swallow
Decreased ability to move tongue
DIAGNOSIS
• Based on clinical presentation and response
to anticholinesterase drugs
• TENSILON TEST
TREATMENT
• Anticholinesterase drugs
– Pyridostigmine (mestinon)
– Neostigmine (Prostigmine)
• Immunosuppressive therapy
(corticosteroids)
• Plasmaphoresis
• Thymectomy
COMPLICATIONS
• Myasthenic crisis: caused by
undermedication
–
–
–
–
–
Sudden marked rise in B/P due to hypoxia
Increased heart rate
Severe respiratory distress and cyanosis
Absent cough and swallow reflex
Increased secretions, increased diaphoresis,
increased lacrimation
– Restlessness, dysarthria
– Bowel and bladder incontinence
• Cholinergic Crisis: caused by excessive
medication
– Weakness with difficulty swallowing, chewing,
speaking and breathing
– Apprehension
– N/V/D/abdominal cramps
– Increased secretions and saliva
– Sweating, lacrimation, fasciculations, and
blurred vision
NURSING CARE
•
•
•
•
Airway management
Suction at bedside
ABGs
Endotracheal intubation if ventilatory support is
needed
• Administer edrophonium chloride (Tensilon) to
determine type of crisis
• Monitor electrolytes, I&O, daily weight
• Tube feeding if unable to eat
CEREBRAL PALSY
• Impaired muscular control due to abnormality in
the brain resulting in abnormal muscle tone and
coordination. Physical signs:
–
–
–
–
–
–
Poor head control after 3 months
Stiff or rigid arms or legs
Pushing away or arching back
Floppy or limp body posture
Cannot sit up without support by 8 months
Use of only one side of body, or only the arms to
crawl
– Clenched fists after 3 months
BEHAVIORAL SIGNS
• Extreme irritability or crying
• Failure to smile by 3 months
• Feeding difficulties
– Persistent gagging or choking when fed
– After 6 months of age, persistent tongue
thrusting
CLINICAL MANIFESTATIONS
• Delayed gross motor movement (universal
•
•
•
•
•
manifestation)
Abnormal motor performance
Altered muscle tone
Abnormal posture
Abnormal reflexes
Associated disabilities and problems
INTERVENTIONS
•
•
•
•
•
•
Mobilizing devices
Surgery
Speech therapy
Dental care
Hearing aids
Physical therapy
PARKINSON’S DISEASE
• Progressive, degenerative disease
characterized by disability from tremor and
rigidity
– Depletion of dopamine
CARDINAL FEATURES
•
•
•
•
•
•
Tremor at rest
Rigidity
Bradykinesia (slow movement)
Flexed posture of neck, trunk, and limbs
Loss of postural reflexes
Freezing movement
OTHER CLINICAL
MANIFESTATIONS
•
•
•
•
•
•
•
Skin problems
Heat intolerance
Postural hypotension
Constipation
Dementia
Anxiety
Depression
TREATMENT
• Dopaminergics
– Levodopa
– Carbidopa-levodopa (Sinemet)
• Anticholinergics
– Trihexphenidyl (Artane)
– Benztropine (Cogentin)
• Dopamine Agonists
– Bromocriptine (Parlodel
– Pergolide (Permax)
• Surgery:
– Pallidotomy
– Sterotaxic thalamotomy
– Autologous adrenal medullary transplant
(doesn’t work well)
– Fetal tissue transplant (better results)
INTERVENTIONS
• Mobility
–
–
–
–
–
ROM
PT (individualized)
Ambulate qid
Assistive devices
Provide for safety
• Communication
–
–
–
–
Allow time to speak
Encourage deep breathing before speaking
Speech therapy
Alternative methods of communication
• Sleep
–
–
–
–
Quiet environment
Position of comfort
ROM to decrease rigidity
Stay awake during day
(meds may interrupt normal sleep cycle)
• Nutrition
–
–
–
–
–
–
–
–
Calorie count/weekly weight
Assess swallowing ability
Soft, solid food appropriate for the individual
Massage facial and neck muscles before eating
Sit upright for feeding and 30 minutes after
Suction at bedside
Adequate roughage/fiber
Small, frequent meals
• Elimination
–
–
–
–
Drink 3000 cc/day if possible
Increased fiber
Increase mobility to stimulate peristalsis
Stool softeners/suppositories
• Self care:
– Encourage independence but set time limits
– Keep items in reach
– Give a time frame to allow the patient to do
their own care
Bell’s Palsy –Patho & Etiology
• Affects motor aspects of the facial nerve, (7th
•
•
•
•
cranial nerve).
Most common type of peripheral facial paralysis.
Affects women & men in all age groups
Most common between ages 20 & 40 yrs.
Results in a unilateral paralysis of the facial
muscles of expression.
Bell’s Palsy –Patho & etiology
• No evidence of a pathologic cause.
• Facial paralysis central or peripheral in origin.
• Central facial palsy is an upper motor neuron
paralysis or paresis.
– Client cannot voluntarily show teeth on paralyzed side
but can show them with emotional stimulation.
• Called voluntary emotional dissociation
Bell’s Palsy –
Clinical Manifestations
• Typical findings on affected side include:
– Upward movement of the eyeball on closing the eye
(Bell’s phenomenon)
– Drooping of the mouth
– Flattening of the nasolabial fold
– Widening of the palpebral fissure
– Slight lag in closing the eye
• Eating may be difficult
Bell’s Palsy –
Outcome Management
• No known cure.
• Palliative measures include:
– Analgesics if discomfort occurs from herpetic lesions
– Corticosteroids to decrease nerve tissue edema
– Physiotherapy, moist heat, gentle massage, &
stimulation of the facial nerve
– Corneal protection w/artificial tears, sunglasses, eye
patch
Neurological Clinical
Assessment
• History
• Physical examination components
–
–
–
–
–
Level of consciousness (LOC)
Motor function
Pupillary function & eye movement
Respiratory patterns
Vital signs
Bell’s Palsy – Recovery/Prognosis
• Clients experiencing Bell’s Palsy often think they
have had a stroke.
– Reassure client
• Prognosis
– Most clients recover within a few weeks w/o residual
manifestations.
• If permanent facial paralysis occurs, surgery may
be necessary.
– Anastomosis of the peripheral end of the facial nerve
with the spinal accessory or hypoglossal nerve may
allow closure of the eye & restore tone to face
Trigeminal Neuralgia
• Chronic irritation of the fifth cranial nerve
• Trigeminal nerve has 3 division & neuralgia may
occur in any one or more of these divisions
– Opthalmic,
– maxillary, &
– mandibular
Trigeminal Neuralgia – Etiology
• Causes can be intrinsic or extrinsic lesions within
the nerve itself
– Ex: multiple sclerosis
• Extrinsic lesions are outside the trigeminal root &
include mechanical compression by
– Tumors, vascular anomalies, dental abscesses, or jaw
malformation
Trigeminal Neuralgia –
Clinical Manifestations
• Characterized by intermittent episodes of intense
•
•
•
•
pain of sudden onset.
Pain is rarely relieved by analgesics
Tactile stimulation, such as touch & facial hygiene,
& talking may trigger an attack
More prevalent in the maxillary and mandibular
distributions & on the right side of the face.
Bilateral trigeminal neuralgia is rare
Trigeminal Neuralgia –Diagnosis
• None of the current diagnostic studies identify
trigeminal neuralgia
• CT scan, MRI, & angiography can identify a
causative lesion.
• Diagnosis made on basis of in-depth history,
w/attention paid to triggering stimuli & nature &
site of the pain.
Trigeminal Neuralgia –
Nursing Considerations
• Careful history is obtained regarding triggering
stimuli
• Dental hygiene & nutritional intake are evaluated
Trigeminal Neuralgia–Outcome Mgt
• Anticonvulsant agents often prescribed as initial treatment
– Carbamazepine (Tegretol)
– phenytoin
• These drugs may dampen the reactivity of the neurons
within the trigeminal nerve
• For some clients, these medications are all the treatment that
is needed
• Monitor liver enzymes before & during therapy
• Use caution if hx of alcohol abuse
Trigeminal Neuralgia–Outcome Mgt
• Baclofen (Lioresal)
– An antispasmodic that may be used alone or in
conjunction with anticonvulsants.
• Narcotics are not particularly effective
• Help client use & improve any pain control strategy
they have developed.
• Provide emotional support
Trigeminal Neuralgia–Outcome Mgt
• Surgery includes
– Nerve blocks with alcohol & glycerol
– Peripheral neurectomy &
– Percutaneous radio-frequency wave forms
• Relief obtained not always permanent
• 0ften better tolerated by elderly or debilitated clients
– Therefore, present later with symptoms
Trigeminal Neuralgia –
Outcome Mgt
• More invasive techniques involve major surgical
procedures (craniotomy):
• Microvascular decompression
– Removing the vessel from the posterior trigeminal root
• Rhizotomy
– Actual resection of the root of the nerve
TN – Outcome Mgt –
Surgical Complications
• Same as with any surgical procedure
• Facial weakness & paresthesias
• If facial anesthesia present after surgery
–
–
–
–
Test food before placing in mouth
Assess for aspiration & advance diet slowly
Water jet device instead of toothbrush
Visit dentist soon
• If corneal reflex impaired
– Eye care
Guillian-Barre’ Syndrome (GBS)
• Once thought to be single entity characterized by
inflammatory peripheral neuropathy
• Now understood to be a combination of clinical
features with varying forms of presentation &
multiple pathologic processes.
GBS (cont.)
• Most cases do not require admission to CCU
• Prototype of GBS, known as acute inflammatory
demyelinating polyradiculoneuropathy (AIDP)
involves rapidly progressive, ascending peripheral
nerve dysfunction leading to paralysis & maybe
respiratory failure
GBS (AIDP)
• Because of the need for ventilatory support, AIDP is
•
•
•
•
one of the few peripheral neurologic diseases that
necessitate a critical care environment.
Annual incidence of GBS is 1.6 – 1.9 per 100,000
persons.
Occurs more often in males
Most commonly acquired demyelinating
neuropathy.
Clusters of cases reported following 1977 swine flu
vaccinations
GBS - Etiology
• Precise cause unknown
• Syndrome involves an immune-mediated response
• Most patients report a viral infection 1 to 3 weeks
before the onset of clinical manifestations, usually
involving upper respiratory tract.
GBS - Etiology
• Numerous triggering events include:
–
–
–
–
–
–
Viral infections
Bacterial infections
Vaccines
Lymphoma
Surgery
Trauma
GBS - Pathology
• Affects:
– motor & sensory pathways of the peripheral nervous system,
– as well as the autonomic nervous system functions of the cranial
nerves.
• Believed to be an autoimmune response to antibodies
formed in response to a recent physiologic event.
• Once temporary inflammatory reaction stops, myelinproducing cells begin the process of re-insulating
demyelinated portions of PNS.
• Degree of axonal damage is responsible for the degree of
neurologic dysfunction.
GBS – Assessment & DX
• Symptoms include:
– Motor weakness
– Paresthesias & other sensory changes
– Cranial nerve dysfunction
• (especially oculomotor, facial, glossopharyngeal, vagal, spinal
accessory, and hypoglossal); and
– Some autonomic dysfunction
GBS – Assessment & DX
• Abrupt onset of lower extremity weakness that
progresses to flaccidity and ascends over a period
of hours to days.
• Motor loss usually symmetric, bilateral, and
ascending
• In the most severe cases, complete flaccidity of all
peripheral nerves, including spinal and cranial
nerves, occurs.
GBS – Assessment & DX
• Admitted to hospital when lower extremity
weakness prevents mobility
• Admitted to CCU when progression of weakness
threatens respiratory muscles.
• DX based on clinical findings plus CSF analysis &
nerve conduction studies.
• Diagnostic finding is elevated CSF protein with
normal cell count
GBS – Assessment & DX
• Frequent assessment of respiratory system
• Most common cause of death is from
RESPIRATORY ARREST
• As disease progresses & respiratory effort
weakens, intubation & MV are necessary
• Continued, frequent assessment of neurologic
deterioration is required until the patient reaches
the peak of the disease & plateau occurs.
GBS – Medical Mgt
• No curative treatment available
• Disease must run its course, which is characterized
by ascending paralysis that advances over 1 to 3
weeks & then remains at a plateau for 2 to 4
weeks.
• Plateau stage followed by descending paralysis &
return to normal or near-normal function.
GBS – Medical Mgt
• Main focus is the support of bodily functions &
prevention of complications
• Plasmapheresis often used in attempt to limit
severity & duration
– Contraindicated if hemodynamically unstable
• IV imunoglobulin may be used
• Steroids may be used
GBS – Nursing Mgt (cont.)
• Support all normal body functions until the patient
can do so on his or her own
• Requires extensive long-term care,
– recovery can be a long process
GBS – Nursing Mgt (cont.)
• Focuses on:
–
–
–
–
Maintaining surveillance for complications
Initiating rehabilitation
Facilitating nutritional support,
Providing comfort & emotional support
GBS –Monitor for Complications
• Once intubated and on MV
– Observe for pulmonary complications
• (ie: atelectasis, pneumonia, pneumothorax
• Autonomic dysfunction, dysautonomia
– Can produce variations in HR & BP
– Hypertension and tachycardia may require beta-blocker
therapy
GBS – Initiating Rehabilitation
• Immobility may last for months
• Usual course of GBS involves:
– average of 10 days of symptom progression
– 10 days of maximal level of dysfunction
– Followed by 2 to 48 weeks of recovery
• Patient requires physical & occupational
rehabilitation because of the problems of long-term
immobility.
GBS – Rehab (cont.)
• Facilitating Nutritional Support
– Usually accomplished through use of enteral feeding
• Patient education
• Participation in a neurologic rehabilitation program
(if necessary)
GBS – Providing Comfort & Emotional
Support
• Pain control
– A safe, effective, long-term solution to pain
management must be identified.
• Extensive psychologic support
• *GBS does not affect the LOC or cerebral function
– Patient interaction & communication are essential
elements of the nursing management plan.
Clinical Manifestations
Using the Glasgow Coma Scale
Coma, Persistent Vegetative State
Other Complications
Glasgow Coma Scale (GCS) –
A tool for assessment
• For LOC only
• Not a complete neurological exam
• Evaluation of 3 categories
– Eye opening
– Verbal response
– Motor response
Rapid Neurologic Examination
• Organized, thorough, & simple.
• Performed accurately & easily at each assessment
point
• Conscious Patient
• Unconscious Patient
Rapid Neurologic Assessment –
Conscious Patient
•
•
•
•
•
•
•
•
Exam should take less than 4 minutes
LOC
Facial Movements
Pupillary function & eye movements
Motor assessment
Sensory
VS
Change in status
Rapid Neurologic Assessment –
Unconscious Patient
• Assessment takes 3 to 4 minutes
• Initial efforts are directed at achieving maximal
•
•
•
•
•
arousal of the patient
LOC
Pupillary assessment
Motor examination
Respiratory pattern
VS
Neurologic changes Associated with
Intracranial Hypertension
• Increasing ICP can be identified by changes in:
• LOC (*1st Sign of deterioration in a conscious
patient)
– Increased restlessness, confusion, agitation, decreased
responsiveness
•
•
•
•
Pupillary Reaction
Motor Response
Vital Signs
Respiratory Patterns
Diagnostic Procedures
•
•
•
•
•
•
•
Computerized tomograpy (CT Scan)
Magnetic resonance imaging (MRI)
Cerebral Angiography
Myelography
Cerebral Blood Flow Studies
Electrophysiology Studies
Lumbar Puncture
COMA
• A state of unconsciousness in which both
wakefulness and awareness are lacking
• A symptom, rather than a disease
– Occurs as a result of some underlying process
• Can be produced by a wide variety of both
neurologic & non-neurologic conditions
• Comprises a continuum of many levels
COMA - Etiology
• Structural neurologic lesions
• Metabolic and toxic conditions
• Psychiatric disorders
COMA – Structural Lesions
• Vascular lesions
– Ischemic & hemorrhagic strokes
• Trauma
– Loss of consciousness may occur immediately or may
develop several days–weeks after injury
• Brain tumors and brain abscesses
– Compression of neurologic structures
– Often accompanied by motor paralysis
COMA –
Metabolic & Toxic Conditions
• Accounts for more than half of all cases of
coma
COMA –
Cardiopulmonary Decompensation
Any cardiopulmonary condition can precipitate a state
of coma by threatening the state of oxygenation of
cerebral tissue
COMA – Poisoning & Alcohol
• May occur as the result of self-administration,
accidental ingestion, industrial exposure, or
homicidal administration
• Drug overdose – 30% of cases in ED
• Symptoms depend on substance ingested
• Alcohol may not be cause of coma in inebriated
patient
– Trauma, cerebral hemorrhage, subdural hematoma
• Thiamine deficiency
COMA – Hypertensive
Encephalopathy/HTN Crisis
• Sudden onset, usually following hx of kidney
disease, severe HTN, or both
COMA - Meningitis
• Common cause of coma
• Fever or signs of meningeal irritation
• Abrupt onset, severe HA followed by loss of
consciousness
• Hx of infectious process affecting middle ear or
paranasal sinuses should raise suspicion of
meningitis.
CLINICAL MANIFESTATIONS
• Classic symptoms:
–
–
–
–
Nuchal rigidity
Brudzinski’s sign
Kernig’s sign
Photophobia
• Other: fever, tachycardia, h/a, chills, nausea,
vomiting, seizures
• May be irritable at first with progression to
confusion, stupor, and semiconsciousness
COMA
•
•
•
•
•
•
•
Encephalitis
Post-convulsion
Other Metabolic Disturbances
Hyper/hypoglycemia
Hepatic coma
Pneumonia
Ecclampsia, various endocrine disorders;
hyperthermia, & electrolyte, acid-base, or water
imbalance.
COMA – Patho.
•
•
•
•
Slight or moderate cortical depression
Complete cortical suppression
Midbrain depression
Brain stem depression
COMA –Assessment & DX
• Detailed serial neurologic examinations
• CT or MRI
– Usually readily identify structural causes
• Lumbar Puncture (unless contraindicated by signs of
increased ICP)
– Analysis of CSF pressure & content
– **CT precedes Lumbar Puncture to identify patients
at risk for brain herniation
• Laboratory studies to identify metabolic or
endocrine abnormalities
Medical Management
• Identification & tx of underlying cause
• Emergency measures to support vital functions &
prevent further neurologic deterioration
• Protection of airway & ventilatory assist
• If cause not known
– Thiamine (at least 100 mg), glucose, & a narcotic
antagonist suggested
Medical Mgt (cont.)
• Prognosis depends on
– cause of the coma &
– length of time unconsciousness persists.
• Best prognosis is associated with early arousal
• Metabolic coma - better prognosis than coma caused
by a structural lesion
• Traumatic coma - better outcome than non-traumatic
COMA
• Clinical Manifestations of Metabolically &
Structurally Induced Coma
COMA – Nursing Mgt
• **Patient is totally dependent on the health care
team
• Interventions directed toward:
– Assessment
• changes in neurologic status &
• clues to the origin of the coma
– Supporting all body functions
– Maintain surveillance for complications
– Providing comforting and emotional support
– Initiating rehabilitation measures
COMA – Eye Care
• Blink reflex is often diminished or absent
– Results in drying & ulceration of the cornea
• Interventions to protect the eyes
– Instill saline or methyl cellulose lubricating drops &
taping eyelids shut
– Instilling saline drops q 2 hr & applying a polyethylene
film over the eyes
Coma Stimulation Therapy
• Based on the belief that structured brain
stimulation fosters brain recovery
PERSISTENT VEGETATIVE STATE
(PVS)
• State of unconsciousness in which wakefulness is
•
•
•
•
present but awareness is lacking
Absence of any ascertainable cerebral cortical
function
Complete or partial hypothalmic & brain stem
autonomic functions are present,
Sleep-wake cycles are present
There is complete unawareness of self & the
surrounding environment
Diagnostic Criteria for PVS
• No evidence of awareness of self or environment
• Inability to interact with others
• No evidence of sustained, reproducible,
purposeful, or voluntary behavioral response to
visual, auditory, tactile, or noxious stimuli
• No evidence of language comprehension or
expression
Diagnostic Criteria for PVS(cont.)
• Intermittent wakefulness manifested by presence
of sleep-wake cycles
• Sufficiently preserved hypothalmic & brain stem
autonomic functions to permit survival with
medical & nursing management
• Bowel & bladder incontinence
• Variably preserved cranial nerve reflexes and
spinal reflexes
PVS - Assessment & DX
• Differentiating feature between PVS & coma is the
wakefulness of the PVS patient
• Most difficult differential diagnosis is between
PVS & a locked-in state
– Locked-in state patient is conscious but unable to
communicate because of severe paralysis
Differentiating characteristics of PVS & other related
conditions
PVS - Assessment & DX
• Diagnosis must be made by a specialist with
expertise in this area.
• Moral, ethical & legal issues pertaining to PVS are
the subject of much debate
• Positron-emission tomography (PET) &
electroencephalography (EEG) are used to support
diagnosis
PVS - Medical Mgt
• No treatment to reverse PVS is known
• Coma sensory stimulation is being studied
• Prognosis depends on the cause of the underlying
brain disease
• For patient in a PVS that resulted from
degenerative or metabolic brain disease
– No chance for recovery is possible
• Average life expectancy is 2 to 5 years
PVS - Medical Mgt
• Collaboration between physicians & family to
determine appropriate level of medical
management
• Decisions must be made regarding:
–
–
–
–
Resuscitation status
Medications (including antibiotics & O2)
Hydration, nutrition, and
Long-term placement
PVS - Nursing Management
• Primarily comprised of:
–
–
–
–
Performing a detailed neurologic assessment
Providing supportive & hygienic measures, and
Preventing complications of immobility
Psychosocial & informational support of the family
REYE SYNDROME (RS)
• A disorder defined as toxic encephalopathy
associated with other characteristic organ
involvement.
• Very uncommon now- review from PEDS
ASSESSMENT OF
INTRACRANIAL PRESSURE
INTRACRANIAL PRESSURE
• Intracranial space comprises 3 components:
– brain substance (80%),
– cerebrospinal fluid (CSF) (10%),
– and blood (10%).
• Under normal conditions, the ICP is maintained
below 15 mm Hg mean pressure
INTRACRANIAL PRESSURE
• Monroe-Kellie hypothesis proposes that
– an increase in volume of one intracranial component
must be compensated by a decrease in one or more of
the other components so that total volume remains
fixed
ICP
• As ICP rises, small increases in volume may
cause major elevations in ICP.
• Cerebral blood flow (CBF) corresponds to the
metabolic demands of the brain & is normally 50
ml/100 g of brain tissue/minute.
• Brain requires 15% to 20% of the resting cardiac
output & 15% of the body’s O2 demands
ICP
• MAP of 50 – 150 does not alter CBF when
autoregulation is present
• Acidosis (causes cerebrovascular dilation)
– Hypoxia, hypercapnia, ishcmia
• Alkalosis (causes cerebrovascular constr.)
– hypocapnia
• Changes in metabolic rate
– Increases increase CBF
– Decreases decrease CBF
Operative Terms
Burr hole
Craniotomy
Craniectomy
Cranioplasty
Supratentorial
Intratentorialy
Mgt of Intracranial Hypertension
• Once identified, therapy must be prompt
• Most current evidence suggests that ICP generally
must be treated when it exceeds 20 mmHg
• All therapies are directed toward reducing the
volume of one or more of the components (blood,
brain, CSF) that lie within the intracranial vault.
ICP
• Major goal of therapy is to determine the cause of
the elevated pressure, and if possible, to remove the
cause
• In absence of a surgically treatable mass lesion,
intracranial hypertension is treated medically.
ICP – Nsg Interventions for intracr.
HTN
•
•
•
•
Patient positioning
Maintaining normothermia
Controlled ventilation to ensure normal PaCO2
Administering meds
– Keep CPP near 80 mmHg to provide adequate blood
supply to the brain
– CPP = MAP – ICP
• Performing ventricular drainage
ICP – Nursing Interventions
POSITIONING
• Head elevation increases venous return
– May place some patients at risk for intracranial HTN &
cerebral ischemia caused by increases of CPP
• Recent trend is to individualize head position to
maximize CPP & minimize ICP measurements
ICP – Nursing Interventions
POSITIONING
• Obstruction of jugular veins or an increase in
intrathoracic or intrabdominal pressure is seen as
increased pressure through the open venous system,
– impeding drainage from the brain and increasing ICP.
ICP – Nursing Interventions
POSITIONING
• Positions that decrease venous return from the
head must be avoided if possible.
• Examples of positions to avoid:
–
–
–
–
Trendelenburg,
prone,
extreme flexion of the hips,
angulation of the neck
ICP – Nursing Interventions
POSITIONING
• If have to place in Trendelburg
– Monitor ICP & VS closely
• May use mechanisms to reduce intracranial pressure
– Sedation and/or ventricular drainage
ICP – Nsg Interventions
• Associated with increased ICP:
–
–
–
–
–
Use of PEEP > 20 cm H20 pressure
Coughing, suctioning
Tight tracheostomy tube ties
Valsalva maneuver
Care activities performed one after another
• Associated with decreased ICP:
– Family contact & gentle touch
ICP – BP control
• Maintenance of arterial BP in the high normal range
is essential in the brain-injured patient.
• Inadequate perfusion pressure decreases the supply
of nutrients & O2 requirements for cerebral
metabolic needs.
• A blood pressure too high increases cerebral blood
volume and may increase ICP
ICP – BP Control MEDICATIONS
• Sedatives – small, frequent doses
• Antihypertensive agents
– Avoid use of nitroprusside & NTG (potent peripheral &
cerebral vasodilators)
• To reduce vasodilating effect of anti-hypertensives,
co-treatment with beta-blockers
– Metoprolol, Labetalol
SEIZURES
• Episodes of excessive and abnormal
discharges of electrical activity within the
CNS
• Epilepsy is a syndrome of recurrent,
paroxysmal episodes of seizure activity
– Partial
– Generalized
PARTIAL (FOCAL, LOCAL)
SEIZURES
• Simple partial seizures
– Seizure activity occurs in a specific body part
• Jacksonian March
– Sensory phenomena
– Autonomic manifestations
– Psychic manifestations
GENERALIZED SEIZURES
• Absence: sudden, brief sensation of motor
activity accompanied by a blank stare and
unconsciousness
• Myoclonic:sudden, uncontrollable jerking
movements of either a single muscle group
or multiple groups, sometimes causing the
patient to fall. Patient loses consciousness
for a moment and is then confused
postictally
TONIC CLONIC SEIZURE
•
•
•
•
May or may not have an aura
Sudden loss of consciousness
Tonic phase
Clonic phase
• Tonic-clonic phase
• Clonic seizures: rhythmic muscular
contraction and relaxation lasting several
minutes
• Tonic seizures: an abrupt increase in
muscular tone and muscular contraction
• Tonic-Clonic “Grand Mal”
STATUS EPILEPTICUS
• Continuous seizing activity and may have
brief periods of calm. Because the patient is
in a constant state of seizing, they may
develop hypoxia, acidosis, hypoglycemia,
hyperthermia, and exhaustion
• Complex Partial Seizures
– With automatisms: purposeless repetitive
activities
– Complex partial evolving to secondary
generalized
PHARMACOLOGY
• Phenytoin (Dilantin)
– Therapeutic level: 10 – 20 mcg
– SE: nystagmus, diplopia, ataxia, slurred
speech, insomnia, dizziness, gingival
hyperplasia, n/v/c, measles like rash, rust
colored urine, Steven Johnson’s syndrome
• Phenobarbital
– Therapeutic range: 10 – 40 mcg/ml
– SE: drowsiness, dizziness, h/a, n/v/d, jaundice,
mild rash
– Nursing Interventions
• No abrupt withdrawal
• Use caution
• No alcohol, CNS depressants, other
barbiturates
• Medic alert identification
• No calcium products
• Deep IM
• Nursing interventions for Dilantin:
–
–
–
–
Don’t give IM
Incompatible with dextrose
Not faster than 50 mg/min IV
Monitor for hypotension, bradycardia,
bradypnea
– Do not give po with milk, calcium, antacids,
MOM
– Hold tube feeding
– Teaching
Neural Tube Defects
Neurological
Dysfunctions
HYDROCEPHALUS
• Blockage of the drainage of cerebrospinal
fluid from the ventricles of the brain or from
impaired absorption of CSF within the
subarachnoid space
• Many causes
CLINICAL MANIFESTATIONS
• Bulging fontanels with or without head
•
•
•
•
•
•
enlargement
Dilated scalp veins
Frontal protrusion (Bodding)
Eyes rotated downward (setting sun sign)
Sluggish pupils, unequal response to light
Irritability
Poor feeding
•
•
•
•
Lower extremity spasticity
Difficulty swallowing, feeding
Shrill, high pitched cry
seizures
TREATMENT
• Preferred procedure: ventriculoperitoneal shunt
• Preoperative
– Elevate HOB
– Prevent crying which increases intracranial pressure
– Avoid jarring, bouncing or any activity that will
increase intracranial pressure
– Head measured daily
– Monitor fontanels for bulging
• Ventriculoperitoneal shunt
• Post op care
– Position flat, on unoperative side
– Monitor for increased ICP (indicates obstruction
of shunt)
– NPO restriction for 24 – 48 hours
– IV fluid caution to prevent overload
• Revised as child grows
• Complications
– Infection
– Malfunction due to obstruction
SPINA BIFIDA OCCULTA
• A neural tube defect that is not visible
externally
• Skin depression or dimple, port wine
angiomatous nevi, or dark tufts of hair may
be the only visible sign
• No treatment is necessary unless neurologic
problems develop (abnormal weight gain,
problems with bowel or bladder, etc.)
SPINA BIFIDA CYSTICA
• Neural tube defect with external sac-like
protrusion
– Meningocele: encases meninges and spinal
fluid but no neural elements
– Myelomeningocele: contains meninges, spinal
fluid and nerves
MYELOMENINGOCELE
• Located anywhere on the neural tube
• May be covered with a fine membrane, the
dura, meninges, or skin
• Most frequently occurs in the lumbar or
lumbar sacral area
• 80-85 % have associated hydrocephalus
PATHOPHYSIOLOGY
• Failure of the neural tube to close during the
first 28 days of pregnancy
• Can also occur due to splitting of the
already closed tube due to increase in
cerebrospinal fluid pressure during the first
trimester
CLINICAL MANIFESTATIONS
• Usually not uniform on both sides
• Affects bowel and bladder sphincters
(constant dribbling or overflow
incontinence; lack of bowel control or rectal
prolapse – no rectal temps for these
children)
• May have lower joint deformities (from
contractures in utero)
DIAGNOSIS
•
•
•
•
MRI
CT
Ultrasound
Elevated maternal alpha fetoprotein level
(done at 16 – 18 weeks gestation)
PREOPERATIVE CARE
• Warm incubator without clothing (clothing may irritate
•
•
•
•
•
•
•
sac)
Moist dressing changes every two hours (0.9% Normal
Saline)
Cleanse carefully if soiled
Keep prone
Diapering is contraindicated until repaired
ROM (restricted to foot, ankle and knee)
Prone position when held by parents (may not be able
to do)
Tactile stimulation (caressing, stroking, other comfort
measures)
POSTOPERATIVE CARE
•
•
•
•
Maintain prone or side lying position
Frequent vital signs and daily weights
Measure head circumference daily
Examine fontanels for signs of tension or
bulging
• Catheterization for urinary retention
• Monitor for infection
PROGNOSIS
• Assessment
–
–
–
–
Neurologic
Urinary
Orthopedic
Bowel
Complications
•
•
•
•
•
•
Increased intracranial pressure
Unconsciousness
Systemic Infections
Neurogenic Shock
Seizure disorders
Others
INCREASED ICP
• Risk factors: head injury, brain tumors,
cerebral bleeding, hydrocephalus, and
edema from surgery or injury
• Most often associated with a space
occupying lesion
PATHOPHYSIOLOGY
• The skull is a hard, bony vault filled with
brain tissue, blood, and CSF. A balance b/w
these 3 maintains the pressure w/in the
cranium
• B/C the bony skull can’t expand, when one of
the 3 components expands, the other 2 must
compensate by decreasing in volume in order
for the total brain volume to remain constant
INCREASED INTRACRANIAL
PRESSURE
• Decreased LOC is the first sign
–
–
–
–
–
Alert
Lethargic
Obtunded
Stuporous
Semicomatose
DECORTICATE POSTURING
DECEREBRATE POSTURING
MORE CLINICAL
MANIFESTATIONS
• Pupillary responses:
– Early: diplopia, blurring, decreased acuity
• Changes in motor function:
– Early: progressive muscle weakness
– Late: decorticate, decerebrate, flaccid
• Headache
– Early: vague but present
– Late: accompanied by projectile vomiting without
nausea
• B/P and Pulse:
– Early: relatively stable
– Late: increased SBP while DBP stays the same (widened
pulse pressure); bradycardia
• Temperature:
– Early: normal, then increases – hyperthermia followed
by hypothermia as CSF increases
• Respirations:
– Early: normal
– Late: decreased at first together with increased SBP and
decreased pulse. As ICP increases, the character
changes: deeply yawning, signing, Cheyenne Stokes.
DOLL’S EYES
•
•
•
•
Unconscious patient’s only
Hold eyes open
Briskly turn head side to side
If eyes move in the opposite direction than the
way the head is turned, then the patient has
positive doll’s eyes. This is normal
• If they stay fixed at midline, this is negative.
• Do not perform on a patient with a cervical
fracture
TREATMENTS
•
•
•
•
•
•
•
•
Mannitol
Corticosteroids
Antipyretics
Barbiturates to induce coma
Anticonvulsants
Antibiotics
IV fluids (NS is best but ½ NS may be used)
Surgery
SEIZURES
• Episodes of excessive and abnormal
discharges of electrical activity within the
CNS
• Epilepsy is a syndrome of recurrent,
paroxysmal episodes of seizure activity
– Partial
– Generalized
PARTIAL (FOCAL, LOCAL)
SEIZURES
• Simple partial seizures
– Seizure activity occurs in a specific body part
• Jacksonian March
– Sensory phenomena
– Autonomic manifestations
– Psychic manifestations
• Complex Partial Seizures
– With automatisms: purposeless repetitive
activities
– Complex partial evolving to secondary
generalized
STATUS EPILEPTICUS
• Continuous seizing activity and may have
brief periods of calm. Because the patient is
in a constant state of seizing, they may
develop hypoxia, acidosis, hypoglycemia,
hyperthermia, and exhaustion
ACTIONS DURING SEIZURES
• Airway
–
–
–
–
–
Loosen clothing around neck
Turn to side if possible
Do not force anything into the mouth
Oxygen as ordered via mask
Suction as needed
• Injury
–
–
–
–
Bed in low position with wheels locked
Side rails up
Padded side rails
If standing, lie down; place padding under head—
protect the head from injury
– Remove potentially harmful objects
– Teaching
• Don’t smoke alone or in bed, avoid alcohol, avoid
being tired, grab the bars in the bathroom, don’t
lock doors, avoid excessive caffeine