Transcript Alterations in Neurologic Function

Alterations in Neurologic
Function
Ball & Bindler
Donna Hills APN EdD
Pediatric Differences
head is large:neck musc
underdeveloped
– prone to HI with falls
unfused sutures < 18mo
– prone to fracture
highly vascular brain;less CSF to
cushion
– brain prone to hemorrhage and trauma
cervical spine immature: incr
mobility
Pediatric Differences (cont.)
ossification of vertebral bodies
incomplete
– greater risk for compression fxs of
vertebrae with falls
myelination, responsible for smooth
motor movements, incomplete at
birth
– proceeds in cephalocaudal direction
– usually complete by 4-5yrs of age.
Level of Consciousness:LOC
most important indicator of
neurologic dysfunction
if neurologic insult continues, pt will
progress from alert thru stages to
coma:
– confusion:where am I?
– Delirium: fear, anxiety, agitation
– obtunded: limited response, falls asleep
– stupor: resp to vigorous stim only
– coma: even painful stim will not arouse
Increased ICP: intracranial
pressure
ICP: the force exerted by brain
tissue, csf, and blood within cranial
vault
decline in loc follows a sequential
pattern of deterioration
initial changes may be subtle
severe: posturing
– decordicate: rigid flexion
– decerebrate: rigid extension
Clinical Manifestations of
Increased ICP (child/adol)
HA, n, v, visual disturbances
pupils sluggish
sunsetting eyes
seizures
slight change in LOC
Clinical Manifestations of Incr
ICP (in infant)
above signs plus:
bulging fontanel
wide sutures: incr head circ
dilated scalp veins
high-pitched cry: catlike cry
Late Signs of Incr ICP
significant decrease in LOC
Cushing’s Triad:
– incr syst BP
– widening pulse pressure
– bradycardia (typo in book)
– irregular respirations
fixed and dilated pupils
B&B (pg 1302 Table 33-1)
Clinical Therapy
assess for recent trauma, infection,
ingestion
has a shunt, tumor or other medical
condition that could affect LOC
determine child’s baseline from
someone who knows him/her.
Work up: labs, LP, EEG, CT, and/or
MRI.
Glascow Coma Scale:GCS
fairly objective tool that attempts to
quantify LOC and functioning
part of VS of any child with altered
neuro state =NVS
don’t need a doctor’s order to start
them
B&B pg 1303 Table 33-2: adaptation
to pedi. with developmentally approp
response.
Treatment for Child with Altered
LOC
goal: optimized cerebral perfusion
O2 to keep sats > 95%
correction of fluid/electrolyte,
acid/base or any other metabolic
distrubance
antibiotics administered AFTER
cultures obtained.
If incr ICP is severe, ventricles may
be tapped or a VP shunt may be
externalized.
Nursing Care of Child with
Altered LOC
What abnormal vital sign findings
should be reported to the physician?
What emergency equipment should
be kept at the bedside?
If the corneal reflex is absent, what
is your most appropriate nursing
action?
What is the appropriate interval for
vital signs in a pt with altered LOC?
Approp action for pt w/o gag reflex?
Headaches
Four major types of headaches:
–
–
–
–
–
Migraine (vascular)
Tension (muscular)
Medication overuse (caffeine,aceto,nsaids)
Inflammatory(sinusitis/dental)
Structural (space occupying lesion)
each type of HA has specific clinical
manifestations and treatment
B&B pg 1323
Clinical Management of HA in
Children/Adol
good history to determine the clinical
manifestations
headache journal can be helpful to
clarify characteristics, associations
(with food, time, activity,
medications), duration, and what
helps.
assess for abnormal neurologic signs
assoc with a HA
determine strategies to relieve them.
Seizure Disorders
common in children (2-4% of pedi
pop)
most common in infancy (1 in 1,000
infants)
incidence decreases with age
Epilepsy: chronic seizure disorder
(1:100 people).
Clinical Manifestations of Sz.
types of seizures B&B pg 1306-7
focal seizures are isolated and
manifestation related to the cortical
area affected
– unilateral and specific
generalized seizures results from
diffuse electrical activity: tonic/clonic
– assoc with paleness, cyanosis, hypoxia,
hypoglycemia, incr metabolic demands
– bilateral and symmetric
Clinical Manifestations of Sz
(cont.)
postictal period: phase following a sz
characterized by decreased LOC.
– difficult to arouse
– length in children is variable
– spontaneous breathing is intact.
visual or olfactory auras may
precede the sz.
febrile sz: sudden rise in temp; may
be familial; no other cause.
Clinical Therapy
history: determine desc and length
of sz, if child lost consciousness and
if it was preceded by an aura (see
Box 33-4 p. 1308)
PE, neuro exam, labs, diagnostic
tests are ordered.
if taking anticonvulsant(s), levels
should be ordered
maintain airway, ensure safety,
admin meds and provide emotional
FIGURE 33–6
A child who has a seizure when standing should be gently assisted to the floor and
placed in a side-lying position. Clear the area of any objects that might cause harm to the child.
Status Epilepticus
a continuous sz lasting more than 30
min or a series of sz between which
consciousness is not regained.
monitor for electrolytes, glucose,
blood gases, temp, VS incl BP, O2 sat
and cap refill to assess perfusion.
often give Diastat rectally
(Diazepam)
be prepared to assist if airway is lost
– RN’s resp to provide approp equipment
Anticonvulsants
list of meds B&B( p 1310)
know generic and brand names of
emergency and first line meds if not
already familiar.
should witness all anticonvulsants
taken by the patient
regular dental care is impt d/t the
effect of some anti-sz meds on the
gingiva.
Anticonvulsants
Diazepam
Phenobarbital
Phenytoin
Carbamazepine
Valproic Acid
Clonazepam
Ketogenic Diet
used for children with myoclonic and
absence seizures
high fat/ low (no) carbohydrate, low
protein
stay on diet 2-3yrs to try to decrease
or irradicate sz
child and family motivation must be
high
Nursing considerations of caring
for a child on a ketogenic diet
the child’s metabolism is forced into
ketosis by dietary management
– urine checked Q void; UA Q day; finger
sticks Q 6hr; lytes and CO2 Q day.
ketones are measured in both the
urine and the blood
all products and meds need to be
evaluated for their CHO content
assess for sx of hypoglyc + acidosis
Ketogenic Diet
FIGURE 33–5
The family must make an effort to make the high-fat diet appealing to the child on a ketogenic diet,
despite their personal feelings about eating large amounts of food such as mayonnaise, as this child is doing
Nursing care of the child having
a seizure
make note of the time sz started, the
type of movements, whether they
changed/progressed, LOC
prevent harm; don’t hold down.
Position of comfort (as long as
airway is open)
jaw thrust if needed; O2 blow by if
sat <95
call for help/physician; check ID
band for allergies
ABOVE ALL
remain calm and
reassure family.
Care of the child with a Sx
disorder at home
(good practical common sense for
any child)
children are at increased risk for
death due to drowning
don’t leave in the bathtub alone; use
the shower
lifesaver when swimming
life vest when boating
avoid fall risks
Infectious Diseases
Bacterial Meningitis
Viral (aseptic) Meningitis
Encephalitis
Reye Syndrome
Guillain-Barre Syndrome
Bacterial Meningitis
bacterial etiology high M&M
infants at greatest risk; 70% of
children with Bacterial Meningitis are
<5yr
may occur secondary to: OM,
sinusitis, pharyngitis
may occur after head trauma or
neurosurg intervention
3 common organisms: HIB, PCV,
Neisseria Meningitidis
Effects of Immunizations
rates of HIB meningitis and
pneumococcal have declined with
increased use of the HIB and PCV
vaccines.
Neisseria Meningitidis may show a
rise in incidence.
Meningococcal Meningitis has incr
incidence in the college age
population.
Effects of Immuniz (cont)
Meningococcal vaccine recommended
for those living in dorms or highly
populated living
Some schools now require it.
Teaching point:
– It only prevents meningitis from
meningococcal infection
Clinical Manifestations:BM
onset usually abrupt but may also be
insidious over about a week.
infant: fever, change in feeding, v/d,
ant fontanel flat or bulging, alert,
restless, lethargic or irritable.
However, if irritable, the child can not
be consoled by their caregiver: what
usually works no longer works to
calm the infant.
Clinical Manifestations: BM
older child: fever, irritable, lethargic,
confused, combative or change in
personality.
c/o muscle or joint pain, back/neck
pain, HA, photophobia, esotropia,
nuchal rigidity.
rash: petechae, purpura, necrotic
patches (assoc with meningococcal
meningitis)
positive Kernig and/or Brudzinski sx
Kernig Sign
To test forKernig sign, raise the child’s leg with the knee flexed.
Then extend the child’s leg at the knee.
If any resistance is noted or pain is felt, the result is a
positive Kernig sign. This is a common finding inmeningitis
.
Brudzinski Sign
To test Brudzinski sign, flex the child’s head while in a supine position. If this action makes the
knees or hips flex involuntarily, a positive Brudzinski sign is present. This is a common sign in
meningitis.
Opisthotonis:
hyperextension of the head and neck
Clinical Therapy:BM
Hx, PE, labs (CBC with diff, Bld cult,
lytes and osmolality, clotting factors.
LP to evaluate opening pressure,
WBC’s, protein and glucose levels in
CSF.
Gram stain and culture on the CSF,
bld cx.
A/B admin as soon as all culture
specimens are obtained.
Common antibiotics used
Ampicillin
Aminoglycosides
– Gentamicin
Ceftriaxone
Cefotaxime.
Sequelae of Bacterial Meningitis
neurologic damage
cranial nerves at risk, esp VIII
(Aucoustic or Vestibulocochlear)
results in hearing loss
seizures, hydrocephalus in the infant.
DD: cognitive soft signs; LD
SIADH:hypersecretion of ADH
meningococcal septicemia with
DIC,organ failure.
Nursing Care of Pt with BM
see NCP in B&B (1317-19).
Viral (aseptic) Meningitis
inflammatory process
increased number of WBC and
protein in CSF
culture will not grow any bacterial
gram stain will be negative
does not appear as ill
are treated aggressively until 48hr
cultures are negative
Encephalitis
inflammation of the brain
usually caused by viruses
Herpes Simplex Type I most common
cause in newborn period: assoc with
high M&M
high fever, irritability, vomiting,
disoriented, confused
sx of meningeal irritation
uncommon: nucchal rigidity,
photophobia, Kernigs and Brudzinski
Reye Syndrome
acute encephalopathy: cerebral
dysfunction caused by a toxin, injury,
inflammatory or anoxic insult
may result in permanent
damage;dysfunction may improve
over time
associated with hepatic dysfunction
mortality high
Clinical Manifestations of Reye
Syndrome
n/v, mental status changes, seizures
and progressive unresponsiveness.
5 stages that outline progressive
neurologic deterioration:
hyperreflexivity, followed by
decorticate rigidity then posturing,
decerebrate rigidity, then posturing,
coma with flaccidity and eventual
arrest.
Decerebrate Posturing
Decerebrate posturing, distinguished by rigid extension, is associated with lesions of the brainstem.
FIGURE 33–3A (continued)
Decorticate Posturing
FIGURE 33–3A
Decorticate posturing, characterized by rigid flexion, is associated with lesions
above the brainstem in the corticospinal tracts.
Etiology of Reye Syndrome
Unclear
assoc with viral illness and use of
ASA.
now rare with acetominophen and
nsaids.
Because of assoc of Reye with use of
ASA post viral syndrome, counsel
parents preventively.
Guillain-Barre Syndrome
Postinfectious Polyneuritis
acute inflammatory demyelinating
polyneuropathy
deteriorating motor function and
paralysis in ascending pattern
immune response to an infectious
organism: GI or resp 2-3 wks prior
respiratory diffic may require
ventilation
Clinical Management of GBS
LP: incr protein levels
EMG: abnormal nerve conduction
hx and PE consistent with
progressive motor weakness; weak
or areflexia LE>UE.
Rx: IgG or plasmaphoresis if unable
to ambulate.
Autonomic nerv sx dysf linked to
fatal arrhythmias; nurs assessement
crucial
Structural Defects
Hydrocephalus
Spina Bifida
Craniosynostosis
Hydrocephalus
FIGURE 33–10
A, Normal size of ventricle. B, Enlarged ventricles, characteristic of hydrocephalus
Hydrocephalus
imbalance of production and
absorption of CSF
communicating
– blockage of flow or absorption of CSF in
subarachnoid space or villi
– acquired from postinfectious meningitis
or IVH
– congenital: sm amt cases d/t x-linked
– or unknown etiology
Hydrocephalus (cont.)
non-communicating
– responsible for majority of cases;usually
a developmental defects
– blockage in ventricles preventing flow
CSF
– caused by infection (toxoplasmosis, or
CMV) hemorrhage, tumor or structural
deformity
– often associated with myelomeningocele
(spina bifida)
Clinical Manifestations of
Hydrocephalus:infants
first sign in infancy is bulging
fontanels, then head enlargement,
sutures become palpably separated
to produce the “crack-pot sound”
(Macewen Sx) when percussed.
Frontal protrusion or bossing
eyes depressed downward: setting
sun sign (sclera visible above pupil).
Pupils may be sluggish with unequal
response to light.
Clinical Manifestations of
Hydrocephalus: older children
sx of presentation are different than
infants after closure of the cranial
sutures
children present with sx of incr ICP
and sx related to the focal lesions.
space occupying lesions: HA(upon
wakening with improvement
following emesis or upright position).
Papilledema, strabismus and
extrapyramidal tract sx (ataxia).
Arnold-Chiari Malformations
Type II seen exclusively with
meningomyelocele
herniation of a small cerebellum,
medulla, pons and fourth ventricle
into the spinal canal through an
enlarged foramen magnum.
The resulting obstruction of CSF flow
causes hydrocephalus
Ventriculoperitoneal(VP) Shunt
a pathway to divert excess fluid from
ventricles to peritoneum
replaced as child grows
can become blocked, kinked or
infected
shunt malfunction causes recurrent
sx of hydrocephalus, and incr ICP
infection is most serious complication
if severe, may need to externalized.
FIGURE 33–12
The tubing drains the excess cerebrospinal fluid from the ventricles to the
abdomen. The main goal of treatment is to reduce the intracranial pressure and to preserve central
nervous system function.
Spina Bifida: Meningomyelocele
congenital neural tube defect
anywhere along the spine
cause unknown but environmental
and genetic factors suspected
– maternal valproic acid use, insulin
dependency, folic acid deficiency
higher the defect, the greater the
neurologic dysfunction
LE paralysis, ortho prob, bowel and
renal.
Clinical Management of Spina
Bifida
early surgical closure (24-48 hrs)
cover sac with sterile saline gauze
place child prone, hips flexed and
knees abducted
observe latex sensitivity precautions
observe for sx incr ICP, before and
after correction.
Meningomyelocele
External view
Craniosynostosis
premature closure of the cranial
sutures
can cause deformity of the skull
can palpate over riding of the sutures
reconstructive surgery before age
1yr has a better outcome
Plagiocephaly
flat occiput in healthy newborn
due to placing child supine to sleep
to avoid risk of SIDS
helmet device can be worn to remold
the skull
– 4 hrs /day brings results in 4 months
Cerebral Palsy
non-progressive motor and posture
dysfunction
secondary to CNS insults: congenital,
hypoxic, ischemic or traumatic origin
prenatal, perinatal or postnatal (up
to 2 yrs)
most common chronic disorder is
childhood
four types of motor dysfunction:
spastic, dyskinetic, ataxic and mixed
Clinical Manifestations of CP
spastic type: persistent hypertonia,
neonatal reflexes, rigidity, incr DTR’s,
contractures, abnormal curve of the
spine
dyskinetic: impairment of voluntary
muscle control, twisting movements,
tremors, diffic with fine and
purposeful movements, exaggerated
posturing, inconsistent muscle tone.
ataxic:abnl bal and gait, hypotonia.
Clinical Manifestations(cont.)
wide variety of symptoms
frequently have other problems: DD,
strabismus, nystagmus, refractory
errors, hearing loss, language delay,
speech impediments, seizures,
and/or mental retardation.
May have altered nutrition d/t diffic
chewing and swallowing; risk for
aspir.
Clinical Therapy
any child with DD and poor suck
should be referred for eval.
Focus is on child reaching his/her
maximum potential
referrals to PT,OT, speech, special ed,
EI, ortho (as needed) and hearing
and vision.
Psych and Social Work referral
should be an integrated part of the
family’s care.
Nursing care of the child with
CP
see NCP B& B pg. 1341-2.
Traumatic Brain Injury
30,000 children and adolescents
under 19yrs of age develop a
permanent disability from a
moderate or severe brain injury (ie)
epilepsy, cognitive impairment,
learning problems and behavioral or
emotional problems.
Occurs from falls, abuse, poor
judgement errors, MVA, sports
related, risk taking behaviors.
Types of traumatic brain injuries
concussion
skull fractures
hematomas: subdural, epidural,
intracerebral
coup(direct blow) or contrecoup
injury(accel/decel)
cerebral contusion
penetrating injuries
Concussions
grade of severity 1,2,3.
– Grade1: mental status changes <15 min
– Grade 2: MSC > 15 min.
– Grade 3: LOC.
Pediatric concussive synd: stunned,
no LOC. Later become pale, clammy,
lethargic, may vomit. Admit for obsv.
Postconcussive synd:HA, dizzy,
vertigo, CMS, photophobia, poor
conc/memory
Clinical Management of
Concussions
parental teaching for parameters to
follow up.
Limited activity until return to normal
mentation
risk of falls and poor judgement
athletes should be protected from
second impact syndrome: cumulative
effects of second concussion, could
cause cerebral edema, cognitive
deficits or sudden death
Skull fractures
linear: no sx, superficial hematoma
depressed: assoc intracranial
injury/epilepsy
compound:depressed and/or
penetrating fx:incr risk of infection
basilar:fx of base of the skull: assoc
with CSF leak, dura tear.
– Bld behind TM, raccoon eyes, battle
sign, cranial nerve damage (hearing
loss).
Depressed Skull Fx
Intracranial hematomas
Epidural:extradural: between the
cranium and the dura
– bleeding is usually arterial
– momentary unconsciousness followed
by normal period, then rapid
deterioration
– uncommon in children <4yrs.
– If undiagnosed, herniation and death
will result
Subdural hematomas
subdural;between the dura and the
cortex
– bleeding is usually venous
– more common than epidurals and freq
occur in infancy
– develop slowly(48-72 hr post injury)
– more than half die: 25% develop sz
– assoc with child abuse;esp Shaken Baby
Syndrome
Contracoup Injury:
subdural hematoma
Intracerebral Hematoma
result of deep contusion
surgical treatment not indicated
– usually self absorbs over time
neuro deficits depends upon size and
location of the lesion
Usually with altered consciousness
may result in hemiplegia or visual
loss.
Penetrating Injuries
gun shot wounds
– high or low velocity
– approx 50% die
– survivors have high risk for multiple
deiecits and seizures
impaled objects: must be left in
place and removed by neurosurgeon
in OR
– high risk for focal injuries, seizures and
infection.
Clinical Manifestations of
Traumatic Brain Injuries
changes in LOC
changes in respiratory status
headache
vomiting
lethargy
retinal hemorrhages (65-90% with
HI)
Cushing’s Triad:
incr ICP
HTN
incr systolic pressure
widening pulse pressure
bradycaradia
irregular respirations
Clinical Therapy:Eval.
thorough history and PE,
observation, determine LOC and/or
vomiting at time of the injury, child’s
memory of event.
VS and use of Glascow Coma Scale
Labs, including toxicology, probable
CT and MRI
consider cervical spine injury
Cervical Spine Injury
If MOI indicates possible injury to cervical
spine, a hard cervical collar will be applied
in the ER AND LEFT ON until the patient is
conscious.
Pt must have a normal cervial spine xray
series AND be able to verbally reassure
the Neurosurgeons that there is no
cervical pain/involvement.
DO NOT REMOVE A CERVICAL COLLAR
WITHOUT AN ORDER FROM THE NEURO
OR TRAUMA TEAM
Clinical Management:
Traumatic Brain Injury
ABC;s supported as needed
perfusion to brain priority: keep bed
flat until this is assured
shock is treated aggressively with
fluid boluses
Cerebral Edema
incr in intracellular and extracellular
fluid in brain
– results from anoxia, vasodilation or
vascular stasis
treated with Mannitol and furosemide
goal is to prevent hypoxia and
hypercapnia since they cause
(cerebral) vasodilation and incr ICP.
Long term effect can’t be eval until 1
yr.