Transcript Neonatal Neurological and Neuromuscular System

Neonatal Neurological System
Susan L Hicks, RN
Nurse Manager, NICU
Madigan Healthcare System
Objectives
Discuss pathophys
 Identify Neural Tube Defects and care
 Discuss Seizures
 Discuss Glucose Management
 Discuss IVH’s
 Discuss HIE

Central Nervous System
The most complex system in the human
brain
 Early recognition of infants at risk for
neurological dysfunction is crucial for
long term outcomes of these infants

Development of the CNS
Neurolation
– 2-3 weeks gestation
Procencephalic--2-3 months
 Neuronal proliferation 3-5 months
 Organization 5 months gestation to 1
year after birth
 Myelinization 8 months gestation to 1
year after birth

Spinal Defects
Occur during neurolation
 3-4 weeks gestation
 Folic Acid supplementation is decreasing
incidence

Anecephaly
Failure of neural tube to close in the
cranial area
 1:1000 live births, decreasing with folic
acid supplementation
 20% are alive at 1 week of age
 Supportive care measures

Encephalocele
Failure of closure of the anterior neural tube
 1:2000 live births
 Can occur over any region of the spine, 75%
over occipital region
 Contain very little or large amounts of neural
tissue not related to the size of the defect
 Surgical closure with possibility of VP shunt
in the presence of hydrocephalus

Spina Bifida
Deformations in the closure of the neural
tube in the spine or vertebrae
 Open or closed defects
 Clinically vary- can have minimal
neuromuscular effects, to paraplegia or
quadriplegia with loss of bowel and
bladder control

Spina Bifida

4 types
–
–
–
–
Closed Spina Bifida Occulta
Meningocele
Myelomeningocele
Myeloschesis
Closed Spina Bifida Occulta
pilonidal / sacral dimple or hair tuft
 10-30% of general population
 Little or no clinical significance

Meningocele
Cystic sac with meninges, but spinal cord
and nerve roots are in normal position
 Excellent outcome following surgical
repair

Myelomeningocele
Cystic sac containing meninges, spinal
cord, and vertebral elements
 Sac exposed on back and covered with
epithelium or a thin membrane
 1:1000 births, decreasing with Folic Acid
supplementation
 Most frequently in the lumbar region of
the spine

Myelominingocele

Treatment
–
–
–
–

stabilization
surgical correction
bowel and bladder care
range of motion/ flexed positioning
Outcome
– These infants are usually otherwise healthy
and outcome dependent on location and
severity of disease
Myeloschesis
Spinal cord is open and exposed
 Most of these infants are stillborn

Nursing Care and Prep for
Transport
Keep infant off site (may cut donut)
 Keep site with sterile drsg on
 Monitor VS closely – especially
temperature
 Give IVF, monitor glucose
 Observe for change in neuro status
 Transport as soon as possible.

Seizures
The most common sign of neurological
dysfunction in the neonatal period
 A sign of underlying disease process
resulting in acute disturbances of the
brain
 If left untreated can lead to permanent
Central Nervous System Damage

Seizures
Neonatal seizures are usually acute and
resolve within the first few weeks of life
 .15 % of term and 22.7% of premature
infants experience neonatal seizures
 Seizures result from excessive
simultaneous electrical discharge or
depolarization of neurons

Risk Factors for Seizures
Asphyxia
 Metabolic disturbances
 Intraventricular Hemorrhage
 Infection
 Congenital Anomalies

Seizures- Clinical Presentation
Because of immature brain organization
at birth, especially in premature infants,
the is an inability to propagate and
sustain generalized seizure activity
 In neonates, especially premature infants,
the symptoms are subtle

Seizures- Clinical Presentation

Abnormal movement or alteration of tone
in the trunk and extremities
– clonic, tonic, bicycling or swimming, general
loss of tone

Facial, oral and tongue movements
– sucking, grimacing, twitching, chewing,
swallowing, yawning
Seizures- Clinical Presentation

Ocular Movements
– eye deviation, blinking staring

Respiratory
– apnea, usually accompanied by one of the
other subtle movements
– labored, irregular respirations
Seizures
Seizure type is difficult to differentiate in
newborns
 It often mimics activity seen in the active
sleep state

Jitteriness or Seizures
Jitteriness Seizures
Stimulus Sensitive
Yes
No
Eye Deviation
No
Yes
Predominant Movement Tremors
Ceases with Passive
Flexion
Yes
Clonic, Rhythmic
Jerking
No
Seizures- Management
Treat underlying cause
 Anticonvulsant- Phenobarbital (most
common)

– also dilantin, diazepam, lorazepam
Careful monitoring of serum toxicology is
crucial to prevent toxicity
 Controversy exists in the literature over
how long to use anticonvulsant
medications in neonates

Seizures- Nursing Care

Assessment
– time of the beginning and end of abnormal
activity
– description of movements and areas involved
– respiratory status and color
– state
Hypoglycemia
May be seen as jittery infants (which
could just be immature neurological
system)
 Anticipate which infants identified as “at
risk’ and will need close monitoring.

– SGA, LGA, Potential for Sepsis, Mag moms,
– Diabetic moms!
Hypoglycemia Management
Follow your hospital guidelines for d-stix
protocol.
 Know acceptable blood glucose values
at your hospital

– <40 usually feed, then recheck?
– <20 automatically get IV ?
– Continues with problem then continuous
IVF?
Hypoglycemia
If treating with feeding, colostrum
excellent. Use of formula should be last
option.
 If treating with D10: use 2ml/kg bolus
dosing.
 Always recheck Dstix according to your
policies.

Intraventricular Hemorrhage
Capillary bed of the germinal matrix in
premature infants is immature
 Neurological Autoregulation

– Maintains consistent cerebral blood flow
despite changes in systemic blood flow
– asphyxia and hypoxemia alter autoregulation

brain becomes a pressure passive system
Germinal Matrix
Intraventricular Hemorrhage

Risk of IVH
–
–
–
–
–
–
–
–
prematurity
PPV
Medications/ Volume expansion
hypercapnea
care giving events
suctioning
pain
high pressure ventilation
Intraventricular Hemorrhage
90% of IVH within the first 72 hours of
life
 50% within the first 24 hours

Intraventricular Hemorrhage

Clinical signs
– unexplained drop in Hematocrit
– Decrease in BP support despite pressor
support
– full fontanel
– change in activity and state
– decreased tone
Grades of IVH
Grade 1
Subpendymal only
Grade 2
Extension into ventricles
Grade 3
Extension into dilated ventricles
Grade 4
Extension into the brain
parenchyma
Treatment of IVH
Indomethacin is used for IVH
prophylaxis in premature infants
 Treatment includes cardiopulmonary
support, treatment of seizures, control of
pain, and possibly ventriculo-peritoneal
shunting or tapping
 Outcome dependent of degree of IVH,
unilateral or bilateral, and whether the
bleed is resolved or develops PVL

Hypoxic/ Ischemic
Encephalopathy
2-4% of term infants
 60% of very low birth weight infants
 3 stages

Stage 1 HIE
Hyper-alert, hyperresponsive to
stimulation
 Dilation of pupils, reactive
 Scarce secretions
 EEG within normal limits

Stage II HIE
Lethargic, Hypotonic, weak suck
 Seizure activity frequent
 Pupils constrictive and reactive
 Periodic variable respiration
 Critical period- either improve or
deteriorate

Stage III HIE
Unresponsive, comatose, seizures within
6-12 hours
 Pupils unequal, variable reactivity
 Absent or depressed reflexes
 Mechanical ventilation is required
 Survivors take days to months to improve
 Feeding difficulties and neurological
abnormalities frequently develop

HIE

Outcomes
– 20-50% die during newborn period
– 17-75% with significant sequelea
– disappearance of abnormal neurologic signs
by 2 weeks offers good prognosis
Subgaleal Hemorrhage
Occurs when emissary veins are damaged
and blood accumulates in the potential
space between the galea aponeurotica
and the periosteum of the skull
 Potentially life threatening injury

Subgaleal Hemorrhage
This space has no containing membranes
or boundaries, the subgaleal hematoma
may extend from orbital ridges to the
nape of the neck
 There is a large potential space for blood
to accumulate, and the possibility of life
threatening hemorrhage

Subgaleal Hemorrhage
Subgaleal Hemorrhage
Subgaleal Hemorrhage

Clinical presentation
– Diffuse swelling of the head
– Signs of hypovolemic shock





pallor
hypotension
tachycardia
tachypnea
prolonged capillary refill time
Subgaleal Hemorrhage

Clinical presentation
– The symptoms may be present at delivery, or
may not become clinically apparent until
several hours or up to a few days following
delivery
Subgaleal Hemorrhage

Clinical presentation
– The swelling is usually diffuse, and shifts
depending on position, and indents easily
upon palpation
– In some cases, swelling is difficult to
distinguish from edema of the scalp
– Occasionally, the cranial findings are
unremarkable, and hypotension and pallor
are the dominant signs
Subgaleal Hemorrhage

Patient Care Management
– Close documentation of vital signs per policy
– Closely monitor any infant with signs of poor
perfusion following vacuum delivery





blood pressure
capillary refill time
pulses
heart rate
respiratory rate and effort
Subgaleal Hemorrhage
Document any findings, interventions,
and outcomes thoroughly
 Follow hospital policy regarding
physician notification
 Outcome

– Once infant has survived the acute phase,
recovery will occur in 2-3 week