Neonatal Neurology Review Leslie A. Parker, PhD, ARNP, NNP-BC Clinical Assistant Professor University of Florida, Gainesville, FL
The speaker has signed a disclosure form and indicated she has no significant financial interest or relationship with the companies or the manufacturer(s) of any commercial product and/or service that will be discussed as part of this presentation.
Session Summary
This session will provide a general overview of the diagnosis and management of neurologic diseases and conditions to help attendants prepare for certification exams.
Session Objectives
Upon completion of this presentation, the participant will:
understand embryology, physiology and pathophysiology of common neurologic conditions in the newborn;
understand etiology and clinical manifestations of common neurologic conditions in the newborn;
understand the treatment of common neurologic conditions in the newborn.
Test Questions
1. Which of the following is not true of a subgaleal hemorrhage?
a. It occurs in the subaponeurotic space b. It is associated with vacuum extraction deliveries c. It can be life threatening d. Can lead to seizures due to irritation of the nervous system
2. Intraventricular hemorrhages:
a. Occur most commonly in the germinal matrix b. Occur most commonly during the birth process c. Often develops after 1 week of age d. Are easily confused with PVL
3. Severe HIE affects which of the following systems:
a. Heart b. Liver c. Kidneys d. All of the above
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4. Neonatal seizures:
a. Are always seen on EEG b. Are easily diagnosed clinically c. Often occur as generalized seizures d. Considered a symptom of neurologic dysfunction
5. Which of the following is true of spin bifida occulta?
a. A defect in the vertebral arch b. Often associated with significant spinal cord defects c. Associated with protrusion of membranes d. Associated with Arnold Chiari syndrome
References Bassan, H. (2009). Intracranial hemorrhage in the preterm infant: Understanding it, preventing it. Clinics in
Perinatology, 36: 737.
Brand, C.M. (2006). Part 2 Examining the newborn with an open spinal dysraphism. Advances in Neonatal Care, 6(4): 181.
Brand, C.M. (2007). Part 3 Examining the newborn with closed spinal dysraphism. Advances in Neonatal Care, 7(1): 30.
Jenson, F.E. (2009). Neonatal seizures: An update on mechanisms and management. Clinics in Perinatology, 36: 881.
Laptook, A.R. (2009). Use of therapeutic hypothermia for term infants with hypoxic-ischemic encephalopathy. Pediatric Clinics of North America, 56(3): 601-16.
McCrea, H.J. & Ment, L.R. (2008). The diagnosis, management, and postnatal prevention of intraventricular hemorrhage in the preterm neonate. Clinics in Perinatology, 35(4): 777-92.
Mwaniki, M.K., Atieno, M., Lawn, J.E. & Newton, C.R. (2012). Long-term neurodevelopmental outcomes after intrauterine and neonatal insults: A systematic review. Lancet, 379(9814): 445-52.
Nyquist, P. (2010). Management of acute intracranial and intraventricular hemorrhage. Critical Care Medicine, 38(3): 946.
Parker, L. (2005). Early recognition and treatment of birth trauma: Injuries to the head and face. Advances in Neonatal Care, 5(6): 288-97.
Robinson, S. (2012). Neonatal post hemorrhagic hydrocephalus from prematurity: Pathophysiology and current treatment concepts. Journal of Neurosurgery: Pediatrics, 9(3): 242-58.
Shah, D.K., Boylan, G.B. & Rennie, J.M. (2010). Monitoring of seizures in the newborn. Archives of Disease in Childhood, Fetal and Neonatal Edition, 97(1): F65-9.
Session Outline See presentation handout on the following pages.
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Leslie Parker RNC, PhD, NNP‐BC
University of Florida
Okay, Let’s Get This Thing Going‐ Birth trauma
‐ Neural tube defects
‐ Holoprosencephaly
‐ Hydranencephalyy p y
‐ Microcephaly/hydrocephaly
‐ IVH/PVL
‐ HIE
‐ Seizures
‐ Meningitis
Is There Anything Else We Could Possibly Cover?? Birth Trauma
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Caput Succedaneum Accumulation of serum above the periosteum
Bruising and petechia
Due to pressure during labor and delivery
C th t li Crosses the suture lines
Avoid confusion with subgaleal hemorrhage
No treatment necessary
Resolves within 24 to 48 hours
Caput Succedaneum Cephalohematoma
Beneath the periosteum
Develops during the first 24 hours of life
Does not extend across the suture lines
Treatment rarely indicated y
Complete recovery occurring by 3 months
Complications include skull fracture, hyperbilirubinemia and mild anemia
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Cephalohematoma
Subgaleal Hemorrhage
Bleeding into the subaponeurotic space
Covers the entire cranial vault
Large enough to hold an infant’s entire blood volume
A i d i h i d d li i Associated with vacuum assisted deliveries
Mortality rate as high as 22%
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Subgaleal Hemorrhage Initial symptoms are vague
Generalized scalp edema and ecchymosis
Ballottable
Periorbital and periauricular edema
M t i t May progress to serious symptoms
Diagnosis
Based on clinical symptoms
CT or MRI confirms diagnosis
Treatment
Careful monitoring
Transfusion of blood products
Prognosis
Subgaleal Hemorrhage
Subgaleal Hemorrhage
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Subarachnoid Hemorrhage The most common intracranial hemorrhage
Bleeding into the subarachnoid space from ruptured vessels
Relatively benign and often asymptomatic
Transient seizure activity on day 2‐3
Abnormal neurologic examination
Generally have an excellent prognosis
Massive hemorrhages occasionally develop
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Subdural Hemorrhage Hemorrhage between the dura and the arachnoid
Overstretching of blood vessels during a difficult delivery
Severity ranges from asymptomatic lesions to massive y g y phemorrhage
Presents within the first 12 to 72 hours
Symptoms
Seizures and neurologic changes
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Subdural Hemorrhage Diagnosis is either CT or MRI
Treatment Varies depending upon location, extent, and progression
Small hemorrhages require careful assessment
d % f Surgery required in 30‐50% of cases
Prognosis
Depends on the extent and severity
Ranges from complete recovery to rapid deterioration and death
Facial Nerve Palsy Injury to the facial nerve
Diagnosis Drooping mouth Perpetually open eye Ineffective suck and swallowing problems Ineffective suck and swallowing problems Persistent drooling
Treatment – Patching and lubricating eye drops– Initial improvement occurs within days– Full recovery may take weeks to months – Surgical intervention may be necessary
Facial Nerve Palsy Brachial Plexus Injury Injury of the upper brachial plexis from C5 to C8 and T1
Due to lateral traction of the neck
Erb’s palsy
– Upper cervical nerves (C5‐C6)
– Paralysis of the arm and shoulder
– Hand muscles remain intact
– Arm lies adducted, prone and internally rotated
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Brachial Plexus Brachial Palsy Injury
Erbs Palsy Brachial Plexus Injury Klumpke’s palsy
– Injury to nerve roots C6 to T1
– Normal upper arm and shoulder movement
– Paralysis of the wrist and hand
Injury to the entire brachial plexus
– Paralysis of the entire upper extremity
– Concurrent sensory loss
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Brachial Plexus Injury Treatment Conservative treatment
– Physical therapy
– 30% of brachial plexus injuries completely recover
Surgical intervention Prognosis Prognosis
– Dependent on degree and location of damage– Full spontaneous recovery if some improvement within 2 weeks
– Partial recovery if initial improvement is delayed until 4 to 6 weeks
– Significant permanent deficit if no improvement by 3 months
Craniosynostosis Premature closure of cranial sutures leading to an
abnormally shaped head
Scaphocephaly
Premature closure of the sagittal sutures
Elongates in the occipitofrontal diameter Elongates in the occipitofrontal diameter
Brachycephaly
Premature closure of the coronal sutures
Overgrowth of the vertex and lateral aspects of the head
Cranial Sutures Scaphocephaly
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Brachycephaly Craniocynostosis Diagnosis
CT
Palpate for sutural ridge
Treatment Surger to remo e a strip of bone Surgery to remove a strip of bone
Neural Tube Defects Failure of the neural folds to fuse and form the
neural tube
Secondary malformations of the skeletal structure and skin
Wide spectrum of abnormalities Wide spectrum of abnormalities
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N l b
Rostral neuropore closing
Forebrain prominence
Heart prominenceRostral neuropore
Neural groove
W.B. Saunders Company items and derived items Copyright (c) 1999 by W.B. Saunders Company
Neural tubeSomites
Connecting stalk
Yolk stalk
A B
Somites
AmnionCaudal neuropore
Caudal neuropore
Spina Bifida Occulta A defect in the vertebral arch
Usually presents as a small dimple with a tuft of hair
Membranes don’t externally protrude
Usually asymptomatic but significant defects of the y y p gspinal cord can occur
Spinal Bifida Occulta Spina Bifida Cystica Protrusion of the spinal cord and/or meninges
through a defect in the arch
May occur anywhere along the vertebral column
Most common in the lumbar region
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Spina Bifida Cystica Menigocele (25%)
Sac contains the meninges
Spinal cord in normal position
A dermal covering presentg
Defective axial skeleton
Prognosis
Usually normal
Spinal cord abnormalities are possible
Meningocele
Spina Bifida Cystica Menigomeyelocele (75%)
Sac contains meninges and neural tissue
The spinal cord is a rudimentary neural tube
Clinical manifestations Clinical manifestations
Dependent on the level of the defect
Functional abnormalities are inferior to the defect
69% in the lumbar region
Paralysis
Loss of sensation
Sphincter paralysis
Meningomyelocele
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Types of Spina Bifida Arnold‐Chiari Malformation Displacement of the medulla oblongata, the fourth
ventricle and some of the cerebellum into the cervical canal
CSF flow is impaired
Diagnosed by CT or MRI
Arnold Chiari MalformationTreatment
Prone position, sterile wrap, antibiotics
Surgery within 24‐48 hours
Treat hydrocephalus
Multidisciplinary approach
Goal: assist each child to develop maximum function and independence
Family counseling Long term prognosis
Genetic counseling
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Prognosis Dependent on the level of the lesion
14% mortality
73% of survivors have IQ >85
87% ambulatory
90% lack bowel and bladder control
Rachischisis Open spinal cord
Failure of neural folds to fuse
Often associated with anencephaly
Rachischisis Congenital Anomalies of the Brain Fairly common due to complex neural
embryology
3:1000
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Cranial Meningocele
Contains only the
meninges
Encephalocele
Affects the meninges and part of the brain
60% are occipital
Can be frontonasal, intranasal, nasopharnyx
Diagnosis
Obvious at birth
CT to assess for other brain abnormalities
Treatment
Prognosis
Encephalocele Anencephaly Failure of the rostral neuropore to close
Missing forebrain
Remainder of the brain is degenerative
Absent cranial vault
50% open spinal cord 50% open spinal cord
Stereotypical movements
Spontaneous/pain induced movements
Intact reflexes
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Anencephaly
Anencephaly Diagnosis
Obvious at birth
Increased alpha fetoprotein
Prenatal ultrasound
Polyhydramnios
Post term delivery
Supportive treatment
Hydranencephaly Complete or nearly complete absence of the cerebral hemispheres
Intact brain stem
Etiology Severe hydrocephaly Severe hydrocephaly
Inutero infection
Vascular occlusion
Clinical manifestations May appear normal at birth
Irritability/Hyper/hypotonia
Intact reflexes
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Hydranencephaly
Prognosis
Usually die early in infancy
No cognitive d ldevelopment
Hydranencephaly
Holoprosencephaly Affect the midfacial region and brain
Failure of the prosencephalon to cleave
Olfactory and optic bulbs
Telencephalon and diencephalon
Wall Cavity
Forebrain(prosencephalon)
Telencephalon
Walls
Cerebralhemispheres
Thalam, etc.
5 Secondaryvesicles
3 Primaryvesicles
Diencephalon
W.B. Saunders Company items and derived items Copyright (c) 1999 by W.B. Saunders Company
Midbrain
Pons
Cerebellum
Medulla
Spinal cord
Diencephalon
Mesencephalon
Metencephalon
Myelencephalon
Midbrain(mesencephalon)
Hindbrain(rhombencephalon)
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Hindbrain Cerebral hemisphere Cerebellum
Midbrain
W.B. Saunders Company items and derived items Copyright (c) 1999 by W.B. Saunders Company
Forebrain Optic cup Olfactory bulb Optic nerve
A B
Slide 18.18
Holoprosencephaly
Clinical manifestations
Wide spectrum
Single or divided eye in a single orbit
Arhinia (absent nose)
Proboscis (fleshy nose‐like appendage) Proboscis (fleshy nose like appendage)
Alobar brain
Holoprosencephaly
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Microcephaly Definition > 2 SD below the mean
Etiology
Small brain = small cranium
Chromosomal abnormalities
TORCH infections
Cerebral atrophy
Perinatal infections
Metabolic causes
Microcephaly Lissencephaly
Near‐total or total absence of cerebral convolutions (agyria)
Pachygyria
few broad gyri and shallow sulci
Lissencephaly
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Microcephaly Clinical manifestations
Small or absent anterior fontanel
Round head
Recessed/sloped forehead
l d Mental retardation
Microcephaly
MicrocephalyHydrocephaly
Imbalance between CSF production and absorption
Excessive CSF in the ventricular system
Excess formation of CSF (Choroids plexus tumor)
Decreased absorption of CSF
Ob t ti f fl Obstruction of flow
Dilated ventricles may compress brain tissue
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Hydrocephalus Hydrocephalus
Hydrocephalus Communicating
Obstruction occurs after CSF exits the ventricles
Noncommunicating
Obstruction occurs along the passages connecting the t i lventricles
Hydrocephalus Etiology
Aqueductal stenosis
Arnold‐chiari malformation
IVH
Tumor
Infection
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Aquaductal Stenosis Hydrocephalus Diagnosis Head circumference
Transillumination
Ultrasound
CT MRI CT or MRI
Treatment – VP shunt Drains CSF from ventricles into peritoneum
Complications Infection
Disconnection
Ventricular Access Device
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Periventricular/Intraventricular Hemorrhage
Incidence
Increasing
25 to 30% of VLBW infants
Most common in the first 12 hours
50% by 24 hours
90% by 72 hours
Subependymal Germinal Matrix
Most common area of origination
Beneath the ventricular wall
Produces glial cells and neurons
Most prominent between 24‐32 weeks
Primitive and highly vascular Primitive and highly vascular
Vessels are immature
Lack muscle and collagen
Susceptible to injury
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Germinal Matrix
Bleeding into germinal matrix
Hematoma forms
Blood is released into Blood is released into ventricular system if the hematoma ruptures
Intraventricular Hemorrhage Catastrophic
Acute presentation
Rapid and severe
Neurologic and systemic deterioration
Hi h li High mortality
Salutatory Evolves over hours to days
Changes in neurologic status
Silent (50%) No overt deterioration
Classification
Papile’s classification Grade I – bleeding into the germinal matrix
Grade II – rupture into the ventricles without ventricular enlargement g
Grade III – ventricles are completely filled and at least one lateral ventricle is enlarged
Intraventricular Hemorrhage
Volpe’s classification Grade I – bleeding into the germinal matrix
Grade II – blood fills less than 50% of the ventricle
Grade III blood fills over 50% of the ventricle Grade III – blood fills over 50% of the ventricle
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Grade I Grade II
Grade III Grade III With Enlarged Ventricles
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Grade IV Hemorrhage Hemorrhagic necrosis of the periventricular
white matter
67% unilateral
80% associated with a large IVH
Hemorrhage due to venous infarction from obstructed blood flow
Grade IV IVHGERMINAL MATRIX HEMORRHAGE
PERIVENTRICULAR VENOUS CONGESTION
PERIVENTRICULAR ISCHEMIA
PERIVENTRICULAR HEMORRHAGIC INFARCTION
Grade IV Pathogenesis of IVH
Fluctuating cerebral blood flow
Lack of autoregulation
Pressure‐passive cerebral circulation
Related to prematurity, asphyxia, hypoxia, p y, p y , yp ,hypercapnea
Arterial hypotension
Ischemia, injury and subsequent rupture of the capillary wall
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Pathogenesis of IVH Increased venous pressure impedes cerebral venous
return causing venous congestion
Heart failure, PPV, high CPAP, labor and delivery
Excess fibrinolytic activity
Platelet and coagulation disturbances
Inflammatory cytokines
Risk Factors for IVH Prematurity Respiratory distress Pneumothorax Asphyxia SeizuresSeizures Apnea Manipulation (tracheal suctioning, positioning,
handling) Rapid infusion of IV fluids/colloids Clotting disorders Breathing out of sync with the ventilator
Diagnosis Clinical
Decreased hematocrit
Bulging fontanele
Change in level of consciousnessg
Ultrasound
Prognosis Grade I + II
Similar to infants with no IVH
Increased risk for learning problems
Grade III
40% have major disabilities
% h h l d ff l 50% have school difficulties
Grade IV
Mortality is 40%
75% risk of neurologic impairment
CP
Low cognitive scores
Seizures
Visual disturbances
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Posthemorrhagic Hydrocephalus
Pathogenesis
Blood clot obstruction
Obstructive inflammation and scarring
Incidence
50% transient venticulomegaly
50% require treatment
Occurs within 4 weeks Monitoring Weekly cranial ultrasound Serial head circumferences
Posthemorrhagic HydrocephalusTreatment
Goals Maintain normal ICP Prevent compression of the periventricular white
matterS b l f Sustain cerebral perfusion
Serial LPs
VP shunts
50% resolve with no treatment
Prenatal Prevention of IVH
Prevention of prematurity
Good luck with this one!
Prenatal transport
Antenatal corticosteriods
Matures blood vessels in the germinal matrix
Decreases incidence by 50%
Postnatal Prevention of IVH Appropriate neonatal resuscitation
Correction/prevention of hemodynamic disturbances
Avoidance of shifts in CBF
Correction of coagulationg
Indomethacin and Ibuprophen Decreases CBF and CBF fluctuations by inhibiting
prostaglandin synthesis
Prostaglandin is important in control of CBF control
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Periventricular Leukomalacia Occurs only in premature infants
Incidence
4‐26% of infants < 1500 grams
27‐30 weeks have highest incidence
Ri k f Risk factors
Often associated with an IVH
Evidence of infective component
PROM > 12 hours
Intra‐uterine infection
PROM + chorio = highest incidence
Pathogenesis of PVL Ischemic lesion
Periventricular white matter necrosis Watershed blood supply
High metabolic rate
Small cysts in white matter Small cysts in white matter
Diagnosis Periventricular echodensities on ultrasound
Ultrasound only detects 40‐60%
MRI
Treatment
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Prognosis Cerebral palsy
Lower limbs
Developmental delays
Hypoxic Ischemic Encephalopathy
Major cause of acute mortality and chronic neurologic disability
Occurs in both term and preterm infants
10‐15% mortality
40% of survivors have permanent handicaps
Mental retardation
Cerebral palsy
Learning disabilities
Epilepsy
Etiology Placental, fetal or maternal 50% predicted by antenatal/perinatal history
Decreased fetal movement Abnormal NST Abnormal biophysical profile Scalp pH Scalp pH Abnormal FHR MSF Decreased amniotic fluid
Effects of HIE Conversion to anaerobic metabolism
Rapid depletion of ATP
Accumulation of lactic acid
Failure of normal metabolic activity
Intracellular pump function failureA l i f di l i d i b i ll Accumulation of sodium, calcium and water in brain cells
Cellular death
Accumulation of fatty acids and free radicals
Excess release of neurotoxic excitatory neurotransmitters
Cell apoptosis
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Phases of HIE Early phase
Decreased brain temperature
Local release of the neurotransmitter GABA
Temporarily decrease cerebral oxygen demand and limit impact
Latent phase Intervention may be effective
Secondary phase of Injury
Apoptosis – programmed cell death
Sarnat Stages A clinical staging tool for HIE
Developed for use in full term infants
Provides information for optimal medical management g
Predicts neurologic prognosis
Sarnat Stages Clinical Manifestations
Depends on severity, timing and duration
Seizures 50‐70%
First 24 hours
E li h i di Earlier the seizure = more severe disease
May be refractory
Abnormal respiration
Abnormal positioning/tone
Irritability
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Clinical Manifestations
Impaired glucose delivery and metabolism
Anaerobic metabolism
Renal failure
Myocardial dysfunction Myocardial dysfunction
Decreased cardiac output
Clinical Manifestations Pulmonary involvement
PPHN
Pulmonary edema
Respiratory depression
P l h h Pulmonary hemorrhage
Surfactant inactivation
Clinical Manifestations Liver
Impaired liver function
Clotting disorders
GI Changes in GI motilityg y
Mucosal damage
NEC
Heme DIC
Decreased clotting factors
Thrombocytopenia
Brain Imaging Early (2‐4 days)
Cerebral edema
Decreased tissue attenuation
Late (2‐4 weeks)
Encephalomalacia
Cerebral atrophy
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Early CT Encephalomalacia
Management Delivery room resuscitation
Maintain ventilation
Maintain oxygenation
Maintain perfusion Maintain perfusion
Correction of acidosis
Inhibits surfactant production
Increases pulmonary vascular resistance
Reduces myocardial contractility
Management Monitor for renal impairment
Treat DIC
Monitor electrolytes
Maintain normal metabolic state
May require 9‐15 meq/kg/min glucose
Increased calcium requirements
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Management Control seizures
Control cerebral edema
Fluid restriction
Hyperventilation
Diuretics
Withdrawal of treatment
Hypothermia
Insult Primary Neuronal Death
Opportunity for Opportunity for Neuronal Rescue
Delayed Neuronal Death
Hypothermia Evidence is compelling
Effective in mild to moderate HIE
Decreases rate of cellular death
D ll l b li Decreases cellular metabolism
Conserves ATP stores
Limits free radical release
Hypothermia Criteria vary among institutions
Initiate less than 6 hours after insult
Continue for 48‐72 hours
Cool to approximately 34‐35 degrees
Rewarm over 12‐24 hours
Complications Decreased heart rate, cardiac output and stroke
volume
Renal impairment
Acid‐base and electrolyte abnormalities
Coagulation abnormalities
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Prognosis Indicators of poor outcome
Apgars less than 3 at 10 minutes Early onset and/or refractory seizures Abnormal neurologic signs at discharge Persistently abnormal CT Markedly abnormal EEG or an abnormal EEG after 3 Markedly abnormal EEG or an abnormal EEG after 3
days
Indicators of normal outcome
Normal neuro exam within the first week
Normal EEG within 3 days
Neonatal Seizures Symptom of neurologic dysfunction
Excessive simultaneous electrical discharge or depolarization
Excessive excitatory amino acid release
fi i i hibi i (i GA A) Deficient inhibitory neurotransmitters (ie GABA)
Critical to recognize, determine etiology and treat
May represent significant illness needing treatment
Interference with supportive measures
Can cause brain injury
Etiology of Seizures HIE
Most common cause
Subtle, multifocal clonic or focal clonic
Intracranial/intraventricular hemorrhage
Subarachnoid hemorrhage
Subdural hemorrhage
Arterial or venous stroke
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Etiology of Seizures Metabolic disturbance
Hypoglycemia
Hypocalcemia
Hyponatremia
Hypernatremia Hypernatremia
Inborn errors of metabolism
Etiology of Seizures Intracranial Infection
Bacterial
Toxoplasmosis
CMV
Herpes
Developmental Defects
Migrational abnormalities
Cerebral cortical dysgenesis
Drug withdrawal
Etiology of Seizures Benign familial neonatal seizures
First 48‐72 hours
Positive family history
Normal development
Benign idiopathic neonatal seizures
Fifth‐day fits
Day 4‐6
Normal development
Classification of Seizures Subtle
Ocular phenomena Horizontal deviation +/‐ jerking of eyes Sustained eye opening with ocular fixation
O l b l li l Oral‐buccal‐lingual movements Rowing of arms or pedaling Autonomic changes
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Classification of Seizures Clonic Rhythmic Slow (1‐3 jerks/sec)
Focal clonicF d/ l i i id Face, upper and/or lower extremities on 1 side
OR Axial structures (neck or trunk) on one side
Multifocal clonic Several body parts in a migrating fashion Seen in term infants
Classification of Seizures Classic Generalized clonic seizures
Bilateral symmetric and synchronous movements
Rare in neonate
Diagnosis HISTORY, HISTORY, HISTORY
Electrolytes
Sepsis workup including LP
Ultrasound/CTUltrasound/CT
EEG
80% of neonatal seizures are not seen on EEG
Electrical seizures may not correlate with clinical seizures
Video EEG
aEEG
Treatment Treat underlying etiology
Medications
Phenobarbitol
Phosphyntoin
Benzodiazepines
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Prognosis
Prognosis and etiology are interdependent
Controlling seizures improves outcome
Sequelae include Developmental delays
Motor deficits
Persistent seizures
Meningitis Inflammation of the membranes lining the brain
and the spinal column
Dura mater, pia mater, arachnoid
Purulent exudate covering the meninges and ventricles ventricles
FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
B2: NEUROLOGY REVIEW Page 40 of 41
Clinical Presentation Nonspecific symptoms of infection
Irritability
Lethargy
Increased ICP (bulging fontanele, HTN, tremors)( g g , , )
Persistent and severe vomiting
Seizures (20‐50%)
Diagnosis Who do we tap? – controversial
Abnormal CSF findings
> 30 wbc (> 60% PMNs)
Glucose (50% serum)
Protein >100 mg/dl Protein >100 mg/dl
Positive culture/gram stain
Treatment and Prognosis 2‐3 weeks of antibiotics
Repeat CSF studies until sterile
Prognosis 20‐50% have permanent sequlae
Hearing/speech difficulties Hearing/speech difficulties
Hydrocephaly
Blindness
Seizures
Mental retardation
Cerebral palsy
The End
Questions?
FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
B2: NEUROLOGY REVIEW Page 41 of 41