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Neonatal Encephalopathy
Julie Parsons, M.D
Assistant Professor, Pediatric Neurology
November 19, 2009
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Disclosures
PTC Therapeutics PTC 124 Clinical Trial for Duchenne Muscular Dystrophy
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Objectives
To promote understanding between legal and medical professionals
To explain the role of a pediatric neurologist To define neonatal encephalopathy To define cerebral palsy To explore the relationship between neonatal
encephalopathy and cerebral palsy
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Pediatric Neurologist
A pediatric subspecialist whose expertise is diagnosing and treating disorders in the developing nervous system
This requires completion of a five year residency training program
Board Certification through the American Board of Psychiatry and Neurology Special Qualification in Child Neurology
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The Top 10 Neurologic Conditions 1. Attention Deficit Hyperactivity Disorder 2. Seizures and epilepsy 3. Developmental Delay 4. Headache 5. Newborn disorder 6. Mental Retardation 7. Macrocephaly/Microcephaly 8. Motor disturbance 9. Central Nervous system infection 10. Neuromuscular Disturbance
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Neonatal Encephalopathy A depression in mental status or alteration of
consciousness Seizures Abnormal muscle tone and reflexes Abnormal respiratory function
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Risk Factors for Neonatal Encephalopathy Increased maternal age Family history of neurologic problems Maternal thyroid disease or other autoimmune
disorder Coagulopathy or thrombotic disorders Maternal hypertension Vaginal bleeding Maternal infection Infertility Intrauterine growth restriction
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Sarnat StagingStage 1:Mild Stage 2:
ModerateStage 3: Severe
Level of consciousness
Excessively irritable or somnolent, but awakens with light stimulation
Unarousable, but withdraws purposefully
Comatose, minimal if any response to pain
Brainstem and Autonomic function
No brainstem deficits. Sympathetic predominance
Parasympathetic predominance
Depressed or absent brainstem reflexes. Disordered breathing
Motor Function Tone normal to increased
Generalized hypotonia
Flaccid
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Sarnat StagingStage 1: Mild Stage 2:
ModerateStage 3: Severe
Reflex abnormality
Exaggerated deep tendon reflexes
Exaggerated deep tendon reflexes: depressed neonatal reflex behaviors
Depressed or absent deep tendon reflexes: absent neonatal reflex behaviors
Paroxysmal Movements
Seizures or myoclonus
Sarnat and Sarnat, 1976
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Correlation of Severity of Clinical Abnormalities and OutcomeSeverity of Encephalopathy % with abnormal outcome
MildJittery, increased irritability and DTRs, exaggerated Moro response
0%
ModerateLethargy, hypotonia, suppressed DTRs, + or – seizures
20 % to 40%
SevereComa, hypotonia, seizures, brainstem and autonomic dysfunction, + elevated intracranial pressure
100%
Sarnat and Sarnat 1976; Volpe 1995
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Sarnat and Sarnat Staging
Stage 3 More than 7 days at Stage 2 Both associated with poor neurologic prognosis
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Hypoxic Ischemic Encephalopathy
Hypoxia= Lack of Oxygen Ischemia= Lack of Perfusion
Hypoxic Ischemic Encephalopathy is caused by a combination resulting in a decreased supply of oxygen to cerebral tissue
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Hypoxic Ischemic Encephalopathy Recognizable Pattern of Progression
1st 12 hours—bilateral hemispheric involvement leads to decreased level of consciousness
12 to 24 hours—”apparent improvement” in level of consciousness, but may have seizures which are often refractory
24 to 72 hours—worsening brainstem dysfunction with altered eye movements, abnormal pupillary response, apnea, bulbar dysfunction (may result in death)
Persistent dysfunction may indicate thalamic or basal ganglia involvement which usually predicts poor prognosis
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Diagnosis of HIE: History
Complications of pregnancy, labor, delivery Placenta previa, cord prolapse, placental abruption,
maternal shock Presence of meconium Placental condition
chorioamnionitis Apgar scores (<3 at 5 minutes) Acid Base status (cord pH <7, BE -12) Evidence of multiorgan system involvement
Kidney, liver, heart
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Differential Diagnosis: Neonatal Encephalopathy
Sepsis Meningitis Sedation Neuromuscular Disease Trauma Metabolic
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Sepsis Common antecedent to low Apgar scores and
depression Hypotension Seizures Meconium Aspiration Chorioamnionitis Bacterial Infections—Meningitis or Group B Strep
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Sepsis Inflammation
Release of cytokines Widespread endothelial injury
Coagulopathies Germinal matrix injury Intraventricular hemorrhage Stroke
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Metabolic Disorders
Biochemical Derangements Hypoglycemia Hypocalcemia Hyponatremia Hyperammonemia Acidosis
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Metabolic Disorders
Inborn Errors of Metabolism Symptoms after hours or days of appearing normal Prominent unexplained vomiting Hyperpnea in absence of lung disease Unusual Odor Family history , or excess fetal loss Physical Exam findings: cataracts, hepatosplenomegaly
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Diagnosis of HIE: EEG Characteristic Sequence Initially marked suppression of amplitude and
slowing 24 to 48 hours discontinuous pattern of burst
suppression May deteriorate to isoelectric Rapid resolution of abnormalities favors good
prognosis
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Burst Suppression EEG
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Diagnosis of HIE: Imaging
Cranial Ultrasound—increased echogenicity and effacement of sulci although 50% read as normal
Computerized Tomography (CT) 2 to 5 days maximal extent of parenchymal hypodensities Atrophy or multicystic encephalomalacia develops later
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Diagnosis of HIE: MRI
T2 prolongation 12 to 18 hours-transient edema T1 high signal after 3 days T2 shortening after 6 to 7 days denotes permanent
injury DWI (diffusion weighted imaging) more sensitive
especially in signaling injury to the thalami and basal ganglia. Maximum sensitivity at 2 to 4 days
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Neuropathology
Parasagittal Injury (>34 wks)– spastic quadriplegia Periventricular White Matter in preterm—spastic
diplegia Basal Ganglia—acute, near total ischemia
associated with poor neurologic outcome chorioathetosis and feeding difficulty
Focal/Multifocal– reflects the area of injury Selective Neuronal Necrosis—HIE
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Normal Cranial CT Scan
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Cerebral Edema on Cranial CT Scan
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Hypoxic Ischemic EncephalopathyBasal Ganglia Injury
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Hypoxic Ischemic EncephalopathySevere Global Injury
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Cerebral Palsy
A chronic neuromuscular disability of central nervous system origin, characterized by abnormal control of movement or posture appearing early in life and not the result of a progressive disease Intellectual , sensory or behavior problems may
accompany but are not a part of the diagnosis Only 10-15% of children with CP have a history of
severe hypoxic ischemic encephalopathy (NCPP)
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Diagnosis of Cerebral Palsy
Delayed Milestones Persistence of developmental reflexes Pathologic Reflexes Failure to develop maturational reflexes No progression or loss of skills by history
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Type of Cerebral Palsy
Spastic Choreoathetotic Ataxic Dystonic Ballismic Mixed
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Clinical Syndromes
Spastic Quadriplegia is the form of CP most commonly associated with Hypoxic Ischemic Encephalopathy
Spastic Hemiparesis is associated with stroke
Athetosis is associated with kernicterus
About 30% of children with CP have a brain malformation or cortical dysgenesis
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Homunculus
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Association of Neonatal Encephalopathy and CP In <10% of children with CP or MR was there an
association with intrapartum or perinatal asphyxia 75% of children with CP had normal Apgar scores Apgar < 3 at 15 min 36% with CP at 20 min 57% with CP Persistently low Apgar scores at 10, 15, 20 min are
associated with poor neurologic outcome
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Criteria for Exposure Birth Asphyxia
Clinical history Clinical Markers
Abnormal fetal heart rate Meconium
Laboratory Markers Fetal Acidosis (cord pH)
Newborn Status Apgars Encephalopathy
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Conclusions ACOG guidelines provide a reasonable framework There is an association between HIE and CP Neonatal Encephalopathy is a non specific clinical
syndrome Neonatal Encephalopathy must be documented to
consider HIE as causation for CP Continued scientific studies are needed to further
understand etiologies of CP