Neonatal Encephalopathy - PowerPoint PPT Presentation

Neonatal encephalopathy
1 / 36

  • Uploaded on
  • Presentation posted in: General

Neonatal Encephalopathy. Julie Parsons, M.D Assistant Professor, Pediatric Neurology November 19, 2009. Disclosures. PTC Therapeutics PTC 124 Clinical Trial for Duchenne Muscular Dystrophy. Objectives. To promote understanding between legal and medical professionals

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.

Download Presentation

Neonatal Encephalopathy

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript

Neonatal encephalopathy


Julie Parsons, M.D

Assistant Professor, Pediatric Neurology

November 19, 2009



  • PTC Therapeutics

    • PTC 124 Clinical Trial for Duchenne Muscular Dystrophy



  • 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

Pediatric neurologist

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

The top 10 neurologic conditions

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

Neonatal encephalopathy1

Neonatal Encephalopathy

  • A depression in mental status or alteration of consciousness

  • Seizures

  • Abnormal muscle tone and reflexes

  • Abnormal respiratory function

Risk factors for neonatal encephalopathy

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

Sarnat staging

Sarnat Staging

Sarnat staging1

Sarnat Staging

Sarnat and Sarnat, 1976

Correlation of severity of clinical abnormalities and outcome

Correlation of Severity of Clinical Abnormalities and Outcome

Sarnat and Sarnat 1976; Volpe 1995

Sarnat and sarnat staging

Sarnat and Sarnat Staging

  • Stage 3

  • More than 7 days at Stage 2

  • Both associated with poor neurologic prognosis

Hypoxic ischemic encephalopathy

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

Hypoxic ischemic encephalopathy1

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

Diagnosis of hie history

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

Differential diagnosis neonatal encephalopathy

Differential Diagnosis: Neonatal Encephalopathy

  • Sepsis

  • Meningitis

  • Sedation

  • Neuromuscular Disease

  • Trauma

  • Metabolic



  • Common antecedent to low Apgar scores and depression

  • Hypotension

  • Seizures

  • Meconium Aspiration

  • Chorioamnionitis

  • Bacterial Infections—Meningitis or Group B Strep



  • Inflammation

    • Release of cytokines

    • Widespread endothelial injury

  • Coagulopathies

    • Germinal matrix injury

    • Intraventricular hemorrhage

    • Stroke

Metabolic disorders

Metabolic Disorders

  • Biochemical Derangements

    • Hypoglycemia

    • Hypocalcemia

    • Hyponatremia

    • Hyperammonemia

    • Acidosis

Metabolic disorders1

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

Diagnosis of hie eeg

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

Burst suppression eeg

Burst Suppression EEG

Diagnosis of hie imaging

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

Diagnosis of hie mri

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



  • 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

Normal cranial ct scan

Normal Cranial CT Scan

Cerebral edema on cranial ct scan

Cerebral Edema on Cranial CT Scan

Hypoxic ischemic encephalopathy basal ganglia injury

Hypoxic Ischemic EncephalopathyBasal Ganglia Injury

Hypoxic ischemic encephalopathy severe global injury

Hypoxic Ischemic EncephalopathySevere Global Injury

Cerebral palsy

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)

Diagnosis of cerebral palsy

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

Type of cerebral palsy

Type of Cerebral Palsy

  • Spastic

  • Choreoathetotic

  • Ataxic

  • Dystonic

  • Ballismic

  • Mixed

Clinical syndromes

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



Association of neonatal encephalopathy and cp

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

Criteria for exposure

Criteria for Exposure

  • Birth Asphyxia

    • Clinical history

  • Clinical Markers

    • Abnormal fetal heart rate

    • Meconium

  • Laboratory Markers

    • Fetal Acidosis (cord pH)

  • Newborn Status

    • Apgars

    • Encephalopathy



  • 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

  • Login