Neonatal Encephalopathy
Mary E. D’Alton, MDMary E. D’Alton, MDWillard C. Rappleye Professor of Obstetrics & GynecologyWillard C. Rappleye Professor of Obstetrics & Gynecology
New York Presbyterian HospitalNew York Presbyterian Hospital
Columbia University College of Physicians & SurgeonsColumbia University College of Physicians & Surgeons
Facts
• CP rate 1.5/1000
• No change in last 40 years
• No geographic/economic boundaries
Clark S, Hankins GDV. AJOG 2003
0
5
10
15
20
25
1970 1975 1980 1985 1990 1995 2000
Cesarean Section Rate
Cerebral Palsy Rate
Charge by Dr. Frank Miller
“To create a multidisciplinary task force to
review and consider the current state of
scientific knowledge about the mechanisms
and timing of possible etiologic events which
may result in neonatal encephalopathy and
cerebral palsy.”
Task Force on Neonatal Encephalopathy and Cerebral Palsy Committee Members
Gary Hankins, MD, FACOG, Chair
Mary D’Alton, MD, FACOG
Mark Ira Evans, MD, FACOG
Larry Gilstrap, MD, FACOG
Richard Depp, III, MD, FACOG
Roger K. Freeman, MD, FACOG
Richard P. Green, MD, FACOG
Task Force on Neonatal Encephalopathy and Cerebral Palsy Committee Members
James A. McGregor, MD, FACOG
Karin B. Nelson, MD
Susan Ramin, MD, FACOG
Robert Resnik, MD, FACOG
Michael Speer, MD
Louis Weinstein, MD, FACOG
Stanley Zinberg, MD, MS
Neonatal Encephalopathy andCerebral Palsy Task Force Consultants
James Barkovich, MD – Professor of Radiology, Neurology, Pediatrics, and Neurosurgery
Kurt Benirschke, MD – Professor Emeritus of Pathology and Reproductive Medicine
Robert R. Clancy, MD – Professor of Neurology and Pediatrics, Pediatric Regional Epilepsy Program
Gabrielle A. DeVeber, MD – Director, Canadian Pediatric Ischemic Stroke Registry
Ronald Gibbs, MD – Professor and Chairman, OB/Gyn
Gregory Locksmith, MD – Assistant Professor, OB/Gyn
Neonatal Encephalopathy andCerebral Palsy Task Force Consultants
Jeffrey Perlman, MD, PhD – Professor of Pediatrics and OB/Gyn
Julian N. Robinson, MD – Assistant Professor, OB/Gyn
Dwight J. Rouse, MD – Associate Professor, OB/Gyn George R. Saade, MD – Professor, OB/Gyn
Diana E. Schendel, PhD – Centers for Disease Control and Prevention
Rodney E. Willoughby, Jr., MD – Associate Professor, Pediatrics
Marjorie R. Grafe, MD – Professor, Placental Pathology
Methods
• Five meetings over 3 years
• Extensive consultation with clinicians and scientists
• Consensus development
• Draft and redraft
Methodology
• Throughout the process, primary source documents were cited to the fullest extent possible.
• Comments solicited from a number of professional organizations:– American Academy of Pediatrics– The Canadian Paediatric Society– The Child Neurology Society– The Society for Maternal-Fetal Medicine– The March of Dimes Birth Defects Foundation
• The Centers for Disease Control and Prevention, Department of Health and Human Services
• The National Institute of Child Health and Human Development
• The Royal Australian and New Zealand College of Obstetricians and Gynaecologists
• The Society of Obstetricians and Gynaecologists of Canada.
Methodology
Most Peer-Reviewed Document
on the Subject
Neonatal Encephalopathy – “A clinically defined syndrome of disturbed neurological function in the infant at or near term during
the first week after birth, manifested by difficulty with initiating and maintaining
respiration, depression of tone and reflexes, altered level of consciousness,
and often seizures.”
Differential Dx: Neonatal Encephalopathy
• Developmental abnormalities
• Metabolic abnormalities
• Autoimmune disorders
• Coagulation disorders
• Infections
• Trauma
• Hypoxia
• IUGR
• Multiple gestations
• Antepartum hemorrhage
• Chromosomal abnormalities
• Persistent breech/transverse lie
Blair, Devel Med Child Neurol 35:449
On the Diagnosis of Birth Asphyxia
• Relies on:– Clinical markers of fetal distress (MSAF/Abn FHR)– Laboratory markers (Cord pH or base excess)– Newborn status (Apgars, time to respirations)
• No data to support:– Equivalence of criteria– Specificity to intrapartum asphyxia
• Potential for misclassification enormous
Relationship of Intrapartum Asphyxia to Neonatal Encephalopathy and Cerebral Palsy
IntrapartumAsphyxia
NeonatalEncephalopathy
CerebralPalsy
x
“Epidemiological studies suggest that in about 90% of cases of cerebral palsy intrapartum hypoxia could not be the cause of cerebral palsy and in the remaining 10% intrapartum signs compatible with damaging hypoxia may have had antenatal or intrapartum origins.”
Key Publications - ACOG• Committee Opinion #49, Nov 1986/1989
– Use and Misuse of the Apgar Score– Committee on Obstetrics: MFM (ACOG)– Committee on Fetus and Newborn (AAP)
• ACOG Technical Bulletin #163, January 1992– Fetal and Neonatal Neurologic Injury
• Committee on Obstetric Practice #137, April 1994– Fetal Distress and Birth Asphyxia
• Committee on Obstetric Practice #197, Feb 1998– Inappropriate Use of the Terms Fetal Distress and Birth
Asphyxia
Badawi, BMJ 317:1549
Antepartum Risk Factors for Newborn Encephalopathy:
The Western Australian Case-Control Study
• Metropolitan Western Australia June 93-Sept 95• All 164 term infants with moderate/severe encephalopathy• Controls – 400 randomly selected• Stats
– Birth prevalence of moderate/severe newborn encephalopathy 3.8/1000 term live births
– Neonatal Fatality 9.1%• Conclusions
– Causes of newborn encephalopathy are heterogeneous and many of the causal pathways start before birth
Badawi, BMJ 317:1549
3.57
2.97
2.07
3.82
2.23
2.17
2.73
2.55
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
Intrapartum Fever
Mod/Severe Antepartum Bleeding
Viral Illness
Family Hx Neurological Disorder
Family Hx Seizure
Instrumental Delivery
Emergency C/S
Abnormal Placental Appearance
Adjusted Odds Ratio
Preconceptional
Intrapartum
Antepartum
Risk Factors for Newborn Encephalopathy
Badawi, BMJ 317:1549
Risk Factors for Newborn Encephalopathy
9.7
6.3
4.37
4.44
4.29
4.43
0 2 4 6 8 10 12
Maternal ThyroidDisease
Severe Preeclampsia
Acute IntrapartumEvent
Infertility Treatment
IUGR 3-9%tile
OP Presentation
Adjusted Odds Ratio
Preconceptional
Intrapartum
Antepartum
38.23
2.07
0 5 10 15 20 25 30 35 40 45
IUGR <3%tile
Abnormal PlacentalAppearance
Antepartum
Risk Factors for Newborn Encephalopathy
0.17
0.17
00.51
Elective C/S
No Labor
Risk Factors for Newborn Encephalopathy
Badawi, BMJ 317:1557
Distribution of Risk Factors for Newborn Encephalopathy
Antepartum risk factors only (69%)
Antepartum risk factors and intrapartum
hypoxia (25%)
Intrapartum hypoxia only (4%)
Unknown (2%)
Blair & Stanley, J Pediatr 112:515
Intrapartum Asphyxia: A Rare Cause of Cerebral Palsy
“It was estimated that in only 8% (15/183) of all
the children with spastic cerebral palsy was
intrapartum asphyxia the possible cause of their
brain damage.”
Badawi, BMJ 317:1557
Theoretical Scenarios for Timing of Neurological Insult in
Newborn Encephalopathy
Antepartum period Intrapartum period Neonatal period Newborn
outcome
1 Insult Encephalopathy
2 Insult Further Insult Encephalopathy
3 Insult Encephalopathy
4 Insult Encephalopathy
Nelson, NEJM 334:613
Uncertain Value of Electronic Fetal Monitoring in Predicting Cerebral Palsy
• Population– Four California counties 1983-1985– Singleton – Birthweight > 2500 gm– Survival to age 3 and EFM (N=78)– Moderate/severe cerebral palsy
• Abnormal FHR– Multiple late decelerations– Decreased beat to beat
• Controls– Matched appropriately (N=300)
Nelson, NEJM 334:613
Uncertain Value - Continued
PatternCP
N=78ControlN=300 OR
Tachycardia N (%) N (%)
> 160 22 (28.2) 85 (28.3) 1.0 (0.6-1.7)
> 180 5 (6.4) 16 (5.3) 1.3 (0.4-3.4)
Bradycardia
< 100 27 (34.6) 75 (25.0) 1.5 (0.9-2.5)
< 80 13 (16.7) 35 (11.7) 1.5 (0.8-3.0)
Multiple Lates 11 (14.1) 12 (4.0) 3.9 (1.7-9.3)
Mult. Lates or BTB 21 (26.9) 28 (9.3) 3.6 (1.9-6.7)
NEJM 334:613
Nelson
“The 21 children with cerebral palsy who had
multiple late decelerations or decreased
variability in heart rate monitoring represented
only 0.19 percent of singleton infants with birth
weights of 2500 g or more who had these fetal-
monitoring findings, for a false positive rate of
99.8%.
Extrapolation from Nelson by Hankins
1. Based on multiple lates or persistent decreased beat to beat variability 500 cesarean sections are required to prevent 1 case of cerebral palsy!
2. Future uterine rupture rate 0.5% = 2.5 ruptures
40% risk of neonatal death or CP = 1.0
3. Future risk of previa and accreta 10-20 x RR
4. Excess maternal risk of cesarean– EBL at least doubled– Infection 5-10 x RR– DVT/PE 5 x RR
“It is not possible at the current time to
prospectively recognize during labor
the point in time when a reduction in
cerebral perfusion results in
irreversible brain injury.”
Jeffrey M. Perlman, M.D.
“Any claims to the contrary are not
supported by any scientific merit.”
ACOG Task Force on Neonatal
Encephalopathy and Cerebral Palsy
Key Publications: www.bmj.com
A Template for Defining a Causal Relationship Between Acute Intrapartum Events and Cerebral Palsy
• Method:– Multidisciplinary review of pertinent medical literature– Open to any and all who might add
• Goal:1. Benefit research into causation and prevention of CP2. Help those who offer expert opinion when counseling (parents or
would be parents) or giving opinions in court.
• Participation Invited:– All members Perinatal Society ANZ– International scientific contributors
• Paper redrafted 8 times until consensus reached• Need for timely updates acknowledged
Panel Members Discipline Institution
Alastair MacLennan (Chair) Obstetrics and Gynecology University of Adelaide
Fiona Stanley EpidemiologyInstitute for Child Health Research, Perth
Eve Blair EpidemiologyInstitute for Child Health Research, Perth
Greg Rice Fetal PhysiologyRoyal Women’s Hospital, Melbourne
Peter Stone Obstetrics and Gynecology University of Otago
Jeffrey Robinson Obstetrics and Gynecology University of Adelaide
David Henderson-Smart Perinatal Medicine University of Sydney
Victor Yu Neonatal Intensive Care Monash Medical Centre
Michael Harbord Pediatric Neurologist Flinders Medical Centre
Panel Members Discipline Institution
Leon Stern Pediatric RehabilitationCrippled Children’s Association of South Australia
Helen Chambers Perinatal PathologyWomen’s and Children’s Hospital, Adelaide
Margaret Furness RadiologyWomen’s and Children’s Hospital, Adelaide
Tina Hayward RadiologyWomen’s and Children’s Hospital, Adelaide
Kerena Eckert Midwifery ResearchWomen’s and Children’s Hospital, Adelaide
Christopher Boundy
Barrister and Solicitor Adelaide
Susan Merrett Medical Administrator SA Health Commission
Mark Kenny Medico Legal ServicesWomen’s and Children’s Hospital, Adelaide
International Consensus Conference
Template Criteria to Define an Acute Intrapartum Hypoxic Event
• Essential criteria1. Evidence of a metabolic acidosis in intrapartum
fetal, umbilical arterial cord or very early neonatal blood samples. pH < 7.00 and base deficit > 12 mMol/L and;
2. Early onset of severe or moderate neonatal encephalopathy in infants > 34 weeks gestation and;
3. Cerebral palsy is of the spastic quadriplegic or dyskinetic type.
ACOG/AAP
Criteria Required to Define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy
Essential criteria (must meet all four)
1. Evidence of a metabolic acidosis in fetal, umbilical cord arterial blood obtained at delivery (pH 7.00 and base deficit >12 mmol/L).
2. Early onset of severe or moderate neonatal encephalopathy in infants of 34 or more weeks of gestation.
ACOG/AAP
3. Cerebral palsy of the spastic quadriplegic or dyskinetic type*.
4. Exclusion of other identifiable etiologies such as trauma, coagulation disorders, infectious conditions, or genetic disorders.
Criteria Required to Define an Acute Intrapartum Hypoxic Event as Sufficient to Cause Cerebral Palsy
International Consensus Conference
Criteria That Together Suggest an Intrapartum Timing but by Themselves Are Non-specific
1. A sentinel (signal) hypoxic event occurring immediately before or during labor.
2. A sudden, rapid and sustained deterioration of the fetal heart rate pattern usually following the hypoxic sentinel event where the pattern was previously normal.
3. Apgar scores of 0-6 for longer than 5 minutes.4. Early evidence of multi-system involvement.5. Early imaging evidence of acute cerebral
abnormality.
ACOG/AAP
Criteria That Collectively Suggest an Intrapartum Timing but Are Nonspecific to Asphyxial Insults
1. A sentinel (signal) hypoxic event occurring immediately before or during labor.
2. A sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the presence of persistent, late or variable decelerations, usually after an hypoxic sentinel event when the pattern was previously normal.
ACOG/AAP
3. Apgar scores of 0-3 beyond 5 minutes.
4. Evidence of multi-system involvement up to 72 hours.
5. Early imaging study showing evidence of acute nonfocal cerebral abnormality.
Criteria That Collectively Suggest an Intrapartum Timing but Are Nonspecific to Asphyxial Insults
Need to Educate
• Physicians
• Decision/policy makers
• Public
Conclusion
“This survey identified large knowledge gaps
in this area, suggesting a need to develop
educational projects to address these
deficits by both professional organizations
and individual teachers.”
1. In cases of intrapartum asphyxia sufficient to result in cerebral palsy, injury to organ systems other than the brain most likely to result from:
a) Loss of cerebral vascular autoregulation (15.7)
b) Redistribution of cardiac output (34.3)
c) Diminution in cardiac output (17.2)
d) Don’t know (32.8)
J Perinatol 2005 (34.9)
2. Using electronic fetal heart rate monitoring, it is
possible to prospectively recognize the precise
point in time at which cerebral injury becomes
irreversible following interruption of placental
blood flow.
a) Agree (0.3)
b) Disagree (97.7)
c) Don’t know (2.0)
J Perinatol 2005 (96.4)
3. Required criteria to define an acute intrapartum hypoxic event sufficient to result in cerebral palsy do not include:a) Umbilical arterial cord pH < 7.0 and base deficit
> 12 mmol/L (5.0)
b) Early onset of severe or moderate encephalopathy in infants > 34 wk EGA (16.0)
c) Exclusion of other identifiable etiologies (8.2)
d) Sentinal hypoxic event occurring prior/during labor (42.6)
e) Don’t know (28.3)
J Perinatol 2005 (53.0)
4. In your experience, the most common outcomes for the fetus exposed to an acute catastrophic hypoxic event, but who is born live, is:
a) Neonatal death (10.7)
b) Transient moderate or severe encephalopathy (18.6)
c) Cerebral palsy (4.3)
d) Normal neurologic outcome (65.1)
J Perinatol 2005 (71.2)
5. The most characteristic brain lesion after the death of a co-twin in a monochorionic twin pregnancy is multicystic encephalomalacia. To the best of your knowledge, this is most likely caused by:a) Infection (1.4)
b) Capacitance effect of the dead fetus and hypotension in the surviving twin (42.3)
c) High output cardiac failure of the surviving twin (14.0)
d) Chronic placental abruption (3.7)
e) Don’t know (38.6)
J Perinatol 2005 (55.7)
6. Early imaging studies in the setting of a neonatal encephalopathy may assist in timing the event. Most imaging studies will be able to demonstrate the onset of diagnostic abnormality within…a) 6 h (1.2)b) 24 h (19.2)c) 48 h (14.9)d) 72 h (16.9)e) 7 d (6.1)f) Don’t know (41.7)
7. Randomized controlled clinical trials show
that antepartum fetal testing decreases the
rate of cerebral palsy.
a) Agree (2.0)
b) Disagree (92.6)
c) Don’t know (5.4)
J Perinatol 2005 (92.7)
8. In evaluation of neonatal encephalopathy, do you believe the EEG primarily:a) Is information as to the etiology of the lesion
(2.3)
b) Documents the presence of and severity of the injury (40.8)
c) Rules out an encephalopathy if it is normal (14.7)
d) Can accurately time the occurrence of the injury (1.2)
e) Don’t know (41.0)
J Perinatol 2005 (46.2)
Origin & Timing of Brain Lesions in Term Infants with Neonatal Encephalopathy
• Time: 1 Jan 1992 – 31 Dec 1998• Location: Utrecht, Netherlands
London, England• Population: EGA ≥ 36 weeks
NE or seizures within 72h birth• Recruited: 351 infants
261 met NE criteria
90 seizures within 72h birthCowan, F., et. al., The Lancet, 2003;vol 361:736-742
• Group I – NE defined by abnormal tone pattern, feeding difficulties altered alertness & at least 3 of the following– Late decelerations or MSAF– Delayed onset respirations– Arterial cord blood ph < 7.1– Apgar <7 at 5 minutes– Multi organ failure
Cowan, F., et. al., The Lancet, 2003;vol 361:736-742
• Group II – Seizures within 72h birth but lack NE criteria
• Exclusions:– Major structural anomalies– Major chromosomal abnormalities– Hypothermia
“Proven bacterial or viral infection was not a reason for exclusion”
Cowan, F., et. al., The Lancet, 2003;vol 361:736-742
Group I
Acute Injury Pattern 197/245 (80%) Bilateral 189/197 Focal 8/197
Normal 40/245 (16%)
Findings not compatible with hypoxia 8/245 ( 3%)
Acute hypoxic damage with other disorders 9/245 ( 4%)
Cowan, F., et. al., The Lancet, 2003;vol 361:736-742
MRI Findings in Group I with Neonatal Encephalopathy
Group II
Acute ischemic or hemorrhagic lesions 62/90 (69%)
Concomitant evidence of antenatal injury 2/62 ( 3%)
Focal cerebral infarction 35/62 (56%)
Focal white matter hemorrhage 12/62 (19%)
Extensive parenchymal hemorrhage 8/62 (13%)
Posterior fossa hemorrhage (2), subarachnoid (3) and intraventricular (2) hemorrhage
7/62 (11%)
Cowan, F., et. al., The Lancet, 2003;vol 361:736-742
MRI Findings in Group II with Seizures within 72 Hours of Birth
Interpretation
Although our results cannot exclude the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, our data strongly suggest that events in the immediate perinatal period are most important in neonatal brain injury.
Cowan, F., et. al., The Lancet, 2003;vol 361:736-742
Criticism of Cowan, PhDI. Criteria to define group I
i. Late decels 99% false positive for CPii. MSAF 14-20% of term gestations
II. Umbilical arterial pH <7 ּ1i. Pathologic acidemia agreed by most as <7ּ0ii. Significant number of normal babies can/will have this
level of acidemia. Respiratory versus metabolic?
III. Apgar <7 at 5 minutesWhat is the rate of any of these markers in their general population?
Origin & Timing of Brain Lesions in Term Infants with Neonatal Encephalopathy
• Design: 173 Term newborns with NE• Location: UCSF & Loma Linda
NE or a marker of perinatal depression:– UA pH <7 ּ1– UA base deficit > 10mEq/L– 5 minute Apgar ≤5
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
MRI
• Median – 6 days of age
• Range – 1 - 24 days
• Injury Patterns –1) basal ganglia /thalamus, predominant
2) watershed predominant
3) normal
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
Table I. Clinical characteristics by magnetic resonance imaging pattern
Normal Watershed predominant
Basal ganglia/thalamus
predominant
P value
Number 51 78 44
Male sex 27 (54%) 51 (65%) 24 (56%)
Antenatal
Substance use 8 (16%) 11 (14%) 11 (25%) .3
Gestational diabetes 4 (8%) 9 (12%) 6 (14%) .6
Preeclampsia 2 (4%) 6 (8%) 3 (7%) .7
Prolonged rupture of membranes 6 (12%) 16 (21%) 8 (19%) .4
Intra-uterine growth restriction 0 4 (5%) 2 (5%) .3
Maternal inflammatory state 19 (37%) 35 (45%) 12 (28%) .2
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
Table I. Clinical characteristics by magnetic resonance imaging pattern
Normal Watershed predominant
Basal ganglia/thalamus
predominant
P value
Perinatal
Fetal distress 33 (66%) 51 (66%) 23 (56%) .5
Complicated vaginal delivery 8 (16%) 17 (18%) 10 (23%) .7
Cesarean delivery 24 (47%) 42 (54%) 22 (50%) .7
Emergent Cesarean delivery 18 (75%) 29 (69%) 22 (100%) .006
Placenta/cord insult 16 (31%) 21 (27%) 15 (34%) .7
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
Table I. Clinical characteristics by magnetic resonance imaging pattern
Normal Watershed predominant
Basal ganglia/thalamus
predominant
P value
Postnatal
Gestational age (weeks) 40 (36-42) 40 (36-42) 40 (36-42) .5
Birthweight (kg) 3.5 (2.2-5.2) 3.2 (2.0-5.4) 3.4 (1.6-4.9) .01
Head circumference (cm) 35 (32-38) 35 (31-44) 35 (29-39) .4
Length (cm) 51 (38-56) 51 (41-59) 51 (44-56) .9
Resuscitation score (1-6) 4 (1-6) 4 (2-6) 5 (1-6) .001
Five-minute Apgar score 6 (1-9) 5 (1-9) 4 (0-9) .0005
Meconium aspiration 14 (28%) 17 (22%) 10 (23%) .8
Encephalopathy score (0-6) 2 (0-6) 3 (1-6) 5 (1-6) .0001
Clinical seizures (yes/no) 14 (28%) 34 (44%) 36 (82%) .0001
Seizure score (0-10) 0 (0-6) 0 (0-8) 4.5 (0-9) .0001
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
Table III. Neurodevelopmental outcome of newborns observed to30 months of age by magnetic resonance imaging pattern
Normal Watershed predominant
Basal ganglia/thalamus
predominant
P value
Number 20 48 21
Died* 0 3 5 .01
30-month MDI 101 (77-121) 84 (50-116) 62.5 (50-104) .0007
12-month MDI 93 (53-109) 91.5 (50-120) 58 (50-109) .006
30-month NMS 0 (0-2) 1 (0-5) 5 (0-5) .0001
12-month NMS 0 (0-3) 1 (0-5) 5 (0-5) .0008
30-month head circumference 50 (47-57) 50 (41-53) 47 (39-51) .005
Data is presented as median (range) or number (%). P values refer to comparisons across the 3 groups.
NMS=Neuromotor score. *All infants died before 12 months of age.
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
Although many risk factors are clearly prenatal, recent evidence from prospective cohorts of neonatal encephalopathy using MRI demonstrate that the brain injury happens close to the time of birth. (Cowan).
“The MRI findings in our cohort were also consistent with recent rather that chronic brain injury, and the prenatal conditions measured were remarkably similar in newborns with normal & abnormal results”.
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
“Because of the frequent occurrence of cerebral watershed injury with the basal ganglia/ thalamus predominant pattern, cognitive deficits cannot be directly attributed to damage to the deep gray nuclei themselves”.
“In contrast, the watershed pattern had predominantly cognitive impairments at 30 months that were not detected at 12 months of age”
Miller, Steven P., Barkovich, James A., et. al., J Pediatr, April 2005; 453-460
Conclusion
• Neuroimaging will continue to evolve until they become the gold standard on timing fetal/neonatal HIE.
• Final common pathway to injury of many insults will be the same – ie hypoxia; ischemia; hypoxia and ischemia, infection…
Neonatal Encephalopathy
Mary E. D’Alton, MDMary E. D’Alton, MDWillard C. Rappleye Professor of Obstetrics & GynecologyWillard C. Rappleye Professor of Obstetrics & Gynecology
New York Presbyterian HospitalNew York Presbyterian Hospital
Columbia University College of Physicians & SurgeonsColumbia University College of Physicians & Surgeons