History of Present

Illness
Female born to 34 year old G4P3 mother with

good antenatal care.

Mother hx complicated by GDM.
Mother completely immunized. GBS negative
Mom admitted at 37+2 weeks with active
vaginal bleeding.
US showed placental abruption.
Called to DR.
Infant delivered via stat c/s.

Jennifer Lee
12/1/2017

Presentation
Bag & mask ventilation started
HR >100 @ 3 min, some respiration effort noted at
5 min.

At 7 min had poor sustained respiration,

leading to intubation.
Color improved but remained floppy at 10 min.
APGAR score: 0 @ 1 min, 4 @ 5 min, 5 @ 10
min

What should you ask L&D

staff to do?

Send Cord blood gas!

Cord arterial gas: pH 6.8, PCO2 103, Bicarb 15
and BD19.7
Small changes in umbilical pH occur within 60s
of delivery, and over 60min cord arterial or
venous pH can fall by more than 0.2pH units.

What can cord blood gases provide

information about?
What is next option if none taken?
Arch Dis Child Fetal
Neonatal Ed

Physical Exam
Weight 3720gms (>90%), OFC 35.5 cm
(90%), Length 54.4 (>90%)
Temperature 36.5oC
HR 190bpm, BP 37/23 mmHg.
Pale and poor perfused
On ventilator with periodic respiration
effort
No significant dysmorphic features

Neuro Exam
Level of Consciousness: poor eye
opening to stimulation, no sustained
alertness
Movements and Tone: minimal
spontaneous activity, hypotonia
Brainstem/Autonomic Functions: pupils
constricted but reactive, no suck, no gag
Reflexes: incomplete Moro, no DTR

Lab Tests
Your initial lab work should include which :
A.Check blood glucose
B.CBC
C.BCx, UCx, LP
D.LFTs
E.Coagulation tests
F. Metabolic testing ammonia, lactate, pyruvate,
AA, organic acids

ALL!

Neonatal Encephalopath
HIE

Neonatal
Encephalopathy

American College of Obstetricians and

Gynecologists: Disturbed neurologic function in
earliest days of life in infant born at or beyond 35
weeks of gestation
Reduced level of consciousness or seizures
Often with difficulty initiating & maintaining respiration;
hypotonia and hyporeflexia
Low Apgar scores, weak cry

Etiology and pathology ???

Insults throughout pregnancy or peripartum?
Single/multiple insults?

Diagnosis for Neonatal Encephalopathy

LOOK FOR A CAUSE!
What was our case studys cause?

Careful hx and neuro exam

Neonatal clinical status
Maternal Mhx
Intrapartum factors (fetal HR monitoring and delivery issues)
Placental pathology
Cord Blood Gases
Lab studies to exclude
Neuroimaging
Mutations (MECP2)

Neuroimaging
HUS - may detect basal ganglia and thalamic
injury, not sensitive to cortical injury. Most
useful in detecting and following intracranial
bleeding.
CT - can detect diffuse cortical neuronal injury,
most useful to r/o intracranial hemorrhage that
requiring immediate surgical intervention.
Concerns for radiation.
MRI - is the study choice of assessing HI brain
injury. It provides specific information regarding
the injury pattern, severity and evolution.
EEG - provide evidence for the presence and
severity of encephalopathy. If nml, have good
prognosis.

Diagnosis of HIE
No gold standard
Nonspecific clinical signs low Apgar, low cord
pH, neonatal seizures
Increased likelihood:
Signs consistent with acute
peripartum/intrapartum event Apgar score
<5 @ 5 min and 10 min, fetal umbilical artery
acidemia, neuroimaging with evidence of
injury, multisystem organ failure
Ischemic or hypoxic event immediately before
or during labor and delivery (ruptured uterus,
UCP, amniotic fluid embolus, etc)
Abnml fetal HR pattern during labor
Brain injury on imaging
Developmental outcome of spastic
quadriplegia or dyskinetic CP

Complications of HIE
ARF in 20% of asphyxiated
term infants
Myocardial dysfx and
hypotension in 50% of term
infants
Elevated LFTs in 80-85% of
term infants
Coagulation impairment is

Pathophysiology of HIE
Immature brain can be more
resistant to hypoxic-ischemic
events compared to older
children/adults
Lower cerebral metabolic rate
Immature balance of NTs
Plasticity of immature CNS

 Gestational age is impt for

susceptibility of CNS structures
<20 weeks: neuronal heterotopia &
polymicrogyria
26-36 weeks: insult affects white matter
leading to periventricular leukomalacia
Term: gray matter insult

Distribution of CNS injury

Watershed areas
Areas of higher metabolic rates
Degree of asphyxia

The Details

Hypoxiaischemia
Primary
neuronal
death

Cytotoxic
mechanisms

1
hour

Delayed
neuronal
death
6 hours

Hypothermia

Modified from Gunn and Thoresen, 2006

Days

Treatment
Hypothermia within first 6 hours of
delivery (SHC vs WBC)
Maintained for 72 hrs at rectal temp
33 to 35C (SHC); 33.5 C esophageal
temp for 72 hrs (WBC)
Eligible if gestational age 36 weeks
and 6 hours of age, acidic blood gas
(ph7.0), & either 10 min Apgar of <5
or ongoing resuscitation initated at
birth and continued for at least 10 min
SE: well tolerated; sinus brady,
thrombocytopenia, fat necrosis (rare)
Increased survival with nml neurologic
outcome at 18 mo (40 vs 24 %) but
limited efficacy
Long term efficacy suggested but not
yet proved
But hyperthermia is def correlated to
adverse cause future of
normothermic levels?

Meanwhile.
EPO in animal models of HI brain injury & neonatal
strokes
Improved histological and fx outcomes after hypoxiaischemia
Need larger studies

Allopurinol some trials show decrease in mortality

and decrease free radical formation, CBF, electrical
brain activity
Opioids few demonstrate morphine and fentanyl
have neuroprotective effect but long term effects
need to be assessed

Prognosis

Epidemiology

Neonatal encephalopathy: 3 per 1000 live births

HIE: 1.5 per 1000 live births
No race/sex predilection
25% die or have multiple disabilities
4% have mild to moderate forms of CP
10% have developmental delay (similar to
control population)
Major cause of infant mortality and morbidity
with sig long term neurological deficits