2. Defined as impaired respiratory gas exchange
accompanied by the development of acidosis
ASPHYXIA NEONATORUM
3.
4. Definition of perinatal asphyxia
WHO :
A failure to initiate and sustain breathing at birth.
NNF :
Moderate asphyxia
Slow gasping breathing or an apgar score of 4-6 at 1 minute of age
Severe asphyxia
No breathing or an apgar score of 0-3 at 1 minute of age
5. HOW DOES ASPHYXIA OCCUR?
Inadequate oxygenation of maternal blood due to maternal hypoxic states
Interruption of umbilical cord blood flow, eg: cord compression during labour
Failure of exchange across the placenta, eg: abruption
Inadequate perfusion of maternal side of placenta, eg: maternal hypotension
Compromised fetus who cannot tolerate transient intermittent hypoxia of normal
labour
Failure to inflate lungs
6. CHARACTERSITICS OF
PERINATAL ASPHYXIA
Profound metabolic acidosis (pH<7.00)
Persistence of an Apgar score of 0 to 3 beyond 5 minutes
Clinical neurologic sequelae in the immediate neonatal period
Evidence of of multiorgan system dysfunction in the immediate
neonatal period
- derived from the 1992 joint statement of the AAOP and ACOG and the
1999 International Cerebral Palsy Task Force
7. TO ASSESS THE SEVERITY OF
ASPHYXIA - Apgar Scores
Signs 0 1 2
Colour Blue/pale Blue peripheries Pink
Heart rate 0 <100 >100
Respiration 0 Weak, gasping Regular
Suction response 0 Slight Cries
Tone 0 Fair Active
A -Appearance P- Pulse G- Grimace A-Activity R-Respiration
8. Quiz:
At birth, a newborn infant is noted to have the following findings: heart
rate – 70/min, respiratory effort – poor and irregular, limp, no reflex
irritability, blue all over the body.
The Apgar score of the baby at this point is?
HR 1, RR 1, Tone 1, reflex 0, color 0
APGAR=3
11. PATHOPHYSIOLOGY
Fetal adaptation to oxygen lack
1. Preferential flow to heart, brain and adrenals
Acidosis
aerobic anaerobic metabolism
glucose pyruvic acid lactic acid Acidosis failure of
autoregulation impaired perfusion
increasing acidosis Death unless resuscitated
12. PATHOPHYSIOLOGY
2. Primary and Secondary apnoea
Occur as an attempt to minimize metabolic work
3.Fetal response to asphyxia
Respiratory metabolic acidosis
4. EEG changes
Loss of faster rhythm iso-electric rhythms
Prolonged voltage suppression with burst of spike
waves indicating risk of significant brain damage
16. PATHOLOGY OF BRAIN DAMAGE
Acidosis alteration in cell membrane
permeability fluid shift cerebral edema
Anoxia chromatolytic changes in neuron
neuron necrosis and neuroglia reactions
Neuron necrosis may be focal, multifocal or
diffusely over the cerebral cortex, brainstem,
17.
18. PATHOLOGY OF BRAIN DAMAGE
Extent of damage depends on:
duration of asphyxia
severity of asphyxia
gestational age
alteration in cerebral blood flow
changes in glucose/glycogen metabolism
in vulnerable areas of brain.
19. Pathology
•Severity and distribution is dependent on several factors
•Certain vulnerable areas
- cerebral cortex , hippocampus , basal ganglia, thalamus, brain stem,
subcortical and periventricular white matter
•In full term infants gray matter structures affected and in
premature infants white matter
•Four basic and clinically important lesions
- Neuronal necrosis, status marmoratus, para-sagittal cerebral injury,
periventricular leucomalacia
23. SEVERITY OF HIE - SARNAT & SARNAT STAGE
Consciousness
Muscle Tone
Stage I
Hyperalert
NAD
Reflexes active
Stage II
Lethargic
Mild Hypotonia
Reflexes active
Primitive Reflexes Present
sucking weak
Autonomic Function Sympathetic
Incomplete
suck weak or -ve
Parasympathetic
Stage III
Stuporose
Flaccid
intermittent
decerebration
Absent
suck -ve
Both depressed
depressed
Seizures
EEG
depressed
None
Normal
Common
Seizure,
background
mildly abnormal
None
Isopotential
burst
suppression
24. Mild HIE
• Muscle tone may be increased slightly
• Deep tendon reflexes may be brisk during the first few
days.
• Transient behavioral abnormalities, such as poor feeding,
irritability, or excessive crying or sleepiness, may be
observed.
• By 3-4 days of life, the CNS examination findings
become normal.
25. Moderate HIE
• Lethargic, significant hypotonia
• Diminished deep tendon reflexes.
• Grasp, Moro, and sucking reflexes may be sluggish or
absent.
• Occasional periods of apnea.
• Seizures may occur within the 1st 24 hours of life.
• Full recovery within 1-2 weeks is possible and is
associated with a better long-term outcome.
26. Severe HIE
• Stupor or coma is typical.
• may not respond to any physical stimulus.
• Breathing may be irregular, and the infant often requires ventilatory
support.
• Generalized hypotonia and depressed deep tendon reflexes are common.
• Neonatal reflexes (e.g., sucking, swallowing, grasping, Moro) are absent.
• Disturbances of ocular motion, such as a skewed deviation of the eyes,
nystagmus, bobbing, and loss of "doll's eye" (i.e., conjugate) movements may
be revealed by cranial nerve examination.
• Pupils may be dilated, fixed, or poorly reactive to light.
27. Preventing asphyxia
• Perinatal assessment
– Regular antenatal check ups
– High risk approach
– Anticipation of complications during labour
– Timely intervention ( eg. LSCS)
• Perinatal management
– Timely referral
– Management of maternal complications Prevention,
28. PREVENTION
decelerations
Recognition of at risk pregnancies
Antenatal monitoring
fetal movements, fetal growth
CTG for change in baseline, loss of variability,
fetal scalp pH
< 7.2 --------------------- immediate delivery
7.2 - 7.25 -------------
7.25
repeat in 1 hour
normal
Co-ordinated care at delivery by paediatrician
29. MANAGEMENT-Investigations
Hx - of pregnancy and resuscitation
O/E to exclude other abnormality
Metabolic tests - sugar, Ca/P04/Mg, cord BG, ABG, metabolic
screen
CSF - to exclude infection; assay brain specific creatine kinase
EEG - to help with seizure Dx and prognosis
Tech. scan - for abnormal uptake in damaged area
30. MANAGEMENT
U/S - to exclude PV-IVH
CT scan - to exclude IVH/trauma, demonstrate severity of edema and for
prognosis
MRI scan
• Supportive care
Monitor B/p, To, blood sugar, correct acidosis and electrolyte inbalance
Care of renal failure - low fluid, dialysis
Care of cardiac failure - Dopamine, restrict fluid
Management of inappropriate ADH secretion - prevent overhydration
31. MANAGEMENT-1
BASIC CARE :Should be a daily routine in the management of all
these babies -
1. Strict asepsis.
2. Ensure neutral thermal environment.
3. Monitor vital parameters – HR,RR,BP,and Pulse Oximetry.
4. Urine output.
5. Daily weight.
6. Nutrition.
32. 1. Management of shock
1.Hypovolumic shock needs replacement with fluids, plasma, or
blood.
2.Cardiogenic shock warrants use of pressors like dopamine and /
or dobutamine. In case of refractory shock inspite of use of
pressors of 20 microgram/kg/mt steroids may be tried.
3.Septic shock should be suspected based on intrapartum risk
factors for sepsis, core axillary mismatch and results of sepsis
screen.
33. 2-MANAGEMENT of Cerebral Oedema
• Minimise cerebral edema
Ventilation - to prevent apnoea and maintain PC02 of 25 - 30 mmHg
Ensure adequate oxygenation
Restrict fluid intake
Mannitol/frusemide - if urine output is established
34. • Not all seizures require treatment. Only lif seizures are more
than 3 in a hour or lasting for 3 mts or more they warrant
anticonvulant.
• Phenobarbitone,Phenytoin,initially by loading dose followed by
maintenance dose are the first line drugs.
• In refractory seizures use of drip of midazolam,lorazepam or
diazepam may be required.
• Role of sodium valproate is occasional. Use of newer
anticonvulants like lamotrigene,clobazam,gabapentin etc is not
well known in neonates.
3-Manangement of seizures
35. 4-MANAGEMENT OF KIDNEY FAILURE
Urine output is by itself not a reliable marker renal
parameters need to be monitored.
2.Fluid restriction is required once renal failure sets in. A
careful evaluation of electrolytes would direct the fluid
management.
3.Daily monitoring of urine output, urine specific gravity,
and body weight are adjuvant to basic care.
4.Rarely peritoneal dialysis is required in case of
persistent oliguria
36. 5-Management of metabolic
derangement
1.Hypoglycemia needs to be corrected by 10 % D.Only if it is
symptomatic it warrants a bolus otherwise in asymptomatic cases
maintenance infusion is all that is required.
2.Only symptomatic hypocalcemia needs correction.Evaluate for
hypomagnesemia in case of persistent hypocalcemia.
3.Hyponatremia should be anticipated and prevented by restricted
fluid administration.
38. Hypothermia as a Treatment for HIE
• Studies have shown that hypoxic ischemic injury can be reduced
by brain cooling.
• Favorable effect on many of the pathways contributing to brain
injury
– Excitatory amino acids
– Cerebral energy state
– Cerebral blood flow and metabolism
– Nitric oxide production
– Apoptosis
40. OUTCOME
Death CNS sequelae
Stage I 0% 0%
Stage II 5% 21%
Stage III 75% 100%
Outcome generally good in those who do not reach stage
III and spend < 5/7 in stage II
42. Prognosis based on Apgars
•Score at 1, 5 minutes does not give prognosis indicator
•The longer the score remains lower, the greater its significance
•0-3 @ 1min has mortality of 5-10%
•may be increased to 53% if at 20min apgars score 0-3
•0-3 @ 5min , CP risk app. 1%
•may be increased to 9%if for 15min
•dramatic rise to 57% CP risk if for 20min
43. Predictors of poor neuro-developmental
outcome
1. Failure to establish resp. by 5 minutes
2. Apgar score of 3 or less at 5 minutes
3. Onset of seizures with in 12 hours
4. Refractory seizures
5. Inability to establish oral feeds by 1 wk
6. Abnormal EEG, neuro-imaging
