Asphyxia neonatorum

1. Dr Varsha Atul Shah
Senior Consultant
Department of Neonatal and Developmental Medicine
Singapore General Hospital
ASPHYXIA NEONATORUMASPHYXIA NEONATORUM

2. Defined as impaired respiratory gas exchange
accompanied by the development of acidosis
ASPHYXIA NEONATORUMASPHYXIA NEONATORUM

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?
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

9. PREDISPOSING FACTORS
Maternal Causes
Medical conditions eg Pulmonary hypertension
Chronic HPT
Antenatal conditions eg Abnormal uterine contraction
Antepartum haemorrhage
Prolapsed cord
Malpositions etc

10. PREDISPOSING FACTORS
Fetal Causes
Multiple pregnancies
Big baby with CPD
Fetal anomalies - Congenital abnormalities
of the lung

11. PATHOPHYSIOLOGY
Fetal adaptation to oxygen lack
1. Preferential flow to heart, brain and adrenals

aerobic anaerobic metabolism
glucose pyruvic acid lactic acid Acidosis
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

13. CLINICAL FEATURES
 Apnoea, bradycardia
 Altered respiratory pattern - grunting, gasping
 Cyanosis
 Pallor-shock
 Hypotonia
 Unresponsiveness

14. ORGANS INVOLVED IN ASPHYXIA (1)
Asphyxia results in alteration in blood flow to various organs, hence
multiple organ injury
Kidney abnormalities occur in 50% of asphyxiated infants CNS
abnormalities in 30% & CVS & pulmonary abnormalities in 25%
•Renal abnormalities - Oliguria, elevated β2 , microglobulin,
•azotaemina, elevated serum creatinine, acute tubular necrosis

15. ORGANS INVOLVED IN ASPHYXIA (2)
CNS abnormalities - HIE, PV-IVH
CVS abnormalities - Ventricular failure (R > L)
Tricuspid regurgitation
Hypotension
Pulmonary abnormalities - PFC, pulmonary haemorrhage
GIT abnormalities - bleeding GIT, NEC
Bone marrow abnormalities - Thrombocytopenia etc

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,
thalamus, basal ganglia etc

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

20. In hypoxic-ischaemic encephalopathy, as the
cerebral edema develops, the brain function is
affected in descending order.

21. PATHOCLINICAL CORRELATION
Full term infant
Pathology Clinical Signs
•Parasagittal cortical and Spastic quadriplegia
subcortical neurosis especially arms
Intellectual deficits
•Cerebellum Ataxia
•Brainstem Pseudobulbar palsy

22. PATHOCLINICAL CORRELATION
Preterm infant
Pathology Clinical Signs
•Periventricular leukomalaciaSpastic diplegia
•Status marmoratus of Dystonia,
•Basal ganglia choreoathetosis
•Thalamus Mental retardation
•Cerebral Cortex Mental retardation

23. SEVERITY OF HIE - SARNAT & SARNAT STAGE
Stage I Stage II Stage III
Consciousness Hyperalert Lethargic Stuporose
Muscle Tone NAD Mild Hypotonia Flaccid
Reflexes active Reflexes active intermittent
decerebration
Primitive Reflexes Present Incomplete Absent
sucking weak suck weak or -ve suck -ve
Autonomic FunctionSympathetic Parasympathetic Both depressed
depressed depressed
Seizures None Common None
EEG Normal Seizure, Isopotential
background burst
mildly abnormal 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 1
st
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
Recognition of at risk pregnancies
Antenatal monitoring
 fetal movements, fetal growth
 CTG for change in baseline, loss of variability, decelerations
 fetal scalp pH
< 7.2 ---------------------immediate delivery
7.2 - 7.25 -------------repeat in 1 hour
7.25 -------------------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, T
o
, 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.

37. Newer modalities
•Antagonists of excitotoxic neurotransmitter receptors
- NMDA receptor blockers
•Free radical inhibitors / scavengers
- vitamin E, superoxide dismutase
•Ca channel blockers
•Nitric oxide synthetase inhibitors
•Hypothermia

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

39. Whole Body Hypothermia
Selective Head Cooling

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

41. DIFFERENTIAL DIAGNOSIS
Drug depression - maternal drugs, GA
Prematurity
Trauma - tentorial tear
Anaemia
Neuromuscular disorder
Infection
Inborn error of metabolism - Pyridoxine Dependency
Respiratory tract malformation

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

44. That’s a wrap
Got questions?