Birth asphyxia occurs when a newborn fails to breathe or has reduced oxygen delivery at birth. It is a major cause of neonatal mortality and morbidity worldwide. Risk factors include maternal infections, post-term pregnancy, fetal anomalies, and complications during delivery. The pathophysiology involves hypoxic cellular damage to vital organs like the brain. Clinical features range from mild to severe and include abnormal heart rate, breathing issues, and multi-organ involvement. Diagnosis is based on history, Apgar scores, blood tests, and neurological exam. Management involves resuscitation and treating complications, while hypothermia therapy may improve outcomes from hypoxic-ischemic encephalopathy. Outcomes depend on severity but can include death or disabilities like

1. BIRTH ASPHYXIA
Bundala
MD

2. Objectives
 Introduction
 Epidemiology
 Etiology /risk factors
 Pathophysiology
 Clinical presentations
 Diagnostic criteria
 Management
 Prognosis
 Complications

3. Introduction
 Failure to initiate spontaneous, sustained breathing
after birth,
OR
 reduction of oxygen delivery and an accumulation
of carbon dioxide owing to cessation of blood
supply to the fetus around the time of birth.

4. Epidemiology
 Birth asphyxia is a common neonatal problem and
contributes significantly to neonatal morbidity and
mortality.
 It ranks as the second most important cause of
neonatal death after infections, accounting for around
30 % mortality worldwide.
 In India, between 250,000 to 350,000 infants die each
year due to birth asphyxia, mostly within the first three
days of life.
 In addition, ante-partum and intra-partum asphyxia
contributes to as many as 300,000 to 400,000
stillbirths.

5. Etiology/risk factors
 Pathologically, any factors which interfere with
the circulation between maternal and fetal blood
exchange could result in the happens of perinatal
asphyxia.
 These factors can be maternal factor, delivery
factor and fetal factor.

6. Cont…
 Maternal factors
Maternal age>35 or <16
Maternal infections
Post term gestation
Multiple gestation
Maternal drug abuse
Poly/oligohydramnios
 Fetal factor:
Multiple birth
Congenital or malformed
Fetus
Abnormal presentation
Meconium aspiration
 Delivery
condition:{Intrapartum}
Abruption of placenta
placenta Preavia
prolapsed cord
premature rupture of
membranes >24hrs
Analgesics, sedation or
drugs depressing the
respiratory centre
Prolonged labour

7. Pathophysiology
 Due to the presence of those different factors may
cause to placental insufficient which later on cause
impaired fetal gas exchange.
 Impaired fetal gas exchange during in utero and
labor resulting in severe hypoxia before delivery
this may predispose to birth asphyxia,
 Resulting to hypo-ventilation, hyper-capnia, hypo-
perfusion and metabolic acidosis
 When fetal hypoxia occurs, the body responds at
least temporarily by blood flow redistribution to
vital organs such as the brain, heart and adrenal
glands to prevent them from hypoxic damage.

8. Cont….
Hypoxic cellular damages:
 Reversible damage(early stage):
-Hypoxia decreases ATP production leading to
cellular dysfunction. But these changes are
initially reversible if hypoxia is corrected in
promptly.

9. Cont…
 Irreversible damage: (late stage)
-Persistent hypoxia leads to irreversible cellular
damage characterized by hypoxemia and marked
loss of Cerebral blood flow autoregulation and
increased celluar damage and cellular energy
dependent pump failure

10. Cont…
Progressive Hypoxia leads to:
a. Primary apnea
-Impaired breathing with normal muscular tone
or hypertonia tachycardia and hypertension
Happens early and shortly, auto regulatory
mechanism to maintain vital organs perfusion
b. Secondary apnea
-Features of severe hypoxemia due to lack or
unsuccessful resuscitation, usually leads to
organ dysfunction.

11. Cont…
Other damages:
a. Persistent pulmonary hypertension (PPHN)
b. Hyper/hypoglycemia
c. Hyperbilirubinemia
d. Electrolyte imbalances hyponatremia and
hypocalcemia

12. Clinical manifestation
Mild to severe birth asphyxia
Fetal heart rate: tachycardia bradycardia
Fetal movement: increase decrease
Blood pressure: Initial ↑ ↓late stages

13. Diagnostic criteria
 History of fetal distress
 Apgar score <3 at 1 min or <6 at 5 min
 Arterial blood lactate >5mmol/L
 Abnormal neurological state
 Multi-organ involvement
 Mixed acidosis
– Ph <7.2 on arterial cord blood
– Base excess >10
– Pa CO2 > 55 mmHg

14. Cont…
 Severity of asphyxia by APGAR score.
Apgar score 8-10: normal
Apgar score 5-7: mild
Apgar score 3-5: moderate
Apgar score <3: severe

15. Management
 1st minute counts (Golden)
Check if the baby is crying and breathing
If baby is not crying or breathing well after
delivery, one need to help baby in the first
minute
 ABCDE resuscitation
• A (air way)
• B (breathing)
• C (circulation)
• D (drug)
• E (evaluation)

16. Airway
 Open airways by placing the head in the neutral
position
 Clear the secretions from the airway by
suctioning as soon as possible
 If meconium-stained-deep tracheal suctioning
should be performed to removal of all the
meconium to avoid chemical pneumonitis - MAS

17. Breathing
 Ensure face mask covers nose & mouth connect
to oxygen bag
 Establish respiration of 30-40/min with chest wall
movement
 No response consider advanced airway
management-intubation & mechanic ventilation

18. Indications for intubation
 When bag and mask is in-effective
 When tracheal suction is required
 When diaphragmentic hernia is present

19. Circulation
 If heart rate <60/bpm, start external cardiac
compression
 Ratio 3:1 ( 90 compressions to 30 bpm)

20. Drugs
 In profound bradycardia, give adrenaline(1:10000, 0.1-
0.3ml/kg) by endotracheal tube or umbilical vein
 If no response, intravenous fluid (saline, albumin,
plasma, blood) with 10ml/kg
 In case of acidosis, give 5% sodium bicarbonate (SB)
with 3-5ml/kg
 Apneic and mum was given opiods consider using
naloxone (0.1mg/kg)

21. Prognosis
 Depends on associated factors, maturity of
the baby, duration and intensity of hypoxia
and acidosis including initiation of
resuscitative measures in the delivery room
 Subsequent competent care and available
facilities also influence the outcome following
birth asphyxia

22. Cont….
 Apgar score < 5 at 10 minutes : nearly 50 %
death or disability (Leicester)
 No spontaneous respiration after 20 min : 60
% disability in survivors (USA).
 No spontaneous respiration after 30 minutes :
nearly 100 % disability in survivors (Newcastle).

23. Complications
 Central nervous system
-infarction, intracranial hemorrhage,
cerebral edema, seizure, hypoxic ischemic
encephalopathy
 Cardiovascular
-bradycardia, ventricular hypertrophy,
arrhythmia, hypotension, myocardial
ischemia

24. Cont…
 Respiratory system
-apnea, respiratory distress syndrome, cyanosis
 KUB
-acute tubular necrosis, bladder paralysis
 Gastrointestinal tract
-necrotizing enterocolitis , stress ulcer

25. Cont…
 Hematology
-Disseminated intravascular coagulation
 Metabolic
-hypoglycemia, hyperglycemia, hypocalcemia,
hyponatremia
 Integument
-subcutaneous fat necrosis

26. Hypoxic Ischemic Encephalopathy
 Acquired syndrome of acute brain injury
characterised by neonatal encephalopathy in the
first 3 days of life and evidence of intrapartum
hypoxia in a term baby
 The immature brain is more resistant to hypoxic-
ischemic events as compared to older children
 NE is characterised by an abnormal LOC, abnormal
tone and primitive reflexes in the first week of life.
 Abnormal breathing and seizures may occur

27. Cont..
 An evolving process initiated by the hypoxic-
ischemic insult leading to decreased blood flow to
the brain followed by the restoration of blood flow
in an injured brain
 This initiates a cascade of pathways which includes
accumulation of extracellular glutamate
 With excessive activation of glutamate receptors,
ca influx and generation of reactive oxygen and
nitrogen species leading to cell death and brain
injuries.

28. Clinical features
 Apnea
 Bradycardia
 Grunting gasping
breaths
 Cyanosis pallor shock
 Hypotonia / hypertonia
 Hyporesponsiveness
The typical presentation
is that of multi-organ
involvement
 Convulsions
 Coma
 Hypotension
 Shock
 Renal failure
 Hypoglycemia
 Risk of infection

29. Diagnostic criteria
 A sentinel hypoxic event immediately before
or during labour.
 A sudden, rapid and sustained deterioration
of fetal heart rate.
 Apgar scores of 0-6 for longer than 5
minutes.
 Early evidence of multisystem involvement.
 Early imaging evidence of acute cerebral
abnormality.

30. Investigations
 Serum electrolytes levels
 Blood sugar levels
 Arterial blood gases
 Renal function tests
 Liver function tests
 Coagulation profile-
PT&PTT
 Cardiac enzymes
 Hb level & FBP
 CXR
 Brain USS
 CT
 MRI
 Echocardigraphy
 EEG
 Retinal and
opthalmological
evaluation

31. Cont…
Neuro-imaging
 MRI: most app technique and is able to show diff patterns
of injury. If available, it can be done at age 10-14 days
 CT scan: less sensitive than MRI for detecting changes in
the central gray nuclei
 Cranial U/S: not the best in assessing abnormalities in
term infants
 aEEG: has prognostic value and is useful in diagnosing
sub-clinical seizures

32. Management
 Aim is to treat symptoms and minimize further
organ damage
 Correct standard management is more important
than adding neuro-protective therapy such as
hypothermia

33. Cont…
 CNS
– Perform a daily neurological assessment and on
admission
– Treat recurrent and persistent
seizures{phenorbabital}
– If mod or severe NE is present at birth, induced
hypothermia may improve the outcome if
commenced asap and not after 6hrs post-del

34. Cont…
Hypothermia MOA
 Reduces cerebral metabolism prevents oedema
 Decreases energy utilisation
 Reduces cytotoxic amino acid accumulation
 Attenuates secondary neuronal damage
 Inhibits cell death
 Reduces extend of brain damage
– Death or severe disability at 18 months has been
reduced significantly

35. Cont…
Respiratory System
 Monitor oxygen sats
– If oxygen is needed but respiratory effort is good,
nasal continuous positive airway pressure is
adeqaute
Renal System
 Fluid balance and electrolytes
– Intrinsic renal failure and SIADH commonly occurs
– Initially restrict fluids to 40ml/kg/24 hrs with K
free 10% glucose and 0.45 % n saline
– Monitor urine output, electrolytes, blood glucose

36. Prognosis And Follow Up
 Neurological examination and aEEG are only
reliable when abnormalities are severe
 Early infant neuro-developmental assessment
can be predictive of the outcome
 Immediate the outcome is Death
 Cerebral palsy, developmental delay and intellectual
disabilities are common in survivors of severe HIE
and multidisciplinary follow-up is required.

37. Prevention
 Perinatal healthy care
 Prevention of asphyxia

38. Love is all we need!!