1) Asphyxia in newborns can result from problems during delivery that deprive the infant of oxygen. Immediate resuscitation is needed to sustain life and prevent brain damage. 2) Predisposing factors include extremes of maternal age, placental problems, preterm or post-term birth, meconium in amniotic fluid and others. 3) Without oxygen, tissues become acidotic which can lead to organ damage. The apgar score is used to assess severity at birth, with low scores indicating need for resuscitation to restore oxygen supply.

1. Kalaba Onesimous
Senior Clinical Care Officer
Kasama District Health Office

2. Introduction
• Asphyxia is deprivation of oxygen in the fetus and
newborn infant.
• A newborn who does not breathe spontaneously or is
in shock requires immediate resuscitation to sustain
life and to minimize the possibility of brain damage
• However not only is ventilation required, but rapid
correction of hypovolemia is also as important

3. Predisposing factors
• Extremes in maternal age (i.e. <20 years or > 35 years)
• Placental abruption
• Placenta previa
• Preeclampsia
• Preterm gestation
• Posterm gestation
• Meconium stained amniotic fluid

4. Predisposing factors
 Fetal bradycardia
 Malpresentation
 Multiple gestation
 Prolonged rupture of membranes
 Maternal diabetes

5. Pathophysiology
 Prenatal asphyxia may be due to placental dysfunction
or neonatal pulmonary dysfunction.
 Infant may be asphyxiated before or during labour and
thus may be in a critical state at time of birth or may
become asphyxiated after delivery due to failure to
establish effective spontaneous respiration

6. Pathophysiology
• Asphyxia in utero may result from severe utero-
placental insufficiency, abruption-placenta, umbilical
cord compression, uterine tetany, maternal
hypotension, umbilical cord compression, foetal
exsanguinations
• Post-delivery the foetus may not be able to breathe due
to prior asphyxiation, placental passage of maternal
analgesics and anaesthetics, malformations e.g.
diaphragmatic hernia, or hypo plastic lungs.

7. Pathophysiology
• A premature infant maybe unable to breathe due to
low lung compliance
• Asphyxia occurs after prolonged periods of deprivation
of oxygen:
• During periods of hypoxia or hypercapnia, blood flow
to the brain is increased ensuring a stable delivery of
oxygen to the brain and metabolism. These flow
changes only fail when there is hypotension.

8. Pathophysiology
 During periods of mild asphyxia, adaptive changes in
blood flow allow adequate oxygen delivery to brain,
heart and adrenal gland. This is accomplished through
and increase and re-distribution of the cardiac output.
 Blood flow to the skin, muscle, kidney and
gastrointestinal tract is sacrificed in order to maintain
perfusion of the vital organs

9. Pathophysiology
• During periods of severe or prolonged asphyxia, the
under-perfused tissues become acidotic due to
anaerobic metabolism and lactic acid production. This
leads to myocardial depression and a gradual decrease
in blood pressure so that blood fails to perfuse the vital
organs with resultant permanent tissue damage in the
organs. The extent of damage depends on amount of
time that elapses before resuscitation is instituted.

10. Pathophysiology
• Asphyxia produces both hypoxemia and hypercapnia.
Respiratory acidosis results form CO2 retention,
superimposed metabolic acidosis occurs as tissues are
deprived of adequate Oxygen and lactic acid
accumulates.
• Secondary effects include a fall in cardiac output (CO)
with a drop in pulse rate and BP, hypovolemia from
pooling of blood in central veins or escape of fluid
from the capillary bed damaged by hypoxemia, and
CNS depression.

11. Pathophysiology
 Anaerobic glycolysis causes increase use of glycogen
stores; therefore asphyxiated infants particularly those
who are small for gestational age are prone to early
hypoglycaemia

12. Events in asphyxia
 The following sequence of events occurs with the onset
of asphyxia. An understanding of these are required
for institution of therapy:-
 Respiratory effort ceases abruptly, and the fetus
experiences primary apnoea. This is followed by a
phase of gasping and if resuscitation is not initiated,
progression to terminal apnoea occurs

13. Events in asphyxia
• A rapid decrease in oxygenation of blood occurs, with
resultant respiratory acidosis followed by a combined
respiratory and metabolic acidosis.
• Hypoxia results in a rapid decrease in heart rate
• Blood pressure initially rises, but with progression to
terminal apnoea falls to hypotensive levels

14. Events in asphyxia
 The fall in blood pressure causes a decrease in the flow
of blood to the organs and results in consequent tissue
damage.
 The above changes can be reversed with appropriate
resuscitative measures (reoxygenation of the CNS)

15. Clinical feature
• The apgar scoring system estimates the severity of
respiratory and neurological depression at birth by
rating certain physical signs.
• Every infant should be rated at 1 and 5 minutes. Low
scores particularly at 5 minutes are more likely to be
associated with residual neurological damage
• A score of < 5 indicates severe depression

16. Clinical features
 However a low apgar score may also be caused
respiratory of neurological depression due to trans-
placental passage of anaesthetic

17. Clinical presentation – postnatal
symptoms of asphyxia
• Effects on brain:
• In mild asphyxia, the infant will initially be depressed.
This is followed by a period of hyperalertness. This
resolves within 1 to 2 days. There is no neurological
sequele
• In moderate asphyxia, the infant is very depressed.
This is followed by a prolonged period of
hyperalertness and hyperreflexia. Generalised seizures
often occur 12-24 hours after the asphyxia but are
easily controlled resolivng in a few days regardless of
therapy. Neurological sequele may occur

18. Clinical presentation - postnatal
 In severe asphyxia, there is coma, intractable seizures,
cerebral oedema, and intracranial haemorrhage. The
patient gets progressively more depressed over the first
3 days. Death may occur during this period due to
cerebral oedema. Survival is often associated with
neurological sequele

19. Clinical presentation
 Effects on Heart:-
 Severe or prolonged episodes of asphyxia may result in
hypoxic cardiomyopathy. Signs and symptoms include
hypotension, poor myocardial contractility,
cardiomegaly and congestive cardiac failure

20. Clinical presentation
 Effect on lung:-
 Respiratory distress occurs due to a delayed fall in
pulmonary vascular resistance.
 Effect on kidney:-
 Decrease renal flow during asphyxia events causes
acute tubular necrosis. This is usually self-limit

21. Clinical presentation
 Effect on gastrointestinal tract:-
 Asphyxia is often associated with poor gastrointestinal
motility or ileus. Hypoxia predisposes to secondary
bacterial invasion and the development of necrotizing
enterocolitis

22. Clinical presentation
 Effect on Blood:-
 Hypoxia depresses bone marrow function and initiates
an intravascualr coagulopathy which results in
thrombocytopenia, prolonged prothrombin time (PT)
and partial thromboplastin time (PTT) and clinical
evidence of bleeding

23. Management
 General principles: the primary objective in treating
perinatal asphyxia is to restore an oxygen supply to the
body tissues, especially the brain. The secondary
objective is to evaluate the degree of hypoxia injury
and to plan treatment

24. management
 Specific therapy
 The most important thing is to resuscitate:-
 Secure airway – quickly clear any secretions – suction
pharynx. (note prolonged suctioning may causes
bradycardia. Intubate if possible
 Ventilate. Positive pressure ventilation can be effected
with bag and mask. Rate – 40/min

25. management
• Secure circulation; if infant does not become rapidly
pink with ventilation, the circulation may be
inadequate. If heart rate is < 80/min, thready pulses
and poor capillary refill (> 2 secs), cardiac massage is
done. Massage rate 120/min. 3 or 4 massages
alternating with one positive pressure ventilation. If
perfusion remains poor, epinephrine 1:10,000 is given;
0.1 to 0.2 mls or 0.2ml/kg endotracheally. Dopamine
and dobutamine may be required

26. management
 For severly asphyxiated, with poor cardic output, rapid
infusion of 10ml/kg of albumin or fresh frozen plasma
will improve circulation. If these are not availabale,
use normal saline.
 10% dextrose, 5mls per kg should be given to counter
hypoglycaemia

27. management
 Depression secondary to narcotics: give naloxene
0.1ml/kg IV is given. There may be need to repeat if
response is good. Every 5 – 10 minutes.
 Hypothermia: The child should be kept warm as
cooling triples the infants Basal metabolic rate thus
increasing oxygen requirements.

28. Management
 Other anticipated problem include:
 Hypotension
 Hypoxic ischemic encephalopathy and seizures
 Hypoxic cardimyopathy
 Persistent pulmonary hypertension
 Ileus and necrotizing enterocolitis
 Acute tubular necrosis

29. Management
 Adrenal haemorrhage and necrosis
 Hypoglycaemia
 Polcythemia
 Hypocalcemia
 Disseminated intravascular coagulation

30. Clinical features – apgar score
 Criteria score

Criteria Score
0 1 2
color Blue, pale Body pink,
extremities blue
All pink
Heart rate absent <100 >100
respiration absent Irregular, slow Good crying
Reflex response
to nasal catheter
none grimace Sneeze, cough
Muscle tone limp Some flexion of
extremities
active