BIRTH ASPHYXIA

INTRODUCTION:Asphyxia Neonatorum is respiratory failure in the new-born, a condition

caused by the inadequate intake of oxygen before, during, or just after birth.
APGAR score at 1 minute < 7
Interruption in oxygen delivery to the fetus
Hypoxia
Hypercapnia
DEFINITION:Asphyxia neonatorum is respiratory failure in the newborn, a condition
caused by the inadequate intake of oxygen before, during, or just after birth.
OR
Health Care Committee Expert Panel on Perinatal Morbidity defined 'perinatal
asphyxia' as"a condition in the neonate where there is the following
combination:
An event or condition during the perinatal period that is likely to severely
reduce oxygen delivery and lead to acidosis,
A failure of function of at least two organs (may include lung, heart, liver,
brain, kidneys and hematological) consistent with the effects of acute asphyxia."
OR
Asphyxia neonatorum, also called birth or newborn asphyxia, is defined as a
failure to start regular respiration within a minute of birth.
OR
Birth asphyxia is defined as a reduction of oxygen delivery and an accumulation
of carbon dioxide owing to cessation of blood supply to the fetus around the
time of birth.

Birth cardiorespiratory depression syndrom of early (in birth, during the first
minutes of life) depression of the main vital functions, including bradycardia,
reduced muscle tone, hypoventilation, hypotension, but usually without
hypoxemia and hypercarbia. As a rule in the newborn are present one or two
signs of these vital functions depression and Apgar score of 4-6 at the first
minute.

TYPES OF BIRTH ASPHYXIA:There are two main types of neonatal asphyxia: Acute asphyxia neonatal asphyxia, which was caused by intranatal
factors only.
Asphyxia, which was developed on the background of prolonged fetal
hypoxia associated with placental insufficiency.

HOW DOES ASPHYXIA OCCUR?

Interruption of umbilical cord blood flow, e g: cord
compression during labor
Failure of exchange across the placenta, e g: abruption
Inadequate perfusion of maternal side of placenta, e g: maternal
hypotension
Compromised fetus who cannot tolerate transient
intermittent hypoxia of normal labor
Failure to inflate lungs

CHARACTERSITICS OF BIRTH 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.

TO ASSESS THE SEVERITY OF ASPHYXIA - Apgar Scores:Signs

Colour

Blue/pale

Blue peripheries

Pink

Heart rate

<100

>100

Respiration

Weak, gasping

Regular

Suction response 0

Slight

Cries

Tone

Fair

Active

A -Appearance P- Pulse G- Grimace A-Activity R-Respiration

Apgar score assessment:7-10 No or mild depression

4-6 Moderate depression
0-3 Severe asphyxia
If Apgar score is 0-3 at the first minute neonatal mortality is 5,6 %. Nelson
and Ellenberg examined Apgar scores in 49 000 infants. Of infants with an
Apgar score 0 - 3 at 20 minutes, 59% of survivors died before 1 year, and 57%
of the survivors had cerebral palsy. If Apgar score is 0-3 at the first minute and
becomes 4 and more in the 5-th minute possibility of cerebral palsy is 1 %.

ESSENTIAL CRITERIA FOR PERINATAL ASPHYXIA

AAP and ACOG: Profound metabolic or mixed acidemia (pH< 7.00) in umbilical cord
blood
Persistence of low Apgar scores less than 3 for more than 5 minutes
Signs of neonatal neurologic dysfunction (e.g., seizures, encephalopathy,
tone abnormalities)
Evidence of multiple organ involvement (such as that of kidneys, lungs,
liver, heart and intestine).

PREDISPOSING FACTORS: Maternal Causes

Medical conditions e g Pulmonary hypertension
Chronic HPT
Antenatal conditions e g Abnormal uterine contraction
Ante partum hemorrhage
Prolapsed cord
Malpositions etc

Fetal Causes
Multiple pregnancies
Big baby with CPD
Fetal anomalies - Congenital abnormalities of the lung

Delivery condition:
Abruption of placenta

 Placenta Previa
Prolapsed Cord
Premature Rupture Of Membranes

CLINICAL FEATURES:There are different clinical features of the Birth Asphyxia

Apnoea, bradycardia
Altered respiratory pattern - grunting, gasping
Cyanosis
Pallor-shock
Hypotonia
Unresponsiveness

SPECIAL INVESTIGATIONS: Electroencephalography (EEG):

The prognosis is likely to be poor if the EEG shows:
Long periods of inactivity (more than 10 seconds)
Brief period of bursts (less than 6 seconds) with small
amplitude bursts
Interhemispheric asymmetry and asynchrony
Isoelectric and low voltage (less than 5 microvolts) 25
Amplitude-integrated electroencephalography (aEEG)

 simplified form and can be performed on continuous basis in

NICU.
Following abnormalities would indicate poor prognosis:
Wide fluctuations in the amplitude with the baseline voltages
dropping to near zero
Peak amplitudes under 5 mV
Seizure spikes
Cranial ultrasound (US):
Cranial US is not good for detecting changes of HIE in the term
babies.
hypoechoic areas can be seen in very severe cases
In preterm babies, periventricular leukomalacia and
intraventricular-periventricular haemorrhage.
Computed tomography (CT):
CT is more useful after a traumatic delivery and suspected of
having an extra-axial haemorrhage

Magnetic resonance imaging (MRI):

Abnormalities of thalami and basal ganglia in term infants
Abnormalities of white and grey matter in preterm infants
Second most common pattern of injury is injury to the watershed
regions.
MRI is preferred over CT as it has no radiation exposure.

MANAGEMENT:SPECIFIC MANAGEMENT: Maintain temperature, perfusion, oxygenation & ventilation

Correct & maintain normal metabolic & acid base milieu
Prompt management of complications

Management of a neonate with perinatal asphyxia

Delivery room care
Obtain arterial cord blood for analysis
Transfer the infant to NICU if
Apgar score 0-3 at 1 minute
Prolonged bag and mask ventilation (60 seconds or more )
Chest compression
NICU care
1. Maintain normal temperature
Avoid Hyperthermia
2. Maintain normal oxygenation and ventilation
Maintain saturations between 90% and 95% and avoid any hypoxia
or hyperoxia
Avoid hypocarbia, as this would reduce the cerebral perfusion
Avoid hypercarbia, which can increase intracranial pressure and
predispose the baby to intracranial bleed.

. 3)Maintain normal tissue perfusion

Start intravenous fluid
Administer dobutamine (preferred) or dopamine to maintain
adequate cardiac output, as required.
Do not restrict fluid as this practice may predispose the babies to
hypo perfusion.
Restrict fluid only if there is hyponatremia (Sodium<120 mg%)
secondary to syndrome of inappropriate secretion of ADH
(SIADH) or if there is renal failure.
4. Maintain normal hematocrit and metabolic milieu
Maintain blood glucose levels between 75 mg/dL and 100 mg/dl.
Correct Anaemia and maintain haematocrit between 45% and 55%.
Check blood gases to detect metabolic acidosis as needed and
maintain pH above 7.30.
In case of severe asphyxia, provide calcium in a maintenance dose
of 4 mL/kg/day (of 10% calcium gluconate)
5.Treat seizures
6. Nutrition:
Start oral feeding once baby is hemodynamically stable
7. Miscellaneous
Administer Vitamin K (1 mg IM) to all infants with perinatal
asphyxia

NEWER MODES OF THERAPY:a) Therapeutic hypothermia

330C to 340C
in infants of at least 36 wk.

 moderate to severe encephalopathy

initiated within 4- 6 hr
continued for 72 hr of age
reduce mortality and neuro-morbidity by 18 months of age.
selectively cooling the head or the whole body.

b) Prophylactic phenobarbitone
A dose of 40 mg/kg administered prophylactically was associated with a
better neuro-developmental outcome at 3 years of age.
c) Drugs under investigation
A large number of drugs are under investigation for neuro-protection in
HIE which need to be used in the early period.
blockade of free radical generation (allopurinol, oxypurinol)
scavenging of oxidants (superoxide dismutase, glutathione, Nacetyl cysteine and alpha tocopherol)
calcium channel blockade (flunarizine, nimodipine)
blockage of NMDA receptors (magnesium, MK801,
dextromethorphan)
blockage of inflammatory mediators (phospholipase A2,
indomethacin).

PREDICTORS OF POOR NEURO DEVELOPMENTAL OUTCOME: Failure to establish respiration by 5 minutes

Apgar 3 or less in 5 mts
Onset of Seizure in 12 hrs.
Refractory convulsion
Stage III HIE
Inability to establish oral feed by 1 wk.
Abnormal EEG & failure to normalize by 7 days of life

 Abnormal CT, MRI, MR spectroscopy in neonatal period

RESEARCH ABSTRACT:A Study on Birth Asphyxia at Tertiary Health Centre
Ekta A Dalal, Nayan L Bodar.
Abstract
Background: Birth asphyxia is an important cause of morbidity and mortality
in neonatal period.
Methodology: This was the cross sectional study conducted in the tertiary care
centre of Ahmedabad on the full term babies with birth asphyxia. The maternal,
fetal and newborn correlates were recorded according to predesigned proforma.
Results: There were total 401 (6.6%) babies born with apgar score of less than
7 at one minute and among them, 320 (79.8%) were full term babies and 81
(20.2%) were preterm babies. Among the babies 52.5% were male, 56.9% were
primigravida, and only 41.9% had antenatal care present, 42.2% had MSL and
47.2% were small for date babies.
Conclusion: Birth asphyxia is common the babies of the mother who had not
received proper antenatal care. Maternal anaemia, primipara, meconium stained
liquor babies have more chances of getting birth asphyxia.

SUMMARY:As the part of my I have conducted seminar on birth asphyxia and in that I have
explained about the introduction, definition, types, characteristics, predisposing
factors, clinical features, investigations and management of birth asphyxia

CONCLUSION:Birth asphyxia occurs in about four of every 1,000 full-term births. It may be
even more common when babies are born prematurely. The amount of harm to
the newborn depends on how long and how severe the period of asphyxia is,
and how quickly the right treatment is given. Two stages of injury can happen
with birth asphyxia. The first stage happens within minutes without oxygen.
Cell damage occurs with the initial lack of blood flow and oxygen. The second
stage of damage is called "reperfusion injury" and can last for days or even
weeks. This injury occurs after restoration of normal blood flow and oxygen to
the brain, and is due to toxins released from the damaged cells.

REFERANCE: DUTTA D.C, Textbook of obstetrics,Edition 6th, Published by- New Central Book,
Page no. 100- 103
MYLES, Textbook of midwives,Edition 6th , Published By-Jaypee Brothers Pages no.
228- 229
JACOB ANNAMMA, A comprehensive textbook of midwifery Edition by 2nd
,Published by-Jypee brothers, Page no. 116- 120
Daftary N Shirish, Manual of Obstetric, Edition 1st , Published by Elseviser, Page No.
292-298

WEBSITES:www. Google .com

www. Pubmed.com
www. Wikipedia. Com
http://www.gfmer.ch/Obstetrics_simplified/shock_in_obstetrics.htm

SEMINAR
ON
BIRTH ASPHYXIA
SUBMITTED TO:MRS. PINKY MAM
LECTURER
(OBG & GYANE DEPARTMENT)
S.NC., MEERUT
SUBMITTED BY:MS. ANNU PANCHAL
M.Sc.(N) FINAL YEAR
S.N.C., MEERUT