Introduction:
Birth asphyxia is a major cause of neonatal deaths,
especially in rural India and in urban places where birth attendants trained in
resuscitation are not available immediately. It also results into severe
neurological long term morbidity; hardly any specific treatment is available.
Perinataly asphyxiated newborns born in absence of trained manpower results in
higher number of stillbirths. Prevention of the primary events and
complications seem to be the best strategy at present.
Definition of birth
asphyxia designed for use in hospital based settings require evaluation of
umbilical cord pH, Apgar scores, neurologic clinical status, and markers of
multisystem organ function1 and are not feasible for community settings2.
The majority of neonatal deaths occur in the home without medical supervision;
community-based definitions must rely on data gathered from verbal autopsy
methods and use more general symptom- and sign-based algorithms. For example,
the National Neonatology Forum of India has defined birth asphyxia as “gasping
and ineffective breathing or lack of breathing at 1 minute after birth.”3
Such sign-based definitions are not, however, implemented consistently, and
varying study-specific definitions may affect estimation of the proportion of
neonatal deaths attributed to birth asphyxia.
Regarding the definition
according to American College of Obstetricians and Gynaecologists and the
American Academy of Paediatrics, a neonate is labelled to be asphyxiated if the
following conditions are fulfilled: (1) Umbilical cord arterial pH < 7; (2)
Apgar score of 0 to 3 for longer than 5 minutes; (3) Neurological
manifestations (e.g., seizures, coma, or hypotonia); and (4) Multisystem organ
dysfunction, e.g., cardiovascular, gastrointestinal, haematological, pulmonary,
or renal system.4
Outcome of birth asphyxia depends
on Apgar score at 5 minutes, heart rate at 90 seconds, time to first breath,
duration of resuscitation, arterial blood gases and acid –base status at 10,
and 30 minutes of age.5 It is measured as short term (early) and
long-term outcome. The early outcome is either death/or presence of hypoxic ischemic
encephalopathy (HIE) grade I, II or III, according to Sarnat staging.6
Perinatal asphyxia refers to
a condition during the first and second stage of labour in which impaired gas
exchange leads to fetal hypoxemia and hypercarbia. It is identified by fetal
acidosis as measured in umbilical arterial blood.7
Perinatal hypoxia,
ischemia, and asphyxia. These pathophyslogical terms describe respectively,
lack of oxygen, blood flow, and gas exchanges to the fetus or newborn. These
terms should be reserved for circumstances when there are rigorous prenatal,
perinatal, and postnatal data to support their use.7
Perinatal /neonatal depression
is the preferred clinical
descriptive term (over Birth Asphyxia by ACOG, but not in vogue) that pertains
to the condition of the infant on physical examination in immediate postnatal
period (i.e., in the first hour after birth). The clinical features of infants
with these conditions include depressed mental status, muscle hypotonia and
possibly disturbance in spontaneous respiration and cardiovascular function. These
terms make no association with the prenatal or later postnatal condition (i.e.,
beyond the first hour) condition, physical exam, laboratory tests, imaging
studies or electroencephalograms. After the first hour or so life, neonatal
encephalopathy is the preferred descriptive terms for infants with abnormal
mental status and associated findings.7
Neonatal encephalopathy is a
clinical and not an etiologic term that describes an abnormal neurobehavioral
state consists of decreased level of consciousness and usually the other signs
of brain stem and/or motor dysfunction. It does not imply a specific aetiology,
nor does it imply irreversible neurological injury as it may be caused by such
reversible conditions as maternal medications or hypoglycemia.7
Hypoxic ischemic encephalopathy
is a term that encephalopathy as described above with objective data to support
a hypoxic ischemic mechanism as the underlying cause for the encephalopathy.7
Hypoxic ischemic brain injury refers
to neuropathology attributable to hypoxia and/or as ischemia as evidence by
biochemical (such as creatine kinase brain bound [CK-BB] ,elecrtophyiologic
(EEG), neuoroimaging (head ultrasonography), MRI, CT or pathological (post-mortem)
abnormalities.7
Neonatal
Encephalopathy or Neonatal neurological syndrome8
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