BIRTH ASPHYXIA: REVIEW 2014 JAN

BIRTH ASPHYXIA Review Article

Prof Jayendra R Gohil, MD, Professor & head

Dr Heena Hasan, MBBS, Resident

Pediatrics dept, Govt. Medical College & Sir TG Hospital, Bhavnagar- 364002
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ABSTRACT

Birth asphyxia is an important cause of acute neurologic injury, occurring in 2 to 3 cases per 1000 term live births in developed countries, with a higher incidence in less developed countries. Birth asphyxia related neonatal mortality and morbidity including long-term neuro-developmental sequele was seen in 25%-60% of survivors. It is estimated that around 23% perinatal deaths are due to birth asphyxia, with a large proportion of stillbirths. Asphyxia should not be confused with hypoxic ischemic encephalopathy (HIE) or cerebral palsy (CP) since not all asphyxiated neonates develop HIE or CP and there are other causes for the same.  In this article there is description of definitions, aetiologies, pathophysiology, clinical features, basic and recent investigations, older and newer treatment of birth asphyxia.

Conclusion: Although there is no specific treatment for birth asphyxia only supportive treatment (fluid and electrolytes balance, oxygenation and ventilation etc.) to prevent the complications and primary preventive measures (electronic fetal heart monitoring, training to birth attendants, home based newborn care) are helpful.
In the developed world, for the HIE, hypothermia has been the only treatment that has worked somewhat (8 -18%). The preferred cooling is whole body with a heart-lung bypass or ECMO; since that is rarely available, external whole body or external head cooling is the next best option. Prevention of reperfusion injury by early (within 6 hours) antioxidant therapy seems to hold the promise for future and should be studied.

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

-          term infant <7 at="" days="" o:p="" onset="">

-          depressed consciousness level

-          abdominal tone and power

-          feeding difficulty

-          seizure
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