Keywords:
Asphyxia, hypoxia, brain injury
Introduction
Birth asphyxia is defined as insufficient oxygen supply to a baby at or around the time of birth. Around 25% of the 4 million annual global neonatal deaths are attributable to birth asphyxia.1 In high-income countries, following birth asphyxia, Hypoxic-ischemic encephalopathy (HIE) occurs in approximately 1 to 2 infants per 1000 live term births.2 The incidence of HIE has been reported several times higher in low and middle-income countries than in high-income countries. Significant proportions of these infants die or survive with severe long-term morbidity.
Etiology and Pathogenesis
There are several causes for birth asphyxia. It could be before, during, or after delivery. Before delivery, it could be due to hypertension, hypotension, congenital infections, intrauterine growth restriction (IUGR), placental abruption, fetal anemia, and post maturity. Intrapartum could be due to abnormal labor leading to shoulder dystocia or breech presentation and cord prolapse. After birth causes include the inability of the baby to cry immediately after birth and severe circulatory collapse such as in severe blood loss.
Soon after birth, respiration should occur normally along with the removal of the fetal lung fluid and there should be a good oxygen/carbon dioxide exchange between the alveoli and the blood. With the onset of respiration and lung expansion, pulmonary vascular resistance decreases, followed by a gradual transition from fetal to adult circulation. It is the failure of this transition from fetal to adult circulation, the birth asphyxia occurs.
In the early stages of birth asphyxia, blood flow to the less important organs like the liver, kidneys, intestines, muscles, and lungs decreases; however the blood flow to the vital organs such as the heart and brain, and adrenal glands increases. The degree of organ damage is dependent on the oxygen requirement of the organ involved and the severity of the asphyxia.
Clinical Features
In the early phase of birth asphyxia, there is a transient increase in heart rate with associated fast breathing with an increase in cardiac output and peripheral constriction of blood vessels. When birth asphyxia is prolonged, it leads to a decrease in blood pressure and cardiac output. When birth asphyxia becomes ever more prolonged with no further intervention, then secondary apnea ensues with rapid gasps, hypotension, and severe bradycardia. Once HIE has developed, the signs and symptoms could be a low APGAR score, convulsion or unconsciousness, floppy, and symptoms of multiple organ involvement.
Investigations
The diagnosis of birth asphyxia is based on a detailed history, physical and neurological examinations. Supportive investigations include
- Serum electrolytes: Markedly low serum sodium, potassium, and chloride in the presence of reduced urine flow and excessive weight gain may be present in severe HIE
- Renal function studies: Creatinine increases 2-4 days after insult,
- Cardiac and liver enzymes values are an adjunct to assess the degree of hypoxic-ischemic injury to these other organs,
- Amplitude integrated EEG/EEG to evaluate seizure activity and
- Imaging Studies such as cranial ultrasound of the brain and MRI to assess brain injury severity.
Treatment
In birth asphyxia, the infant needs immediate professional care in the neonatal intensive care unit and therapeutic hypothermia is a method for treating HIE following birth asphyxia to reduce the risk of brain injury3. Therapeutic hypothermia has become standard of care for these infants in the past decade after several clinical trials. Hypothermia treatment of the newborn involves cooling the infant for a period of 72 h to a body temperature of 33.5°C. Then, the infant's body temperature is increased by 0.5°C per hour until the normal body temperature (37°C) is reached.
How to Prevent
Advance in antenatal care, the presence of a pediatrician at high-risk delivery has reduced the incidence of birth asphyxia in high-income countries. Continuous intrapartum monitoring including fetal heart rate, timed intervention, and prompt delivery of an at-risk fetus has a role in prevention.
Complications
Complications include deafness, epilepsy, cerebral palsy, learning difficulties, and attention deficit disorders.
1. Lawn JE, Cousens S, Zupan J. 4 million neonatal deaths: when? Where? Why? Lancet 2005;365:891-900.
2. Pierrat V, Haouari N, Liska A, Thomas D, Subtil D, Truffert P. Prevalence, causes, and outcome at 2 years of age of newborn encephalopathy: population based study. Archives of disease in childhood Fetal and neonatal edition 2005;90:F257-61.
3. Edwards AD, Brocklehurst P, Gunn AJ, et al. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal hypoxic ischaemic encephalopathy: synthesis and meta-analysis of trial data. Bmj;340:c363.