Birth asphyxia is a condition of impaired gas exchange occuring during labor leading to progressive hypoxia associated with carbon dioxide retention and significant metabolic acidosis. The word is derived from Greek meaning stopping of the pulse. Birth asphyxia is an important cause of perinatal mortality and neurological morbidity.
During normal labor uterine contractions compress uterine blood vessels, resulting in intermittent interruption to blood flow into the placenta. There is no oxygen delivery to the fetus at the height of conctractions with subsequent restoring of oxygen delivery between contractions when the uterus is relaxed. There is only a slight fall in blood pH in a normal labor with a healthy fetus and placenta. On the other hand all abnormalities in the mother, placenta or fetus which prevent such succesful adaptation to the effects of uterine contractions or factors that prolonge labor result in intrapartum fetal hypoxemia.
The fetus is equipped with wide range of adaptive mechanisms so moderate degree of hypoxemia is tolerated for some time. If the condition persists, the switching to anaerobic metabolism results in increasing production of lactate, acidosis and asphyxia. Prolonged periods of low oxygen concentration and acidosis have adverse effects on the fetal circulation, intrauterine fetal breathing, the brain, kidneys and other organs. Unless immediate delivery the result is irreversible organ damage to susceptible organs and ultimately cardiac arrest and intrapartum death.
Causes of birth asphyxia
All the conditions which predispose to intrauterine hypoxia (fetal distress) prior to the onset of contractions may increase the asphyxial stress during labor.
Signs of fetal hypoxia before and during delivery — fetal heart rate abnormalities, decreased or stopped fetal movements, thick amniotic fluid contaminated by meconium.
Fetal heart rate monitoring using cardiotocography can detect hypoxic episodes well before the developement of asphyxia.
Essential criteria for birth asphyxia after delivery
Asphyxial lesions at autopsy
An episode of hypoxia and acidosis induces intrauterine breathing movements. The period of respiratory effort ends in deep sighing breaths and terminal apnea. The deep breaths result in masses of epithelial squames and amniotic debris being aspirated into the bronchi, bronchioli and acini. These may be visible for many weeks.
Brain
Kidneys
Hemorrhagic lesions
Massive aspiration of amniotic fluid and meconium, birth asphyxia: Aspiration of amniotic fluid, asphyxia, Macro, autopsy (73783) Aspiration of amniotic fluid, asphyxia, Macro, autopsy (73784)