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.
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)
Acute and subacute brain injury due to perinatal asphyxia.
The fundamental abnormality in HIE is a deficit of oxygen supply. This is due to hypoxemia (diminished amount of oxygen in th blood supply) and ischemia (a diminished amount of blood perfusing the brain). Loss of cerebrovascular autoregulation (the ability of brain vessels to maintain a constant cerebral blood flow in spite of fluctuations in the cerebral perfusion pressure) which occurs in asphyxiated newborns also contributes to the injury.
During the perinatal period hypoxemia and/or ischemia result most commonly from asphyxia. Various causes are listed above. Only 10% of cases occur in the early postnatal period with diseases in organs responsible for oxygen delivery. These are pulmonary system diseases (airway obstruction, tracheoesophageal fistula, pneumothorax, pneumonia, hypoplastic lungs, diaphragmatic hernia etc.) and nonpulmonary causes (heart defects, heart failure etc.).
There is no single presentation of this disease. Extension and distribution of brain lesions depend upon the maturational stage of the brain and the severity and duration of asphyxial injury. In premature infant the target region for pathologic damage is the periventricular white matter. Anoxic and ischemic damage to the cerebral cortex is characteristic to the term infant. Ischemic damage to the basal ganglia, thalamus and nuclei od midbrain and brain stem may be seen in infants of any gestational age.
Moderate and severe HIE
Mortality rate is 50 – 75% in severe HIE. Most deaths occur in the first weeks of life due to multiorgan failure, cardiorespiratory arrest or pneumonia. 80% of infants who survive develop serious complications — mental retardation, epilepsy, cerebral palsy or combination of these. Some infants with history of mild to moderate HIE have significant learning disabilities and ADHD in spite of absence of obvious signs of brain injury
Cerebral palsy is non-progressive motor deficit sustained in the perinatal period. The neuropathology of cerebral palsy is complex including not only hypoxic-ischemic encephalopathy itn the perinatal period but also malformations, traumatic lesions, infections and inborn metabolic disordes. The exact time of injury often remains uncertain, probably only 10 — 25% cases are related to intrapartum asphyxia.
Major neuropathological patterns of injury in HIE
Selective neuronal necrosis
White matter lesions
Combined grey and white matter lesions
Late stages of HIE in survivors
Cut slides of normal brain, term neonate:
Normal brain, newborn, Macro, autopsy (73841)
Term infant with severe birth asphyxia due to amniotic fluid
embolism in the mother which suddenly developed during the
delivery. Apgar score 0-3-3-4. Early onset of seizures after
birth, coma, multiorgan failure. Severe hypoxic-ischemic
encephalopathy and death at 1 month of age.
Hypoxic encephalopathy, Macro, autopsy (73808)
Hypoxic encephalopathy, Macro, autopsy (73812)
Hypoxic encephalopathy, Macro, autopsy (73811)
Hypoxic encephalopathy, Macro, autopsy (73815)
Hypoxic encephalopathy, Macro, autopsy (73810)
Hypoxic encephalopathy, Macro, autopsy (73813)
Hypoxic encephalopathy, Macro, autopsy (73814)
Hypoxic encephalopathy, Macro, autopsy (73809)
Severe hypoxic-ischemic encephalopathy in term neonate:
Hypoxic encephalopathy, Macro, autopsy (73804)
Hypoxic encephalopathy, Macro, autopsy (73802)
Hypoxic encephalopathy, Macro, autopsy (73807)
Hypoxic encephalopathy, Macro, autopsy (73805)
Hypoxic encephalopathy, Macro, autopsy (73803)
Hypoxic encephalopathy, Macro, autopsy (73806)
Hypoxic-ischemic encephalopathy in a child surving for 1 year:
Hypoxic encephalopathy, Macro, autopsy (73798)
Hypoxic encephalopathy, Macro, autopsy (73799)
Hypoxic encephalopathy, Macro, autopsy (73800)
Hypoxic encephalopathy, Macro, autopsy (73801)
Hypoxic-ischemic encephalopathy, multicystic:
Hypoxic encephalopathy, multicystic, Macro, autopsy (74385)
Hypoxic encephalopathy, multicystic, Macro, autopsy (74386)
Hypoxic encephalopathy, multicystic, Macro, autopsy (74387)
Hypoxic encephalopathy, multicystic, Macro, autopsy (74388)
Hypoxic encephalopathy, multicystic, Macro, autopsy (74389)
Hypoxic encephalopathy, multicystic, Macro, autopsy (74390)
Hypoxic encephalopathy, multicystic, Macro, autopsy (74391)
Meconium is the first intestinal discharge of newborn, viscous and dark green composed of intestinal epithelial cells, lanugo, mucus, intestinal secretions and swallowed amniotic fluid elements. Meconiumstained amniotic fluid may be than aspirated before or during birth causing neonatal respiratory distress syndrome. The causes of premature meconium passage in utero are not clear, hypoxic stress may play a role. Meconium aspiration syndrome is seen in term and postterm infants, it is rare before 34 weeks.
Failure to reduce pulmonary vascular resistance in the postnatal period
Preacinar and intra-acinar pulmonary arteries and arterioles show medial hyperplasia with extension of smooth muscle into small peripheral vessels. It is likely that the arterial changes begin in utero from increased sensitivity to hypoxia or stress or primary failure of mechanism governing arterial muscularization.
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