CHORIONAMNIONITIS, CHRONIC HYPOXIA, AND PATHOPHYSIOLOGICAL PRINCIPLES OF CARDIOTOCOGRAPHY

Research Article

Abstract

The presence of severe antenatal hypoxia is common and in this case the fetus shows CTG abnormalities. Although many fetuses with cerebral hypoxic ischemic insults arising in the antenatal period may not demonstrate uniform CTG anomalies, nevertheless on the birth test some well-defined CTG characteristics can be identified that may appear in the subsequent intrapartum period.

The peculiar CTG pattern in this situation, with fetuses with pre-existing hypoxia or neurological damage, is characterized by a fixed and relatively non-variable baseline, with reduced or absent variability that does not demonstrate the presence of fetal cyclic activity. Sometimes a tachycardia may be present, usually much higher than 160 bpm, especially if the hypoxic insult is recent. In the case of a hypoxic insult with a more distant onset, however, the baseline appears normal (110-160 bpm). Contrary to the three CTG pictures mentioned above, associated with hypoxia that begins and evolves during labor, this CTG picture constitutes the demonstration of the presence of a stable encephalopathy that cannot be modified by any obstetric intervention, even aggressive ones. If the fetus suffers a further hypoxic insult after such damage or develops intrapartum hypoxemia during labor, decelerations in the fetal heart rate may appear in response to uterine contractions. These appear to have the characteristic of appearing small and superficial. In the absence of acidemia, the CTG does not show the presence of decelerations despite the brain damage. At birth, these children show an increase in red blood cells, a lengthening of the elimination time of erythrocytes, which suggests the possibility of antenatal hypoxic damage with the presence of multi-organ dysfunction, delayed onset of convulsions, damage to the cerebral cortex, presence of long-standing meconium-stained amniotic fluid, meconium aspiration syndrome, and pulmonary hypertension. In this situation there are many fetuses who present an IUGR, who may more easily develop acidemia and show a short-lived bradycardia with a rapid return of the fetal heart rate to baseline after having suffered the acute hypoxemic insult and a tachycardia with return to baseline for increased sympathetic tone. An amniotized chorion can lead to generalized fetal inflammation, called Fetal Systemic Inflammatory Response Syndrome, which is produced, in part, by endothelial damage. This syndrome is associated with hypotension, neonatal seizures, mechanical ventilation of the newborn, meconium aspiration syndrome, multiple organ dysfunction, low APGAR at birth, neonatal depression, neonatal hypoxic ischemic encephalopathy, intraventricular hemorrhage with white matter damage, periventricular leukomalacia, bronchodysplasia pulmonary and cerebral palsy. Unfortunately, we do not have effective tools to diagnose these fetuses at risk of encephalopathy and infectious brain damage. CTG monitoring has low sensitivity in the detection of fetal systemic inflammatory response syndrome, placental inflammation or neonatal sepsis. When the infectious disease occurs isolated or associated with hypoxia, the following may be present: tachycardia, reduced variability, absence of fetal cyclic activity. However, none of these frameworks appear specific. Fetal tachycardia may be present without decelerations, and it seems that in such cases fetuses subject to infectious and/or inflammatory processes are more susceptible to even minimal hypoxic insults. In many cases the symptoms of infection and/or inflammation are not evident and the CTG pictures are non-specific. It appears important first to maintain a high level of suspicion and be aware that there are no reliable and predictive tools for diagnosing damage in an infected fetus. Although there is no evidence that cesarean section, in such cases of suspected or proven intrauterine infection with an uncertain temporal determination of fetal damage, is advantageous, however, especially if risk factors such as stained amniotic fluid, fever, CTG anomalies are present, IUGR, antepartum hemorrhage, it seems appropriate to resort to this operation and extract the fetus. In the case of fetal infection, it is necessary to avoid that intrapartum factors (prolonged labor, reckless use of oxytocin and uterine hyperstimulation, particularly traumatic vaginal operative birth) can aggravate the risk of brain damage. In such cases it is also necessary to avoid resorting to misleading means such as taking blood from the fetal scalp, STAN.