Meconium Aspiration
Meconium in a baby's lungs blocks the thin cell walls and prevents oxygen from passing through them into the bloodstream. Meconium also irritates the lining of the lungs and can cause an inflammation known as chemical pneumonitis. Meconium aspiration is most likely at the time of delivery as the baby takes his or her first full breath of air. The meconium may then be breathed right into the lungs. But if a baby has passed meconium earlier, aspiration can also occur earlier in labor or before labor begins.
In some cases, a baby with meconium aspiration goes on to develop pneumothorax, a dangerous condition in which a hole develops in the lung and air escapes through it into the chest. This air then exerts pressure on the lungs and prevents them from expanding.
Babies most at risk of meconium aspiration syndrome are those who are born after forty-two weeks, who are small for dates or who have been very short of oxygen during or before labor. Babies who develop an infection in the womb may also pass meconium before delivery and may take it in before or during delivery. -When a Baby Dies, by Nancy Kohner & Alix Henley, Thorsons, 1997
Fetal Heart Rate May Point To Meconium Aspiration
To identify the fetus and newborn at risk for meconium aspiration syndrome the perinatal characteristics of 238 infants delivered through meconium stained amniotic fluid were prospectively examined. All infants with meconium stained amniotic fluid were routinely suctioned with a DeLee apparatus before tracheal intubation and suctioning. The type and presence of meconium in the trachea, neonatal breathing before intubation, and Apgar scores were recorded in the delivery room. Despite suctioning with a DeLee apparatus and endotracheal suctioning, meconium was present in the trachea in 87 infants (37 percent) and meconium aspiration syndrome developed in 22 infants (8.6 percent). Of the infants delivered through thick meconium, meconium aspiration syndrome developed in 19 percent, as compared with 2.9 percent and 4.6 percent in the thin and moderate meconium groups.
Thick mecomium, the presence of fetal tachycardia, and absence of intrapartum fetal cardiac accelerations identified the fetus at high risk for meconium aspiration syndrome. The presence of these monitoring findings and thick meconium should alert practitioners to the possibility of a fetus that requires intervention. Low umbilical artery pH, Apgar scores <5, and meconium in the trachea further characterized the newborn at high risk for meconium aspiration syndrome. The combination of these findings may best identify the infant delivered through meconium stained amniotic fluid who requires close observation for meconium aspiration syndrome.
The authors of the study comment: "Our study differs from previous reports in that we analyzed fetal heart monitoring in addition to the intrapartum and newborn characteristics of infants delivered through meconium stained amniotic fluid . . . . The presence of fetal tachycardia may be a response by the fetus to compensate for hypoxemia and acidosis. The absence of intrapartum cardiac accelerations may represent failure of the fetus to compensate for the acidosis. The presence of these specific findings should alert the [practitioner] to a fetus at high risk of in utero aspiration of meconium. If these specific . . . findings and thick meconium are noted the [practitioner] or resuscitation team should be . . . prepared for resuscitation even if the infant undergoes suctioning with a DeLee apparatus and endotracheal suctioning. -Elena M. Rossi MD et al, "Meconium aspiration syndrome: Intrapartum and neonatal attributes," Am J Obstet Gynecol 1989; 161: 1106-10
Fetal Asphyxia
Meconium stained amniotic fluid occurs in approximately 12 percent of live births.In approximately one third of these infants meconium is present below the vocal cords. However, meconium aspiration syndrome develops in only two of every 1,000 live-born infants. Ninety-five percent of infants with inhaled meconium clear the lungs spontaneously. Recent investigations have suggested that a reexamination of our assumptions about the etiology of meconium aspiration syndrome is in order. Evidence has been provided that supports the hypothesis that it is not the inhaled meconium which produces the primary pathologic condition of meconium aspiration syndrome but rather it is fetal asphyxia that is the etiologic agent. Asphyxia in utero produces pulmonary vasospasm and hyperreactivity of the pulmonary vessels. With severe asphyxia the fetal lungs undergo pulmonary vascular damage with pulmonary hypertension. The damaged lungs are then unable to clear the meconium. In the most severe cases there is right-to-left shunting and persistent fetal circulation with subsequent fetal death. The incidence of meconium aspiration may thus be essentially unaffected by current obstetric and pediatric interventions at birth. For the asphyxiated or distressed infant, suctioning at birth and tracheal intubation is recommended. - VL Katz MD & WA Bowes Jr MD, "Meconium aspiration syndrome: Reflections on a murky subject," Am J Obstet Gynecol 1992; 166: 171-83
Postmaturity and Meconium Aspiration
Recent studies have concluded that true post-term babies have a higher morbidity and mortality rate, and may be at greater risk than moderately preterm babies . . . . There is a much higher incidence of meconium staining, premature aspiration of meconium (in utero), and meconium aspiration syndrome. Murray Enkin, et al, in "A Guide to Effective Care in Pregnancy and Childbirth," writes that "Perinatal mortality is increased in post-term pregnancy. Prolonged pregnancy is associated with an increased risk of intrapartum and neonatal death but not of antepartum death. The risk increases with the onset of labor. A higher prevalence of meconium stained amniotic fluid is an outstanding feature among the intrapartum and asphyxial neonatal deaths . . . . It is important, therefore, that the midwife make as accurate an estimation of gestational age as possible, in order to make appropriate care choices." -Valerie El Halta, Midwifery Today Issue No. 38
Reprinted from Midwifery Today E-News (Vol 1 Issue 12, Mar. 19, 1999)
To subscribe to the E-News write: enews@midwiferytoday.com
For all other matters contact Midwifery Today:
PO Box 2672-940, Eugene OR 97402
541-344-7438, midwifery@aol.com, Midwifery Today
|
|