What Is Meconium and What Causes it?
Meconium-stained amniotic fluid is often caused by fetal hypoxia or other physiologic stress
Any reflexive “gasping” of the unborn fetus, due to hypoxia, can depress the fetal diaphragm mechanically, squeezing the contents of the bowels into the amniotic fluid.
Meconium is made up of vernix, lanugo (fine hair), desquamated epithelial cells, and other intestinal contents (bile, mucus, etc.), and it can cause a harmless “meconium staining” of the fetal skin–often a greenish hue
Although the staining itself is harmless, it is a sign of something that can prove very dangerous if the fetus were to aspirate the meconium-stained amniotic fluid (→ causes Meconium Aspiration Syndrome (MAS) after delivery, a severe life-threatening pneumonitis).
The likelihood of this complication depends on the gestational age at delivery:
- 5% for premature babies;
- 15-20% of term babies; and
- 25-30% of post-term babies.
Why Is Meconium Dangerous?
Meconium is very inflammatory and irritating to the fetal lungs and can result in neonatal meconium pneumonitis, which has significant morbidity and mortality in the nursery.
It can result in complete or incomplete airway obstructions.
Complete airway obstructions include atelectasis and a right-to-left shunt across the foramen ovale due to the increased pulmonary pressure that atelectasis creates in the pulmonary vasculature.
Incomplete airway obstructions include “ball-valve” type obstructions, pneumothorax, and chemical irritation pneumonia.
Patient deterioration can occur due to meconium stained amniotic fluid that is aspirated into the fetal lungs before birth.
This results in hypoxia, hypercapnia (elevated CO2), and acidosis (blood pH < 7).
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Why Does Meconium-staining Occur?
Meconium is a sign of fetal distress, either on-going or old.
Meconium-stained amniotic fluid occurs “in utero” (inside the womb before delivery) and is mostly found in post-term and small-for-gestational-age (SGA) newborns.
Meconium AT THE TIME OF BIRTH is normal–merely a squeezing out of the intestines through the anus with the compression/decompression forces of delivery.
In post-term infants, the baby keeps growing (requiring more) but the placenta starts deteriorating (providing less), and these respective, opposing phenomena can clash.
In SGA babies, there usually has been compromise of the placenta that has negatively impacted its ability to oxygenate and provide adequate nutrition for adequate growth.
Both cases result in compromised infants that may lack adequate “reserve” to withstand the normal rigors of labor and delivery, creating hypoxia and with it, the mechanical breathing reflexes that result in the expulsion of meconium into the amniotic fluid.
The events may even possibly have been set in motion before labor! Most feel that the morbidity/mortality associated with meconium is not so much due to events at birth (“fetal distress”) but are a result of limited fetal reserve to tolerate challenges during birth, such as contractions with intermittent hypoxia–that is, events prior to birth that limit a baby’s ability to tolerate stress–events which could not have been controlled and are probably long over before labor and delivery even began. In other words, morbidity/mortality may be associated with the “fetal distress” associated with meconium, but it is the event(s) prior to birth that set the baby up for fetal distress when challenged against a limited fetal ability to withstand.
For all of the reasons above and because of all of the attributes meconium-stained amniotic fluid has, it is a phenomenon that carries with it a
- high mortality rate, an increased risk of hypoxemia,
- increased risk of aspiration pneumonia,
- increased risk of pneumothorax, and
- increased risk of pulmonary hypertension.
Risk factors for meconium-stained amniotic fluid include
- fetal distress during labor and delivery,
- post-term infants,
- infants who are SGA, and
- placental compromise due to smoking, hypertension, or substance abuse.
Types of Meconium: Thin and Thick
The thicker the meconium, the worse the associated morbidity and mortality due to the fact that thicker secretions simply muck up the works worse than thin, dilute secretions can.
Particulate meconium containing discrete globs of meconium is considered “thick” meconium. Whether the meconium is thin or thick is probably irrelevant, because meconium AT ALL is the risk factor for what might come after delivery.
Meconium of either variety may be noticed when spontaneous rupture of membranes shows the amniotic fluid has meconium.
MANAGEMENT OF MECONIUM
For interventions in cases of meconium-stained amniotic fluid or meconium noted with pre-delivery rupture of membranes, the obstetrical/pediatric literature has changed significantly since 2004, and with it, the standard of care.
This will impact any CURRENT EMS guidelines in what to do.
The OLD way of thinking:
This is included here only because some very capable EMS veterans and even many obstetricians will still swear by the technique of suctioning away any meconium at delivery while the head is on the mother’s perineum (before the first breath and the rest of the baby has delivered).
This also includes nasopharyngeal suctioning with a French catheter.
This strategy was developed in hopes of limiting the amount of meconium that might have pooled in the nasopharynx which could be inhaled into the lungs, the very thing that the suction was intended to reduce.
However, a study in 2004 evaluated outcomes in thousands of babies with meconium-stained amniotic fluid who were randomly separated: half had the suctioning, half did not.
The findings: There was no difference in the eventual outcomes–the need for mechanical ventilation, mortality, duration of oxygen therapy, or even length of hospital stay.
This study outcome was because the events that lead to morbidity and mortality occur in the uterus prior to birth and are therefore not affected by any type of suctioning.
In other words, the harm’s already been done and no amount of suctioning at delivery will alter that harm, already well in progress.
In addition, suctioning newborns can result in vagal bradycardia for up to 20 minutes.
“Newborns receiving bulb suctioning showed a statistically significant, lower heart rate (P=.042) during the first 20 minutes and a significantly higher SpO2 level (P=.005) by 15 minutes of age.” https://www.ncbi.nlm.nih.gov/pubmed/24911034
The NEW way of thinking (the current standard of care):
Do not suction the nares or nasopharynx at the time of delivery of the head, nor after completion of the delivery if the infant is “vigorous” (good APGAR).
In cases of “non-vigorous” (poor APGAR), endotracheal suctioning should not be done, either, but instead, guidelines are based on general principles of intubation for inadequate respiratory effort (gasping, labored breathing, or poor oxygenation), or a heart rate < 100 BPM.
If an infant develops signs of respiratory distress, this will usually happen within 15 minutes of birth.
Therefore, full-term infants with meconium-stained amniotic fluid without any sign of respiratory distress or depression immediately or very soon after birth are unlikely to develop complications of meconium aspiration syndrome.
The bottom line if there is meconium-stained amniotic fluid:
If the baby is vigorous, no suction at all is indicated, but merely wiping the face for purposes of reducing loss of heat.
If the baby is non-vigorous, no endotracheal suction, but endotracheal intubation for ventilation support of the bigger problem (that is, actual lung damage).
WHAT DO YOU DO? The old way or the new way?
Old habits die slow, and you may find yourself in a situation where the one in charge pursues the older strategy.
Therefore, you should submit to the chain of command and/or follow the local protocol. Except for a vagal reaction, there won’t be much of a downside.
The whole point is that there isn’t an “up-side” to doing it the old way.
(For purposes of your test, the smart money is probably on the old way due to the lag between the literature and practice.)
Other Considerations in Management:
- Circulation support and pharmacologic intervention should be applied as necessary.
- Possible non-pharmacologic intervention may include needle decompression and hypothermia prevention.
- Transport considerations include the identification of and transport to a facility able to handle high-risk newborns if the baby is non-vigorous, but transport to any obstetrical facility for neonatal surveillance in vigorous babies even with meconium-stained amniotic fluid.
- Psychological support and communication strategies include explaining what is being done for the newborn and refraining from discussing “chances of survival” with the family.
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