Meconium-stained Amniotic Fluid Revisited: A Holistic Perspective

WHAT’S NEW AND WHAT’S CHANGED

Meconium has been considered to be sterile. However, researchers have isolated bacterial remnants and communities within meconium. These are mainly of two types, namely those bacteria that produce lactic acid, such as lactobacillus, and those that belong to the family of the so-called enteric bacteria, such as Escherichia coli.⁹ Needless to say, this has clinical significance. In one study of the singleton pregnancies that ultimately had a cesarean delivery after a trial of labor, 5,883 had MSAF and those with MSAF had a significantly increased incidence of surgical site infection.¹⁰

The mechanisms underlying meconium passage in utero are not clear and appear to be complex. As mentioned before, the association of MSAF with fetal distress has been known since historic times. The explanation could lie in increased parasympathetic activity causing increased intestinal peristalsis and relaxation of the anal sphincter secondary to enhanced vagal output during episodes of fetal hypoxia. A study has also shown that the corticotropin-releasing factor, a known mediator of colonic motility, has been implicated in the pathogenesis of hypoxia-induced MSAF in a rat model.¹¹ Having said that, can we conclusively state that the presence of MSAF is a reliable sign of fetal hypoxia? The nuanced answer to that is that the current evidence does show an association between MSAF and fetal hypoxia, but are all cases of MSAF a reliable indicator of acute fetal distress, the answer has to be no.

Clinicians have associated the consistency and time of passage of meconium with adverse fetal outcomes. The risk of perinatal death is increased five to seven times when freshly passed or thick meconium is present at the onset of labor.¹² Infants with thin or old meconium are more likely to have passed meconium as a physiologic maturational process and they are more likely to be healthy at birth.¹³ Moreover, there is evidence that MSAF was associated with an increase in the rate of pathological intrapartum fetal heart rate patterns, intrapartum fevers, and operative vaginal and cesarean section deliveries, and these complications increased with the staining and thickness of the amniotic fluid.¹⁴ As a consequence of this, the consistency of meconium was an important factor in determining whether a neonate needs immediate endotracheal suctioning at birth. However, current evidence no longer supports this practice. If the infant is vigorous with good respiratory effort and a heart rate >100 beats/minutes, tracheal intubation to aspirate meconium should not be attempted; only the mouth and nose may be suctioned with a bulb or suction catheter. If the neonate is depressed, traditional teaching has always been that in the presence of MSAF, any form of positive pressure ventilation should be preceded by endotracheal suctioning or else it could result in the meconium being pushed further into the air passages. However, the current American Academy of Pediatrics/American Heart Association guidelines no longer recommend endotracheal suctioning before positive pressure ventilation even in depressed infants (2015 guidelines).¹⁵

Perineal suctioning of the oropharynx was recommended in the past in the presence of MSAF. However, based on available evidence, routine perineal suctioning of all babies in the presence of MSAF does not prevent MAS and has the potential risk of delaying proper resuscitative measures.^13,16

In the past, transcervical amnioscopy has been performed to visualize the color of the membranes, to predict the presence of MSAF. This was considered as a means of antenatal assessment of fetal wellbeing. However, this procedure is invasive and is no longer performed in a clinical setting, as meconium staining is no longer considered to be a reliable sign of acute fetal hypoxia.

Amnioinfusion, or transcervical infusion of normal saline, at body temperature, into the amniotic cavity, has been proposed as a method of reducing the risk of the MAS in patients with MSAF. The potential mechanisms include dilution of meconium, thus, reducing its mechanical and inflammatory effects, and cushioning of the umbilical cord, thus, correcting recurrent umbilical-cord compressions that lead to variable fetal heart rate decelerations and fetal acidemia. However, it must be kept in mind that this procedure is not without risk and the complications include uterine overdistension, hypertonus, infection, and amniotic fluid embolism. According to the ACOG Committee report 2006 (reaffirmed in 2018), the current evidence does not show that amnioinfusion reduces the incidence of MAS in patients with MSAF. NICE guidance of Nov 2006 also states that amnioinfusion should not be used routinely as a therapeutic tool and may be used only in a research setting.

Can ultrasonogram (USG) be used to predict the presence of meconium in the amniotic fluid? There is some evidence to show that echogenic amniotic fluid is associated with an increased incidence of MSAF; however, the sensitivity of this investigative modality appears to be poor.¹⁷

MECONIUM ASPIRATION SYNDROME

Meconium aspiration syndrome (MAS) has been defined as respiratory distress in an infant born through meconium-stained amniotic fluid with radiologic changes suggestive of this syndrome and whose symptoms cannot be otherwise explained.¹⁸ It is a common cause of severe respiratory distress in term neonates, with an associated highly variable morbidity and mortality. The pathophysiology of MAS is multifactorial and includes acute airway obstruction, surfactant dysfunction or inactivation, chemical pneumonitis, and persistent pulmonary hypertension of a newborn.¹⁸ Short-term complications include death, respiratory failure, ventilator-induced barotrauma, and development of pulmonary hypertension. Long-term complications include pulmonary sequelae such as wheezing in infancy and asthma in childhood. Long-term complications also include adverse neurodevelopmental outcomes.

This disorder is often life threatening, and approaches to the prevention of MAS have changed over time with collaboration between obstetricians and pediatricians forming the foundations for care. The wide use of surfactant and inhaled nitric oxide as therapeutic tools has led to decreased mortality and the need for extracorporeal membrane oxygenation.¹⁸ In developed countries, mortality rates have been reduced to below 5%.¹⁹

Approximately 30–50% of infants diagnosed with MAS will require continuous positive airway pressure (CPAP) or mechanical ventilation and these conventional ventilatory methods still remain the mainstay in the management of MAS. The optimum modes of ventilation for MAS, however, are yet to be formulated.²⁰

Does cesarean section reduce the incidence of MAS in patients with MSAF? This question has troubled both pediatricians and obstetricians. However, there is no evidence to show a difference in the neurodevelopmental outcomes of surviving infants born by normal spontaneous vaginal delivery vs cesarean section delivery.²¹

FUTURE RESEARCH AND GUIDANCE

Divon et al. evaluated the National Swedish Medical Birth Registry. In 181,524 singleton pregnancies with reliable dates delivered at greater than 40 weeks, the authors found a significant increase in the odds ratio for fetal death, due to MAS, at greater than 41 weeks of gestation.²² Hence, there could be grounds for deliberations on the current definition of postterm pregnancy which still remains 42 weeks or more.

Research in the area of prevention and treatment of MAS is ongoing especially on the role and timing of surfactant therapy and the role of antibiotics. Studies are also being conducted to determine “best” ventilatory strategies for the different grades of MAS.²⁰

A device to visualize the amniotic fluid prior to the rupture of membranes was tried out in the past without much success.²³ This is one area where technology and high-resolution ultrasound can be focused to provide a noninvasive method of detecting MSAF in the future.

CONCLUSION

In conclusion, we can say that the problem of MSAF will be faced by clinicians and the best way to reduce the “chill factor” would be to understand the pathogenesis of meconium release and its effect on the fetal respiratory system, and to be prepared to manage MAS. Multimodal management involving the obstetrician and the neonatologist would be the ideal approach to this problem. Strategies for the prevention of MSAF and MAS need to be formulated and standardized by consultative cooperation between the neonatologist and the obstetrician.

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