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Meconium in labour
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Meconium in labour
of hypoxic stress. It does seem evident; however, that in the preterm fetus, the passage of meconium, although a relatively rare event, is of significance as this group has a particularly high rate of perinatal morbidity and mortality when labour is associated with MSAF. This review aims to discuss the theories behind the production of meconium, its implications during labour, the complications associated with its presence and the evidence for any potential therapeutic options available.
Jeffrey Unsworth Sarah Vause
Abstract Meconium staining of the amniotic fluid is a common occurrence during labour and although a large proportion of these pregnancies will have a normal neonatal outcome, its presence may be an indicator of fetal hypoxia and has been linked to the development of cerebral palsy, seizures and meconium aspiration syndrome. The management of the intrauterine passage of meconium has been controversial but appropriate intrapartum care with early detection and management of fetal hypoxia is important in minimizing the risk from meconium staining of the amniotic fluid. This review looks at the evidence for the potential mechanisms implicated in the passage of meconium; its intrapartum management and possible interventions available to reduce the risk of meconium aspiration. The neonatal complications and immediate delivery room management of the meconium-stained neonate are also discussed.
Formation and composition of meconium The name meconium is derived from the name meconium-arion, meaning “opium-like”, and has been linked with Aristotle’s belief that it induced sleep in the fetus. It first appears within the fetal gastrointestinal tract at 70e85 days gestation as a viscous substance made up primarily of water (70e80%). Other constituents include intestinal epithelial cells, squamous cells, lanugo, amniotic fluid, bile acids and salts (giving the characteristic green colour), phospholipase A2, interleukin-8, mucus glycoproteins, lipids and proteases. The main theories accounting for the passage of meconium before birth are based on those of fetal maturation and fetal stress.
Keywords meconium; meconium aspiration syndrome; meconium liquor
Fetal maturation: although meconium appears very early in the gastrointestinal tract, MSAF rarely occurs before 34 weeks gestation and appears increasingly with advancing gestational age with its incidence increasing to 30e40% over 42 weeks. Motilin, an intestinal polypeptide which stimulates contraction of intestinal muscle, is found in higher concentrations in post-term than pre-term fetal gastrointestinal tracts. Furthermore, intestinal parasympathetic innervation and myelination also increase in later gestations implying that the increasing incidence may reflect the maturation of peristalsis in the fetal intestine. Therefore, at increasing gestations, particularly post-term, MSAF may be a physiological event, simply reflecting the maturation of fetal intestinal function.
Introduction Meconium-stained amniotic fluid (MSAF) occurs as a result of the passage of fetal colonic contents into the amniotic fluid. It occurs in approximately 15e20% of term pregnancies but this number increases to 30e40% in the post-term pregnancy. MSAF has been linked with an increased risk of developing chorioamnionitis and is associated with adverse fetal outcomes including neonatal sepsis, cerebral palsy, seizures and in particular an increased risk of the neonate developing meconium aspiration syndrome, which in itself accounts for approximately 2% of perinatal deaths. The passage of meconium, in part, is thought to be due to physiological fetal gut maturation, thereby, explaining the higher incidence in the post-term pregnancy. It has also been suggested that fetal hypoxia and acidaemia may also be implicated in the pathogenesis of MSAF, thereby, acting as a potential sign of fetal distress. However, the exact relationship between fetal distress and MSAF is uncertain; passage of meconium may occur in the absence of any sustained hypoxia or increased neonatal morbidity or mortality and conversely fetal distress may occur in the absence of any meconium passage. For this reason it is controversial whether the in utero passage of meconium represents normal gut maturation or occurs as a result
Fetal stress: MSAF has also been attributed to a fetal response to intrauterine stress and hypoxia, with the passage of meconium occurring more frequently when umbilical vein oxygen saturations are below 30%. Furthermore, the degree of MSAF is related to the degree of hypoxia with “thick” stained MSAF being associated with lower oxygen concentrations than “light” stained MSAF. One theory to explain this is that of intestinal ischaemia, which is thought to result in relaxation of the fetal anal sphincter and increased gastrointestinal peristalsis, thereby, leading to the passage of meconium. It has been theorized, therefore, that during hypoxia, the fetal circulation shunts blood away from the bowel and directs it to the brain and heart, thereby contributing to intestinal ischaemia and subsequently MSAF. Conversely, in animal studies, term rabbits failed to pass meconium during a hypoxic insult, calling into question, whether this mechanism is a major cause for meconium passage in a hypoxic human fetus. Vagally mediated gastrointestinal peristalsis in response to head or cord compression (the same reflex which initiates variable decelerations) may also be associated with meconium passage in the absence of fetal distress.
Jeffrey Unsworth MB ChB is a Specialist Registrar in Obstetrics and Gynaecology at St Mary’s Hospital, Manchester, UK. Conflicts of interest: none declared. Sarah Vause MD MRCOG is a Consultant Obstetrician and Sub-specialist in Maternal and Fetal Medicine at St Mary’s Hospital, Manchester, UK. Conflicts of interest: none declared.
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Meconium passage, which may be secondary to smooth muscle contraction in the fetal gastrointestinal tract, has also been linked to the use of misoprostol when inducing labour. The exact mechanism for meconium passage in the human fetus is still not completely understood and may be a combination of all the above. It should be emphasized, however, that despite being complicated by the presence of MSAF, many pregnancies do not have any adverse outcome, and indeed fetal distress occurs frequently in the absence of the passage of meconium, therefore, more research is required for us to fully understand the relationship between MSAF and fetal distress.
The Apgar scoring system
Apgar sign Activity (muscle tone) Pulse Grimace (reflex irritability) Appearance (skin colour) Respiration
Grading of meconium For many years attempts have been made to correlate increased meconium thickness with a worse perinatal outcome, but due to the subjectivity of assessing meconium thickness, it makes it very difficult to compare studies with any scientific rigour. Indeed, it has been shown that inter- and intra-observer agreement on visual grading of MSAF thickness is poor (Table 1 illustrates a common grading system of meconium). However, there does appear to be a significant linear association between meconium thickness and abnormal fetal heart rate patterns during labour, low Apgar scores (Table 2) and risk for caesarean section delivery. There also appears to be a higher risk of neonatal intensive care admission in pregnancies with thick meconium as compared to those with clear amniotic fluid, suggesting that thick meconium, not thin, is associated with an increased risk for perinatal complications during labour and delivery. A system of measuring quantitative meconium concentrations using a “meconiumcrit” (percentage by volume of the solid component of meconium) was proposed in the 1990s, but this has not been adopted clinically, as a study investigating the value of measuring meconiumcrit showed no significant correlation with umbilical artery pH or Apgar score and no clinical benefit. However, it should be noted that two cases of meconium aspiration syndrome occurred within this study, both of which were from the “thick” meconium group. Although there is limited good quality evidence suggesting that the use of a system to grade meconium has any significant impact on neonatal outcome, most obstetricians would consider thick meconium a more ominous sign than thin and the National Institute of Clinical Excellence (NICE) recommends a standardized scoring system for the degree of meconium staining and its association with neonatal outcome. Further to this, accurately estimating the degree of meconium thickness is of importance as it helps determine the intensity of monitoring required following birth.
Grade 2 Grade 3 (thick)
Entire body normal Good, crying
Normal, except Pale all over for extremities Slow, irregular Absent
0 Points Absent Absent Absent
Intrapartum management Due to the mechanisms mentioned above, meconium passage may have different clinical significance at different gestations. Meconium in the term fetus As the fetal gut matures, meconium moves closer to the distal colon and rectum. Therefore, at term there is a close proximity between the meconium and the anal sphincter. For this reason, the amount of fetal stress required to initiate the release of meconium may be trivial and unsustained, such as occurs with cord compression during normal labour. However, in the absence of the stress of labour, meconium may be more significant. Risk factors for MSAF in the term fetus are shown in Table 3. The presence of MSAF in early labour is associated with an increased rate of caesarean section delivery compared to the presence of clear amniotic fluid, due to the increased rate of fetal heart rate abnormalities observed in this group, in particular, the presence of early and variable decelerations, explainable by the theory of cord compression. Numerous studies have utilized cardiotocographical fetal heart rate recordings, cord pH measuring and Apgar scores to try and ascertain the relevance of MSAF in the term fetus and its impact on neonatal outcome in order to determine any way of identifying the at-risk pregnancy. The evidence suggests that in
Risk factors for meconium passage Risk factors for meconium-stained amniotic fluid Post-term pregnancy Placental insufficiency Maternal hypertension and pre-eclampsia Maternal diabetes Fetal heart rate abnormalities IUGR Poor biophysical profile Smoking Oligohydramnios Cocaine abuse
Refers to light green or flecking of otherwise clear amniotic fluid Brown but thin uniform staining of the amniotic fluid Bright green or brown thick uniform staining of the amniotic fluid
Table 1
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1 Point Arms and legs flexed <100 Grimace
Table 2
Standard grading system for meconium thickness Grade 1 (thin)
Score 2 Points Active movements >100 Sneeze, coughs
Table 3
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the presence of a normal fetal heart rate pattern there is no significant correlation between MSAF and umbilical cord artery pH. However, when fetal heart rate abnormalities are present, the passage of meconium is associated with a lower umbilical artery pH compared to those with clear amniotic fluid. Regardless of a normal or abnormal fetal heart rate pattern, MSAF is associated with lower Apgar scores at 1 and 5 min than when compared with similar heart rate patterns with clear amniotic fluid, the degree of which is associated with increasing meconium thickness. This could potentially be explained either by vigorous suctioning to clear meconium from the larynx, the degree of neonatal asphyxia or neonatal aspiration of meconium. More objective intrapartum measures have been used to assess whether meconium alone can signify fetal distress. Fetal blood samples taken during labour have shown that the presence of meconium in the absence of fetal heart rate abnormalities is associated with higher fetal scalp pH recordings and better Apgar scores than compared to MSAF with fetal heart rate abnormalities. This suggests that meconium passage, in the absence of other signs of fetal distress, is not a sign of hypoxia and therefore, is not an indication for fetal blood sampling. Fetal heart rate abnormalities are thus a better predictor of fetal hypoxia than meconium alone, and the appearance of an abnormal heart rate tracing in the presence of MSAF is a strong indicator of fetal distress, above and beyond that seen with fetal heart rate abnormalities alone. Furthermore meconium-stained amniotic fluid, in the absence of fetal heart rate abnormalities, is associated with reduced Apgar scored and an increased perinatal morbidity and mortality, likely due to meconium aspiration following birth of an otherwise healthy fetus. The early detection and management of fetal hypoxia are important in minimizing the risk from meconium staining of the amniotic fluid. For this reason, NICE has made several recommendations related to the intrapartum management of meconium staining: 1. Continuous electronic fetal monitoring for any women with significant MSAF, defined as dark green or black amniotic fluid that is thick or tenacious or any amniotic fluid containing lumps of meconium 2. Continuous electronic fetal monitoring to be considered for women with light-stained liquor depending on a risk assessment, including as a minimum, their stage of labour, volume of liquor, parity, fetal heart rate pattern, and transfer pathway 3. If there are any cardiotocographical signs of fetal distress, a fetal blood sample should be obtained. If pH is below 7.21 then an emergency delivery should be performed
increased incidence of cerebral palsy and intraventricular haemorrhage. MSAF in the pre-term fetus, especially in the mid-trimester, may also be associated with acute ascending infections, and it has been speculated that intra-amniotic infections may cause fetal gastroenteritis and diarrhoea. Women in pre-term labour with meconium-stained liquor have a higher incidence of clinical chorioamnionitis when compared to those with clear liquor. Amniocenteses conducted on women presenting with pre-term labour with intact membranes have shown a significantly increased rate of positive amniotic fluid microbial cultures when meconium liquor is present and these women are more likely to deliver pre-term, suggesting that meconium passage is a risk factor for microbial invasion, chorioamnionitis and pre-term delivery. Haematogenous Listeria infection has also been associated with pre-term MSAF. However, the incidence of this has been found to be quite low and the presence of meconium is not a useful indicator of listeriosis infection.
Complications of meconium-stained amniotic fluid MSAF in the presence of fetal heart rate abnormalities is a strong indicator of fetal distress; however, it is also associated with complications in the newborn. Meconium directly alters the amniotic fluid, reducing its antibacterial activity, thereby; increasing the risk of perinatal bacterial infection, however, the most severe complication of MSAF is meconium aspiration syndrome. Meconium aspiration syndrome Various components of meconium, in particular, bile salts and enzymes can cause complications if aspirated into the lungs of an infant prior to, during or immediately after birth, thereby, resulting in the Meconium Aspiration Syndrome. This occurs in approximately 5% of infants born with MSAF and has a mortality rate in the region of 3e5%. Meconium aspiration syndrome describes a wide spectrum of respiratory disease, ranging from mild respiratory distress to severe disease and death despite mechanical ventilation. Prior to the late 1970s it was thought that aspiration of amniotic fluid and meconium only occurred during the first few breaths after delivery, however, meconium has been found distally as far as the alveoli in stillborn infants. Further to this, studies with radio-opaque contrast and Cr51 labelled erythrocytes injected into amniotic fluid have demonstrated that amniotic fluid enters the fetal lungs in the non-asphyxiated human fetus, suggesting that meconium aspiration occurs in utero. Animal studies have also shown that intrauterine gasping, resulting in greater aspiration of meconium, occurs in fetuses exposed to hypoxia, implying that fetal distress is a risk factor for development of meconium aspiration syndrome. Currently, there is no way to distinguish those who develop meconium aspiration from intrauterine gasping and those who develop it by inhalation at birth. Perhaps the most significant risk factor for meconium aspiration syndrome is post-term delivery, due to the high prevalence of MSAF in this population and the increased incidence of oligohydramnios in these pregnancies. Oligohydramnios predisposes to cord
Meconium in the pre-term fetus The incidence of MSAF in the pre-term fetus is approximately 5% but is associated with a poorer neonatal outcome when compared to similar gestations with clear amniotic fluid, suggesting that meconium-stained amniotic fluid is a gestational age independent risk factor. At term, only a relatively small amount of stress is required to result in the passage of meconium, however, in the pre-term fetus, the greater colonic distance over which the meconium has to travel, implies a greater severity and/or duration of stress, and may explain the increased perinatal morbidity and mortality seen in this group, particularly the
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compression which may help explain the higher frequency of meconium passage at this gestation, but more importantly, meconium passage in the presence of oligohydramnios results in a thicker meconium-stained amniotic fluid which can result in a more serious meconium aspiration syndrome and poorer neonatal outcome.
leading to decreased lung compliance and oxygenation. If persistent hypoxia occurs then pulmonary hypertension may develop, a common finding in fatal meconium aspiration syndrome. The pathophysiology of meconium aspiration syndrome is summarized in Figure 1.
Pathophysiology: the mechanism by which meconium induces this syndrome is likely to be a combination of mechanical airway obstruction, chemical irritation resulting in a pneumonitis, surfactant inactivation and a predisposition to secondary infection. Airway obstruction is usually the initial problem encountered by the neonate with meconium aspiration syndrome, although complete obstruction is unusual. Small amounts of meconium may migrate to the distal airways leading to pulmonary air trapping, hyperinflation of the lungs and possibly subsequent pneumomediastinum or pneumothorax. A pneumonitis may develop due to the direct toxic effect of meconium contents and the infiltration of a large number of polymorphonuclear leucocytes and macrophages into the airways and lung parenchyma mediating an intense inflammatory response resulting in direct tissue injury. This inflammatory response is mediated by chemotactic cytokines present in meconium which lead to high levels of vasoactive mediators (leukotrienes, prostaglandins) resulting in pulmonary vasoconstriction. Meconium may also displace surfactant from the alveolar surface, thereby, reducing its tension lowering abilities
Management: the management of babies born with meconiumstained liquor has been controversial; many believe that the most effective intervention for preventing meconium aspiration syndrome involves removal of meconium from the pharynx and trachea either before or after birth. For this reason it was previously proposed that all babies born through meconium-stained amniotic fluid should receive suction to the mouth and oropharynx before delivery of the shoulders and trunk and then undergo tracheal intubation and tracheal aspiration through the endotracheal tube. However, this was repeatedly challenged and more recent evidence suggests a more liberal approach can be used depending on the neonatal condition at birth and the degree of meconium staining of the amniotic fluid. Oropharyngeal and nasopharyngeal suctioning prior to birth of the shoulders, once almost universally accepted, has more recently been shown to have no effect on the incidence of meconium aspiration syndrome, the need for mechanical ventilation or duration of hospital stay when compared to not suctioning. Therefore, NICE recommends against its use prior to delivery.
Pathophysiology of meconium aspiration syndrome Physiological meconium passage
Fetal distress
Meconium stained amniotic fluid
Postpartum aspiration
Intrauterine gasping
Meconium aspiration
Airway obstruction
Cytokine induced pneumonitis
Surfactant inactivation
Hypoxia acidosis
Decreased lung compliance
Pulmonary air trapping Atelectasis Ventilation/perfusion mismatch
Persistent pulmonary hypertension
Figure 1
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Tracheal suctioning has been a matter of controversy for many years, some proposing suctioning for all pregnancies complication by meconium, others proposing no suction for any case and some proposing the use of selective suctioning based on the degree of meconium thickness and infant vigour. It appears that neonates born with good muscle tone and a normal heart rate (>100 beats per minute) do not benefit from tracheal suctioning; there is no reduction in meconium aspiration syndrome or improvement in neonatal outcome. Additionally, a vigorous baby can make visualization of the vocal cords difficult, thereby, potentially increasing the risk of oesophageal or tracheal injury. NICE, therefore, recommends that the upper airways should only be suctioned if there is thick or tenacious meconium present in the oropharynx. If, however, the infant is depressed, laryngoscopy and suction under direct vision should be carried out by a healthcare professional trained in advanced neonatal life support. Suctioning to empty the stomach of meconium at birth has also been proposed to reduce the risk of meconium aspiration syndrome, the rationale being that it could later be regurgitated and aspirated. However, there is insufficient evidence to recommend for or against it. The risk of developing meconium aspiration syndrome is thought to be related to the circumstances in which meconium passage occurred. Postdate pregnancies associated with the passage of thin meconium are unlikely to develop any serious complications following delivery. Those who suffer an acute intrauterine hypoxic event during labour are more likely to pass thick meconium and are at high risk of the obstructive and local inflammatory effects of meconium and of developing the meconium aspiration syndrome. These are likely to benefit the most from meconium clearing manoeuvres. Those who have suffered from chronic intrauterine hypoxia are more likely to have undergone muscularization and thickening of the pulmonary arteries and are subsequently more likely to develop pulmonary hypertension and to be depressed at birth. Further to this, chronic hypoxia increases the risk of meconium passage and incidence of intrauterine gasping with subsequent aspiration of meconium. Therefore, efforts to remove meconium at birth may be ineffective at reducing the risk of meconium aspiration syndrome in this group. Most vigorous babies born through thick meconium-stained amniotic fluid do not require any intervention besides being monitored for signs of respiratory distress, which if occurs generally develops within 12 h of birth. NICE recommends these neonates should be closely observed at 1 and 2 h after delivery and then every 2 h for the first 12 h of life. Those born through light MSAF should be observed at 1 and 2 h of life and reviewed by a neonatologist if there are concerns at any time. Observations should include: General wellbeing Chest movement and nasal flare Skin colour Feeding Muscle tone Temperature Heart rate and respiration A recent study has shown that meconium aspiration syndrome rarely develops in neonates with Apgar scores above 8 at 5 min
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and suggests that these can be safely discharged shortly after birth; however, this has not yet been put into routine practice. If there are signs of meconium aspiration syndrome then transfer to the neonatal intensive care unit (NICU) may be required, to allow the full range of respiratory support and close monitoring to be undertaken. These neonates may require more invasive treatments including mechanical ventilation, surfactant therapy and extracorporeal membrane oxygenation (ECMO). Infection There is a link between MSAF and the development of chorioamnionitis, with the incidence of clinical and histological chorioamnionitis being higher when associated with intrapartum meconium-stained amniotic fluid compared to clear amniotic fluid. This has several possible implications; namely it increases the risk of neonatal sepsis and subsequent perinatal morbidity and mortality, secondly, it predisposes to dystocias, thereby, increasing the rates of operative delivery, and thirdly, chorioamnionitis is a risk factor for the development of postpartum endometritis and its associated maternal morbidity. Amniotic fluid in general is quite a poor growth medium for bacteria; however, in the presence of meconium there is a three-fold increase in bacterial isolates from meconium-stained amniotic fluid compared to clear amniotic fluid. It is thought that meconium may mediate the increase in bacterial growth by acting as a growth factor, inhibiting bacteriostatic properties of amniotic fluid or by antagonizing host defense systems in particular neutrophil phagocytosis. The most common bacterial isolates are Ureaplasma urealyticum, Escherichia coli, Candida albicans, Streptococci and Listeria monocytogenes. It has been suggested that intrapartum MSAF should be considered a potential marker for infectious morbidity but whether prophylactic antibiotics are of benefit in reducing the maternal and fetal morbidity is unknown and requires further research.
Prevention of meconium aspiration syndrome Many cases of meconium aspiration syndrome can be prevented by assessment of risk factors, continuous fetal monitoring and appropriate removal of meconium from the pharynx and trachea. However, although airway suctioning is thought to reduce the incidence of meconium aspiration it does not eliminate the risks entirely because fetal gasping may result in the entry of meconium into the lungs prior to birth. For this reason, several other methods have been proposed to reduce the perinatal mortality and morbidity caused by meconium-stained amniotic fluid. In under resourced countries, paediatric facilities for the management of meconium aspiration syndrome are frequently absent, thereby, increasing the importance of an intervention. Amnioinfusion Amnioinfusion has been proposed as one method of reducing the risk of meconium aspiration syndrome. It involves infusing normal saline transcervically through a catheter into the uterine cavity, thereby diluting any meconium present and reducing its mechanical and inflammatory effects. As oligohydramnios is associated with thick meconium-stained amniotic fluid, increasing the volume of fluid in the amniotic cavity may also reduce the
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FURTHER READING Baker PN, Kilby MD, Murray H. An assessment of the use of meconium alone as an indication for fetal blood sampling. Obstet Gynecol 1992; 80: 792e6. Hofmeyr GJ, Xu H. Amnioinfusion for meconium-stained liquor in labour. Cochrane Database Syst Rev, http://dx.doi.org/10.1002/14651858. CD000014.pub3; 2010. Art. No.: CD000014. Intrapartum care: care of healthy women and their babies during childbirth. London: National Collaborating Centre for Women’s and Children’s Health, http://www.nice.org.uk/CG55; 2007. Lucas A, Adrian TE, Aynsley-Green A, Bloom SR. Gut hormones in fetal distress. Lancet 1979; 2: 968. Pritchard J. Fetal swallowing and amniotic fluid volume. Obstet Gynecol 1966; 28: 606e10. Sheiner E, Hadar A, Shoham-Vardi I, Hallak M, Katz M, Mazor M. The effect of meconium on perinatal outcome: a prospective analysis. J Matern Fetal Neonatal Med 2002; 11(1): 54e9. Siriwachirachai T, Sangkomkamhang US, Lumbiganon P, Laopaiboon M. Antibiotics for meconium-stained amniotic fluid in labour for preventing neonatal sepsis (protocol). Cochrane Database Syst Rev, http://dx.doi.org/10.1002/14651858.CD007772; 2009. Art. No.: CD007772. Steer PJ, Eigbe F, Lissauer TJ, Beard RW. Interrelationships among abnormal cardiotocograms in labor, meconium staining of the amniotic fluid, arterial cord blood pH, and Apgar scores. Obstet Gynecol 1989; 74(5): 715e21. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM, Vivas NI. Oropharyngeal and nasopharyngeal suctioning of meconium-stained neonates before delivery of their shoulders: multicentre, randomised controlled trial. Lancet 2004; 364: 597e602. Wennerholm UB, Hagberg H, Brorsson B, Bergh C. Induction of labor versus expectant management for post-date pregnancy: is there sufficient evidence for a change in clinical practice? Acta Obstet Gynecol Scand 2009; 88: 6e17.
frequency of umbilical cord compressions, thereby reducing risk of fetal hypoxia and meconium passage. A Cochrane review found no evidence that amnioinfusion caused any significant improvement in rates of caesarean section, meconium aspiration syndrome, severe perinatal morbidity or perinatal death in settings with standard perinatal surveillance; therefore, it is not recommended as standard for pregnancies complicated by meconium. Complications of amnioinfusion include umbilical cord prolapse, uterine scar rupture and amniotic fluid embolus. NICE does not currently recommend its use. Induction of labour at 41 weeks Due to the high prevalence of MSAF in the post-term pregnancy, it has been speculated that induction of labour may decrease the incidence of fetal distress and meconium aspiration syndrome. It has been shown that when compared with expectant management of post-term pregnancies, elective induction of labour at 41 weeks gestation is associated with lower rates of meconium aspiration syndrome and caesarean section, but there is no significant reduction in perinatal mortality. Other potential methods There is no evidence to support the use of maternal narcotics to reduce the incidence of fetal gasping. Various methods of physiotherapy such as postural drainage, cricoid pressure, and vibratory therapy for neonates born through MSAF, have not been shown to be of any benefit, and indeed are not without complications and delay the institution of more effective therapies, therefore, they are not recommended.
Conclusion The management of intrauterine meconium passage has generated considerable controversy. Its exact relationship with fetal distress is complex, dependent on several factors including fetal gestation and heart rate abnormalities and is not completely understood. Meconium passage continues to be a common problem and meconium aspiration syndrome is associated with many cases of neonatal respiratory distress, neurological complications and death. Despite numerous interventions the incidence of meconium-stained amniotic fluid is unlikely to decrease, therefore, the challenge is in identifying those pregnancies which are at risk of adverse neonatal outcome and meconium aspiration syndrome. Those at greatest risk are those with intrauterine hypoxia, those born with thick meconium and those whose fetal vigour is depressed at birth. The finding of meconium, therefore, should prompt a thorough evaluation of the patient and the institution of continuous fetal monitoring for fetal wellbeing; abnormal fetal heart rate patterns being the best predictor of those who will require intervention at birth. Many cases of meconium aspiration syndrome can be prevented by assessment of risk factors, continuous fetal monitoring and removal of meconium from the airways, however this will not prevent all, therefore, it is important that all healthcare professionals who attend delivers have an understanding of the management of MSAF and be trained in the proper obstetric and neonatal interventions required. A
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Meconium-stained amniotic fluid is associated with increased morbidity and mortality in babies. Women with thick meconium should be advised to have continuous electronic fetal monitoring. If significant meconium-stained amniotic fluid is identified healthcare professionals trained in fetal blood sampling should be available during labour and a fetal blood sample taken if cardiotocographical evidence of fetal distress. Healthcare professionals trained in advanced neonatal life support should be available at birth for significantly stained neonates. Vigorous babies born through thick meconium require close monitoring at 1 and 2 h following birth, then every 2 h for 12 h. Vigorous babies born through thin meconium require close monitoring at 1 and 2 h only. Amnioinfusion is not recommended to treat meconium-stained amniotic fluid.
Ó 2010 Elsevier Ltd. All rights reserved.
Meconium in labour
of hypoxic stress. It does seem evident; however, that in the preterm fetus, the passage of meconium, although a relatively rare event, is of significance as this group has a particularly high rate of perinatal morbidity and mortality when labour is associated with MSAF. This review aims to discuss the theories behind the production of meconium, its implications during labour, the complications associated with its presence and the evidence for any potential therapeutic options available.
Jeffrey Unsworth Sarah Vause
Abstract Meconium staining of the amniotic fluid is a common occurrence during labour and although a large proportion of these pregnancies will have a normal neonatal outcome, its presence may be an indicator of fetal hypoxia and has been linked to the development of cerebral palsy, seizures and meconium aspiration syndrome. The management of the intrauterine passage of meconium has been controversial but appropriate intrapartum care with early detection and management of fetal hypoxia is important in minimizing the risk from meconium staining of the amniotic fluid. This review looks at the evidence for the potential mechanisms implicated in the passage of meconium; its intrapartum management and possible interventions available to reduce the risk of meconium aspiration. The neonatal complications and immediate delivery room management of the meconium-stained neonate are also discussed.
Formation and composition of meconium The name meconium is derived from the name meconium-arion, meaning “opium-like”, and has been linked with Aristotle’s belief that it induced sleep in the fetus. It first appears within the fetal gastrointestinal tract at 70e85 days gestation as a viscous substance made up primarily of water (70e80%). Other constituents include intestinal epithelial cells, squamous cells, lanugo, amniotic fluid, bile acids and salts (giving the characteristic green colour), phospholipase A2, interleukin-8, mucus glycoproteins, lipids and proteases. The main theories accounting for the passage of meconium before birth are based on those of fetal maturation and fetal stress.
Keywords meconium; meconium aspiration syndrome; meconium liquor
Fetal maturation: although meconium appears very early in the gastrointestinal tract, MSAF rarely occurs before 34 weeks gestation and appears increasingly with advancing gestational age with its incidence increasing to 30e40% over 42 weeks. Motilin, an intestinal polypeptide which stimulates contraction of intestinal muscle, is found in higher concentrations in post-term than pre-term fetal gastrointestinal tracts. Furthermore, intestinal parasympathetic innervation and myelination also increase in later gestations implying that the increasing incidence may reflect the maturation of peristalsis in the fetal intestine. Therefore, at increasing gestations, particularly post-term, MSAF may be a physiological event, simply reflecting the maturation of fetal intestinal function.
Introduction Meconium-stained amniotic fluid (MSAF) occurs as a result of the passage of fetal colonic contents into the amniotic fluid. It occurs in approximately 15e20% of term pregnancies but this number increases to 30e40% in the post-term pregnancy. MSAF has been linked with an increased risk of developing chorioamnionitis and is associated with adverse fetal outcomes including neonatal sepsis, cerebral palsy, seizures and in particular an increased risk of the neonate developing meconium aspiration syndrome, which in itself accounts for approximately 2% of perinatal deaths. The passage of meconium, in part, is thought to be due to physiological fetal gut maturation, thereby, explaining the higher incidence in the post-term pregnancy. It has also been suggested that fetal hypoxia and acidaemia may also be implicated in the pathogenesis of MSAF, thereby, acting as a potential sign of fetal distress. However, the exact relationship between fetal distress and MSAF is uncertain; passage of meconium may occur in the absence of any sustained hypoxia or increased neonatal morbidity or mortality and conversely fetal distress may occur in the absence of any meconium passage. For this reason it is controversial whether the in utero passage of meconium represents normal gut maturation or occurs as a result
Fetal stress: MSAF has also been attributed to a fetal response to intrauterine stress and hypoxia, with the passage of meconium occurring more frequently when umbilical vein oxygen saturations are below 30%. Furthermore, the degree of MSAF is related to the degree of hypoxia with “thick” stained MSAF being associated with lower oxygen concentrations than “light” stained MSAF. One theory to explain this is that of intestinal ischaemia, which is thought to result in relaxation of the fetal anal sphincter and increased gastrointestinal peristalsis, thereby, leading to the passage of meconium. It has been theorized, therefore, that during hypoxia, the fetal circulation shunts blood away from the bowel and directs it to the brain and heart, thereby contributing to intestinal ischaemia and subsequently MSAF. Conversely, in animal studies, term rabbits failed to pass meconium during a hypoxic insult, calling into question, whether this mechanism is a major cause for meconium passage in a hypoxic human fetus. Vagally mediated gastrointestinal peristalsis in response to head or cord compression (the same reflex which initiates variable decelerations) may also be associated with meconium passage in the absence of fetal distress.
Jeffrey Unsworth MB ChB is a Specialist Registrar in Obstetrics and Gynaecology at St Mary’s Hospital, Manchester, UK. Conflicts of interest: none declared. Sarah Vause MD MRCOG is a Consultant Obstetrician and Sub-specialist in Maternal and Fetal Medicine at St Mary’s Hospital, Manchester, UK. Conflicts of interest: none declared.
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Meconium passage, which may be secondary to smooth muscle contraction in the fetal gastrointestinal tract, has also been linked to the use of misoprostol when inducing labour. The exact mechanism for meconium passage in the human fetus is still not completely understood and may be a combination of all the above. It should be emphasized, however, that despite being complicated by the presence of MSAF, many pregnancies do not have any adverse outcome, and indeed fetal distress occurs frequently in the absence of the passage of meconium, therefore, more research is required for us to fully understand the relationship between MSAF and fetal distress.
The Apgar scoring system
Apgar sign Activity (muscle tone) Pulse Grimace (reflex irritability) Appearance (skin colour) Respiration
Grading of meconium For many years attempts have been made to correlate increased meconium thickness with a worse perinatal outcome, but due to the subjectivity of assessing meconium thickness, it makes it very difficult to compare studies with any scientific rigour. Indeed, it has been shown that inter- and intra-observer agreement on visual grading of MSAF thickness is poor (Table 1 illustrates a common grading system of meconium). However, there does appear to be a significant linear association between meconium thickness and abnormal fetal heart rate patterns during labour, low Apgar scores (Table 2) and risk for caesarean section delivery. There also appears to be a higher risk of neonatal intensive care admission in pregnancies with thick meconium as compared to those with clear amniotic fluid, suggesting that thick meconium, not thin, is associated with an increased risk for perinatal complications during labour and delivery. A system of measuring quantitative meconium concentrations using a “meconiumcrit” (percentage by volume of the solid component of meconium) was proposed in the 1990s, but this has not been adopted clinically, as a study investigating the value of measuring meconiumcrit showed no significant correlation with umbilical artery pH or Apgar score and no clinical benefit. However, it should be noted that two cases of meconium aspiration syndrome occurred within this study, both of which were from the “thick” meconium group. Although there is limited good quality evidence suggesting that the use of a system to grade meconium has any significant impact on neonatal outcome, most obstetricians would consider thick meconium a more ominous sign than thin and the National Institute of Clinical Excellence (NICE) recommends a standardized scoring system for the degree of meconium staining and its association with neonatal outcome. Further to this, accurately estimating the degree of meconium thickness is of importance as it helps determine the intensity of monitoring required following birth.
Grade 2 Grade 3 (thick)
Entire body normal Good, crying
Normal, except Pale all over for extremities Slow, irregular Absent
0 Points Absent Absent Absent
Intrapartum management Due to the mechanisms mentioned above, meconium passage may have different clinical significance at different gestations. Meconium in the term fetus As the fetal gut matures, meconium moves closer to the distal colon and rectum. Therefore, at term there is a close proximity between the meconium and the anal sphincter. For this reason, the amount of fetal stress required to initiate the release of meconium may be trivial and unsustained, such as occurs with cord compression during normal labour. However, in the absence of the stress of labour, meconium may be more significant. Risk factors for MSAF in the term fetus are shown in Table 3. The presence of MSAF in early labour is associated with an increased rate of caesarean section delivery compared to the presence of clear amniotic fluid, due to the increased rate of fetal heart rate abnormalities observed in this group, in particular, the presence of early and variable decelerations, explainable by the theory of cord compression. Numerous studies have utilized cardiotocographical fetal heart rate recordings, cord pH measuring and Apgar scores to try and ascertain the relevance of MSAF in the term fetus and its impact on neonatal outcome in order to determine any way of identifying the at-risk pregnancy. The evidence suggests that in
Risk factors for meconium passage Risk factors for meconium-stained amniotic fluid Post-term pregnancy Placental insufficiency Maternal hypertension and pre-eclampsia Maternal diabetes Fetal heart rate abnormalities IUGR Poor biophysical profile Smoking Oligohydramnios Cocaine abuse
Refers to light green or flecking of otherwise clear amniotic fluid Brown but thin uniform staining of the amniotic fluid Bright green or brown thick uniform staining of the amniotic fluid
Table 1
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1 Point Arms and legs flexed <100 Grimace
Table 2
Standard grading system for meconium thickness Grade 1 (thin)
Score 2 Points Active movements >100 Sneeze, coughs
Table 3
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the presence of a normal fetal heart rate pattern there is no significant correlation between MSAF and umbilical cord artery pH. However, when fetal heart rate abnormalities are present, the passage of meconium is associated with a lower umbilical artery pH compared to those with clear amniotic fluid. Regardless of a normal or abnormal fetal heart rate pattern, MSAF is associated with lower Apgar scores at 1 and 5 min than when compared with similar heart rate patterns with clear amniotic fluid, the degree of which is associated with increasing meconium thickness. This could potentially be explained either by vigorous suctioning to clear meconium from the larynx, the degree of neonatal asphyxia or neonatal aspiration of meconium. More objective intrapartum measures have been used to assess whether meconium alone can signify fetal distress. Fetal blood samples taken during labour have shown that the presence of meconium in the absence of fetal heart rate abnormalities is associated with higher fetal scalp pH recordings and better Apgar scores than compared to MSAF with fetal heart rate abnormalities. This suggests that meconium passage, in the absence of other signs of fetal distress, is not a sign of hypoxia and therefore, is not an indication for fetal blood sampling. Fetal heart rate abnormalities are thus a better predictor of fetal hypoxia than meconium alone, and the appearance of an abnormal heart rate tracing in the presence of MSAF is a strong indicator of fetal distress, above and beyond that seen with fetal heart rate abnormalities alone. Furthermore meconium-stained amniotic fluid, in the absence of fetal heart rate abnormalities, is associated with reduced Apgar scored and an increased perinatal morbidity and mortality, likely due to meconium aspiration following birth of an otherwise healthy fetus. The early detection and management of fetal hypoxia are important in minimizing the risk from meconium staining of the amniotic fluid. For this reason, NICE has made several recommendations related to the intrapartum management of meconium staining: 1. Continuous electronic fetal monitoring for any women with significant MSAF, defined as dark green or black amniotic fluid that is thick or tenacious or any amniotic fluid containing lumps of meconium 2. Continuous electronic fetal monitoring to be considered for women with light-stained liquor depending on a risk assessment, including as a minimum, their stage of labour, volume of liquor, parity, fetal heart rate pattern, and transfer pathway 3. If there are any cardiotocographical signs of fetal distress, a fetal blood sample should be obtained. If pH is below 7.21 then an emergency delivery should be performed
increased incidence of cerebral palsy and intraventricular haemorrhage. MSAF in the pre-term fetus, especially in the mid-trimester, may also be associated with acute ascending infections, and it has been speculated that intra-amniotic infections may cause fetal gastroenteritis and diarrhoea. Women in pre-term labour with meconium-stained liquor have a higher incidence of clinical chorioamnionitis when compared to those with clear liquor. Amniocenteses conducted on women presenting with pre-term labour with intact membranes have shown a significantly increased rate of positive amniotic fluid microbial cultures when meconium liquor is present and these women are more likely to deliver pre-term, suggesting that meconium passage is a risk factor for microbial invasion, chorioamnionitis and pre-term delivery. Haematogenous Listeria infection has also been associated with pre-term MSAF. However, the incidence of this has been found to be quite low and the presence of meconium is not a useful indicator of listeriosis infection.
Complications of meconium-stained amniotic fluid MSAF in the presence of fetal heart rate abnormalities is a strong indicator of fetal distress; however, it is also associated with complications in the newborn. Meconium directly alters the amniotic fluid, reducing its antibacterial activity, thereby; increasing the risk of perinatal bacterial infection, however, the most severe complication of MSAF is meconium aspiration syndrome. Meconium aspiration syndrome Various components of meconium, in particular, bile salts and enzymes can cause complications if aspirated into the lungs of an infant prior to, during or immediately after birth, thereby, resulting in the Meconium Aspiration Syndrome. This occurs in approximately 5% of infants born with MSAF and has a mortality rate in the region of 3e5%. Meconium aspiration syndrome describes a wide spectrum of respiratory disease, ranging from mild respiratory distress to severe disease and death despite mechanical ventilation. Prior to the late 1970s it was thought that aspiration of amniotic fluid and meconium only occurred during the first few breaths after delivery, however, meconium has been found distally as far as the alveoli in stillborn infants. Further to this, studies with radio-opaque contrast and Cr51 labelled erythrocytes injected into amniotic fluid have demonstrated that amniotic fluid enters the fetal lungs in the non-asphyxiated human fetus, suggesting that meconium aspiration occurs in utero. Animal studies have also shown that intrauterine gasping, resulting in greater aspiration of meconium, occurs in fetuses exposed to hypoxia, implying that fetal distress is a risk factor for development of meconium aspiration syndrome. Currently, there is no way to distinguish those who develop meconium aspiration from intrauterine gasping and those who develop it by inhalation at birth. Perhaps the most significant risk factor for meconium aspiration syndrome is post-term delivery, due to the high prevalence of MSAF in this population and the increased incidence of oligohydramnios in these pregnancies. Oligohydramnios predisposes to cord
Meconium in the pre-term fetus The incidence of MSAF in the pre-term fetus is approximately 5% but is associated with a poorer neonatal outcome when compared to similar gestations with clear amniotic fluid, suggesting that meconium-stained amniotic fluid is a gestational age independent risk factor. At term, only a relatively small amount of stress is required to result in the passage of meconium, however, in the pre-term fetus, the greater colonic distance over which the meconium has to travel, implies a greater severity and/or duration of stress, and may explain the increased perinatal morbidity and mortality seen in this group, particularly the
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compression which may help explain the higher frequency of meconium passage at this gestation, but more importantly, meconium passage in the presence of oligohydramnios results in a thicker meconium-stained amniotic fluid which can result in a more serious meconium aspiration syndrome and poorer neonatal outcome.
leading to decreased lung compliance and oxygenation. If persistent hypoxia occurs then pulmonary hypertension may develop, a common finding in fatal meconium aspiration syndrome. The pathophysiology of meconium aspiration syndrome is summarized in Figure 1.
Pathophysiology: the mechanism by which meconium induces this syndrome is likely to be a combination of mechanical airway obstruction, chemical irritation resulting in a pneumonitis, surfactant inactivation and a predisposition to secondary infection. Airway obstruction is usually the initial problem encountered by the neonate with meconium aspiration syndrome, although complete obstruction is unusual. Small amounts of meconium may migrate to the distal airways leading to pulmonary air trapping, hyperinflation of the lungs and possibly subsequent pneumomediastinum or pneumothorax. A pneumonitis may develop due to the direct toxic effect of meconium contents and the infiltration of a large number of polymorphonuclear leucocytes and macrophages into the airways and lung parenchyma mediating an intense inflammatory response resulting in direct tissue injury. This inflammatory response is mediated by chemotactic cytokines present in meconium which lead to high levels of vasoactive mediators (leukotrienes, prostaglandins) resulting in pulmonary vasoconstriction. Meconium may also displace surfactant from the alveolar surface, thereby, reducing its tension lowering abilities
Management: the management of babies born with meconiumstained liquor has been controversial; many believe that the most effective intervention for preventing meconium aspiration syndrome involves removal of meconium from the pharynx and trachea either before or after birth. For this reason it was previously proposed that all babies born through meconium-stained amniotic fluid should receive suction to the mouth and oropharynx before delivery of the shoulders and trunk and then undergo tracheal intubation and tracheal aspiration through the endotracheal tube. However, this was repeatedly challenged and more recent evidence suggests a more liberal approach can be used depending on the neonatal condition at birth and the degree of meconium staining of the amniotic fluid. Oropharyngeal and nasopharyngeal suctioning prior to birth of the shoulders, once almost universally accepted, has more recently been shown to have no effect on the incidence of meconium aspiration syndrome, the need for mechanical ventilation or duration of hospital stay when compared to not suctioning. Therefore, NICE recommends against its use prior to delivery.
Pathophysiology of meconium aspiration syndrome Physiological meconium passage
Fetal distress
Meconium stained amniotic fluid
Postpartum aspiration
Intrauterine gasping
Meconium aspiration
Airway obstruction
Cytokine induced pneumonitis
Surfactant inactivation
Hypoxia acidosis
Decreased lung compliance
Pulmonary air trapping Atelectasis Ventilation/perfusion mismatch
Persistent pulmonary hypertension
Figure 1
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Tracheal suctioning has been a matter of controversy for many years, some proposing suctioning for all pregnancies complication by meconium, others proposing no suction for any case and some proposing the use of selective suctioning based on the degree of meconium thickness and infant vigour. It appears that neonates born with good muscle tone and a normal heart rate (>100 beats per minute) do not benefit from tracheal suctioning; there is no reduction in meconium aspiration syndrome or improvement in neonatal outcome. Additionally, a vigorous baby can make visualization of the vocal cords difficult, thereby, potentially increasing the risk of oesophageal or tracheal injury. NICE, therefore, recommends that the upper airways should only be suctioned if there is thick or tenacious meconium present in the oropharynx. If, however, the infant is depressed, laryngoscopy and suction under direct vision should be carried out by a healthcare professional trained in advanced neonatal life support. Suctioning to empty the stomach of meconium at birth has also been proposed to reduce the risk of meconium aspiration syndrome, the rationale being that it could later be regurgitated and aspirated. However, there is insufficient evidence to recommend for or against it. The risk of developing meconium aspiration syndrome is thought to be related to the circumstances in which meconium passage occurred. Postdate pregnancies associated with the passage of thin meconium are unlikely to develop any serious complications following delivery. Those who suffer an acute intrauterine hypoxic event during labour are more likely to pass thick meconium and are at high risk of the obstructive and local inflammatory effects of meconium and of developing the meconium aspiration syndrome. These are likely to benefit the most from meconium clearing manoeuvres. Those who have suffered from chronic intrauterine hypoxia are more likely to have undergone muscularization and thickening of the pulmonary arteries and are subsequently more likely to develop pulmonary hypertension and to be depressed at birth. Further to this, chronic hypoxia increases the risk of meconium passage and incidence of intrauterine gasping with subsequent aspiration of meconium. Therefore, efforts to remove meconium at birth may be ineffective at reducing the risk of meconium aspiration syndrome in this group. Most vigorous babies born through thick meconium-stained amniotic fluid do not require any intervention besides being monitored for signs of respiratory distress, which if occurs generally develops within 12 h of birth. NICE recommends these neonates should be closely observed at 1 and 2 h after delivery and then every 2 h for the first 12 h of life. Those born through light MSAF should be observed at 1 and 2 h of life and reviewed by a neonatologist if there are concerns at any time. Observations should include: General wellbeing Chest movement and nasal flare Skin colour Feeding Muscle tone Temperature Heart rate and respiration A recent study has shown that meconium aspiration syndrome rarely develops in neonates with Apgar scores above 8 at 5 min
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and suggests that these can be safely discharged shortly after birth; however, this has not yet been put into routine practice. If there are signs of meconium aspiration syndrome then transfer to the neonatal intensive care unit (NICU) may be required, to allow the full range of respiratory support and close monitoring to be undertaken. These neonates may require more invasive treatments including mechanical ventilation, surfactant therapy and extracorporeal membrane oxygenation (ECMO). Infection There is a link between MSAF and the development of chorioamnionitis, with the incidence of clinical and histological chorioamnionitis being higher when associated with intrapartum meconium-stained amniotic fluid compared to clear amniotic fluid. This has several possible implications; namely it increases the risk of neonatal sepsis and subsequent perinatal morbidity and mortality, secondly, it predisposes to dystocias, thereby, increasing the rates of operative delivery, and thirdly, chorioamnionitis is a risk factor for the development of postpartum endometritis and its associated maternal morbidity. Amniotic fluid in general is quite a poor growth medium for bacteria; however, in the presence of meconium there is a three-fold increase in bacterial isolates from meconium-stained amniotic fluid compared to clear amniotic fluid. It is thought that meconium may mediate the increase in bacterial growth by acting as a growth factor, inhibiting bacteriostatic properties of amniotic fluid or by antagonizing host defense systems in particular neutrophil phagocytosis. The most common bacterial isolates are Ureaplasma urealyticum, Escherichia coli, Candida albicans, Streptococci and Listeria monocytogenes. It has been suggested that intrapartum MSAF should be considered a potential marker for infectious morbidity but whether prophylactic antibiotics are of benefit in reducing the maternal and fetal morbidity is unknown and requires further research.
Prevention of meconium aspiration syndrome Many cases of meconium aspiration syndrome can be prevented by assessment of risk factors, continuous fetal monitoring and appropriate removal of meconium from the pharynx and trachea. However, although airway suctioning is thought to reduce the incidence of meconium aspiration it does not eliminate the risks entirely because fetal gasping may result in the entry of meconium into the lungs prior to birth. For this reason, several other methods have been proposed to reduce the perinatal mortality and morbidity caused by meconium-stained amniotic fluid. In under resourced countries, paediatric facilities for the management of meconium aspiration syndrome are frequently absent, thereby, increasing the importance of an intervention. Amnioinfusion Amnioinfusion has been proposed as one method of reducing the risk of meconium aspiration syndrome. It involves infusing normal saline transcervically through a catheter into the uterine cavity, thereby diluting any meconium present and reducing its mechanical and inflammatory effects. As oligohydramnios is associated with thick meconium-stained amniotic fluid, increasing the volume of fluid in the amniotic cavity may also reduce the
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FURTHER READING Baker PN, Kilby MD, Murray H. An assessment of the use of meconium alone as an indication for fetal blood sampling. Obstet Gynecol 1992; 80: 792e6. Hofmeyr GJ, Xu H. Amnioinfusion for meconium-stained liquor in labour. Cochrane Database Syst Rev, http://dx.doi.org/10.1002/14651858. CD000014.pub3; 2010. Art. No.: CD000014. Intrapartum care: care of healthy women and their babies during childbirth. London: National Collaborating Centre for Women’s and Children’s Health, http://www.nice.org.uk/CG55; 2007. Lucas A, Adrian TE, Aynsley-Green A, Bloom SR. Gut hormones in fetal distress. Lancet 1979; 2: 968. Pritchard J. Fetal swallowing and amniotic fluid volume. Obstet Gynecol 1966; 28: 606e10. Sheiner E, Hadar A, Shoham-Vardi I, Hallak M, Katz M, Mazor M. The effect of meconium on perinatal outcome: a prospective analysis. J Matern Fetal Neonatal Med 2002; 11(1): 54e9. Siriwachirachai T, Sangkomkamhang US, Lumbiganon P, Laopaiboon M. Antibiotics for meconium-stained amniotic fluid in labour for preventing neonatal sepsis (protocol). Cochrane Database Syst Rev, http://dx.doi.org/10.1002/14651858.CD007772; 2009. Art. No.: CD007772. Steer PJ, Eigbe F, Lissauer TJ, Beard RW. Interrelationships among abnormal cardiotocograms in labor, meconium staining of the amniotic fluid, arterial cord blood pH, and Apgar scores. Obstet Gynecol 1989; 74(5): 715e21. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM, Vivas NI. Oropharyngeal and nasopharyngeal suctioning of meconium-stained neonates before delivery of their shoulders: multicentre, randomised controlled trial. Lancet 2004; 364: 597e602. Wennerholm UB, Hagberg H, Brorsson B, Bergh C. Induction of labor versus expectant management for post-date pregnancy: is there sufficient evidence for a change in clinical practice? Acta Obstet Gynecol Scand 2009; 88: 6e17.
frequency of umbilical cord compressions, thereby reducing risk of fetal hypoxia and meconium passage. A Cochrane review found no evidence that amnioinfusion caused any significant improvement in rates of caesarean section, meconium aspiration syndrome, severe perinatal morbidity or perinatal death in settings with standard perinatal surveillance; therefore, it is not recommended as standard for pregnancies complicated by meconium. Complications of amnioinfusion include umbilical cord prolapse, uterine scar rupture and amniotic fluid embolus. NICE does not currently recommend its use. Induction of labour at 41 weeks Due to the high prevalence of MSAF in the post-term pregnancy, it has been speculated that induction of labour may decrease the incidence of fetal distress and meconium aspiration syndrome. It has been shown that when compared with expectant management of post-term pregnancies, elective induction of labour at 41 weeks gestation is associated with lower rates of meconium aspiration syndrome and caesarean section, but there is no significant reduction in perinatal mortality. Other potential methods There is no evidence to support the use of maternal narcotics to reduce the incidence of fetal gasping. Various methods of physiotherapy such as postural drainage, cricoid pressure, and vibratory therapy for neonates born through MSAF, have not been shown to be of any benefit, and indeed are not without complications and delay the institution of more effective therapies, therefore, they are not recommended.
Conclusion The management of intrauterine meconium passage has generated considerable controversy. Its exact relationship with fetal distress is complex, dependent on several factors including fetal gestation and heart rate abnormalities and is not completely understood. Meconium passage continues to be a common problem and meconium aspiration syndrome is associated with many cases of neonatal respiratory distress, neurological complications and death. Despite numerous interventions the incidence of meconium-stained amniotic fluid is unlikely to decrease, therefore, the challenge is in identifying those pregnancies which are at risk of adverse neonatal outcome and meconium aspiration syndrome. Those at greatest risk are those with intrauterine hypoxia, those born with thick meconium and those whose fetal vigour is depressed at birth. The finding of meconium, therefore, should prompt a thorough evaluation of the patient and the institution of continuous fetal monitoring for fetal wellbeing; abnormal fetal heart rate patterns being the best predictor of those who will require intervention at birth. Many cases of meconium aspiration syndrome can be prevented by assessment of risk factors, continuous fetal monitoring and removal of meconium from the airways, however this will not prevent all, therefore, it is important that all healthcare professionals who attend delivers have an understanding of the management of MSAF and be trained in the proper obstetric and neonatal interventions required. A
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Practice points C
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Meconium-stained amniotic fluid is associated with increased morbidity and mortality in babies. Women with thick meconium should be advised to have continuous electronic fetal monitoring. If significant meconium-stained amniotic fluid is identified healthcare professionals trained in fetal blood sampling should be available during labour and a fetal blood sample taken if cardiotocographical evidence of fetal distress. Healthcare professionals trained in advanced neonatal life support should be available at birth for significantly stained neonates. Vigorous babies born through thick meconium require close monitoring at 1 and 2 h following birth, then every 2 h for 12 h. Vigorous babies born through thin meconium require close monitoring at 1 and 2 h only. Amnioinfusion is not recommended to treat meconium-stained amniotic fluid.
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