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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 5  |  Issue : 3  |  Page : 157-161

Meconium-stained amniotic fluid as a potential risk factor for perinatal asphyxia: A single-center experience


1 Department of Pediatrics, Sri Aurobindo Medical College and Post Graduate Institute, Indore, Madhya Pradesh, India
2 Department of Medicine, Sri Aurobindo Medical College and Post Graduate Institute, Indore, Madhya Pradesh, India

Date of Web Publication28-Sep-2016

Correspondence Address:
Dr. Veerendra Mehar
Department of Pediatrics, Sri Aurobindo Medical College and Post Graduate Institute, Indore - 453 111, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4847.191246

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  Abstract 

Background: The aim of this study was to find out immediate fetal outcome in meconium-stained amniotic fluid in relation to perinatal asphyxia. Materials and Methods: This retrospective study includes medical records of all neonates admitted to Neonatal Intensive Care Unit (NICU) between September 2014 and July 2015. The variables reviewed are age, sex, weight, mode of delivery, gestational age, presence of meconium aspiration syndrome (MAS) and perinatal asphyxia. Results: Out of 399 total admissions in NICU, 62.4% were male babies and remaining 37.6% were female babies. Of the total 6.8% were cases of MAS, making females (10.7%) more prone compared to male (4.4%) while perinatal asphyxia came out to be 11.5%, making male (12%) more prone than female (10.7%). Postterm (odds ratio [OR] =3.50 [CI: 0.39-31.42]) and term (OR = 2.58 [CI: 1.16, 5.75]) babies were having more risk of developing MAS compared to preterm (P < 0.01). Postterm (OR = 9.15 [CI: 1.91-43.75]) and term (OR = 2.67 [CI: 1.41-5.08]) babies were having more risk of developing perinatal asphyxia compared to preterm (P < 0.01). MAS babies are having 6.62 (CI: 2.85-15.38) times more risk of developing perinatal asphyxia (P < 0.01). Conclusion: The management of MAS, which is a perinatal problem, requires a well concerted and coordinated action by the obstetrician and pediatrician. Prompt and efficient delivery room management can minimize the sequelae of aspirated meconium and decrease the chance of perinatal asphyxia.

Keywords: Meconium aspiration syndrome, Neonatal Intensive Care Unit, perinatal asphyxia


How to cite this article:
Mehar V, Agarwal N, Agarwal A, Agarwal S, Dubey N, Kumawat H. Meconium-stained amniotic fluid as a potential risk factor for perinatal asphyxia: A single-center experience. J Clin Neonatol 2016;5:157-61

How to cite this URL:
Mehar V, Agarwal N, Agarwal A, Agarwal S, Dubey N, Kumawat H. Meconium-stained amniotic fluid as a potential risk factor for perinatal asphyxia: A single-center experience. J Clin Neonatol [serial online] 2016 [cited 2020 Feb 17];5:157-61. Available from: http://www.jcnonweb.com/text.asp?2016/5/3/157/191246


  Introduction Top


In early 2000, the prevalence of meconium aspiration syndrome (MAS) ranged from 0.20% to 0.54% in the general population[1],[2],[3],[4] and from 1.0% to 6.8% in infants born through meconium-stained amniotic fluid (MSAF).[1],[2],[3],[4] In a 8 years span from 1990 to 1998, a total of ten reports were reviewed that showed a total incidence of 0.52% of MAS, 13.1% of MSAF 4.2% of MAS among MSAF and 49.7% of MAS needing ventilator support with a 4.6% mortality rate.[3]

However, a lower incidence of MAS was suggested due to the scarcity of large population-based studies: the National US Birth Cohort Study conducted on the basis of singleton term non-Hispanic white live births (1995-2001) showed that the rate of MAS markedly increased with gestational age (GA), that is, from 0.10% at GA of 37 weeks to 0.22 and 0.31% at GA 40 and 41 weeks, respectively.[5] The prevalence of MAS could be extrapolated to 0.18% in this population of term infants. In Australia, the rate of MAS requiring mechanical ventilation in Level III units ranged between 0.024% and 0.046% at GA 36-40 weeks and then increased to 0.080% at GA 41 weeks and 0.14% at GA 42 weeks.[6] In France, the prevalence of mechanically ventilated MAS was estimated to 0.043% by a retrospective national survey among neonates born in 2000-2001.[7]

Among all live births approximately 13% neonates are born through meconium-stained amniotic fluid and out of these 5-10% developed MAS, which increases neonatal morbidity and mortality. Following the first description of the pathophysiology of MAS in 1975, there has been a marked improvement in the survival of infants with MAS[8] due to improved intra- and post-partum management of the same. Although there is a significant decrease in the occurrence of MAS and associated mortality in developed countries MAS remains a major problem in developing countries.

Meconium is derived from the Greek word "mekoni," meaning poppy juice or opium. It is a sterile, thick, black-green (resulting from bile pigments), odorless material first observed in the fetal intestine during the 3rd month of gestation which is the fecal material that accumulates in the fetal colon throughout gestation. It consists of an accumulation of debris, comprising desquamated cells from the intestine and skin, gastrointestinal mucin, lanugo hair, fatty material from the vernix caseosa, amniotic fluid, and intestinal secretions.[9],[10] Most infants have their first bowel movement after birth (within the first 24-48 h after birth). Occasionally, a fetus can pass meconium in uteri. MAS refers to the aspiration of meconium and amniotic fluid by the fetus. This can occur when the fetus is still in the uterus, passing through the birth canal or when it takes its first breath after birth.

MAS is an important cause of respiratory distress in the term newborn, is a serious condition with high morbidity and mortality.[6],[11] MAS has a complex pathophysiology and occurs due to a combination of airway obstruction, pulmonary hypertension, epithelial injury, surfactant inactivation, and inflammation, when there is underlying,[11],[12] fetal asphyxia,[13] and infection.[14],[15] An inflammatory response to meconium is seen in both newborns and animal models with MAS.[16] Intratracheal instillation of meconium in animals results in an intense pulmonary inflammatory reaction with the influx of polymorphonuclear leukocytes, monocytes/macrophages, and T-cells within a few hours. Parenchymal lung cell injury is worsened by the production of proinflammatory cytokines[17],[18] and apoptotic epithelial cells are present in meconium containing lungs.[19],[20]

MAS results in considerable respiratory morbidity in term and near-term infants. It is clinically characterized by early onset of respiratory distress in an infant born through MSAF presenting with poor lung compliance and hypoxemia. Chest X-ray shows patchy opacification and hyperinflation.[21],[22] Mechanical ventilation and intubation is required among one-third of infants suffering from MAS.[23],[24] Newer neonatal therapies include high-frequency ventilation, inhaled nitric oxide, and surfactant.[25],[26]

There has been a marked reduction in the incidence and risk of MAS over the past few decades, mostly restricted to the developed world due to better obstetric practices with great emphasis been paid on avoidance of postmaturity and expeditious delivery in case of fetal distress.[4],[24],[27]

This study was undertaken to find out immediate fetal outcome in meconium-stained liquor in relation to perinatal asphyxia.


  Materials and Methods Top


Study design and the participants

This hospital-based retrospective observational study was conducted in the Department of Pediatrics of a Tertiary Care Center, Indore. The study population included patients admitted to Neonatal Intensive Care Unit (NICU). Data were collected from the medical record department of the patients of NICU. The variable collected were age, sex, weight, mode of delivery and GA.

Outcome variables

MAS, perinatal asphyxia, and other neonatal infections.

Explanatory variables

Factors at the individual level are GA and sex. GA of <37 weeks are coded as preterm, >42 weeks as post-term, and 37-42 weeks as term.

Data management and statistical analysis

The analysis was done using descriptive statistics and testing of hypothesis. The data were analyzed Statistical Package for the Social Sciences (SPSS) for Windows Version 20.0 (SPSS Inc., Chicago, IL, USA). P < 0.05 (two-tailed) was used to establish statistical significance.


  Results Top


[Table 1] depicts that females are (10.7%) more prone compared to males (4.4%). Postterm (odds ratio [OR] =3.50 [CI: 0.39-31.42]) and term [OR = 2.58 [CI: 1.16-5.75]) babies were having more risk of developing MAS compared to preterm (P < 0.01). From the above statistics, it is clear that females formed a dominant group as compared to males among the babies born to MSAF. Along with this, it can also be assumed that post and term neonates are having a larger risk of developing MAS.
Table 1: Relation between demographic data and meconium aspiration syndrome


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[Table 2] shows that 11.5% of the total babies had perinatal asphyxia. Twelve percent of males and 10.7% of female babies suffered from perinatal asphyxia.
Table 2: Relationship of perinatal asphyxia with demographic data and meconium aspiration syndrome


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Postterm (OR = 9.15 (CI: 1.91-43.75)) and term (OR = 2.67 [CI: 1.41-5.08]) babies were having more risk of developing perinatal asphyxia compared to preterm babies (P < 0.01). MAS baby is having 6.62 (CI: 2.85-15.38) times more risk of developing perinatal asphyxia (P < 0.01).

From the table, it can be stated that males are having more risk of developing perinatal asphyxia as compared to females. Postterm and term babies are having a greater risk of developing asphyxia.

Thus, from the results of this study a strong relationship between MAS and perinatal asphyxia can be established, i.e., meconium aspirated neonates are more prone for developing perinatal asphyxia.


  Discussion Top


The increased risk for pulmonary morbidity and mortality among infants born through MSAF is well recognized. Although many reports have noted a clinical spectrum of pulmonary dysfunction from mild tachypnea to severe pulmonary insufficiency, this study also confirms that MSAF is associated with an increased risk for pulmonary dysfunction. The risk for pulmonary disease, however, is not manifested equally in all infants with meconium staining. As it was shown by several previous studies, the greatest risk for pulmonary disease occurred among infants with associated signs of possible intrapartum fetal compromise. Despite following recommended guidelines of airway management, these infants continued to manifest a high rate of pulmonary morbidity.[25],[28],[29],[30]

The recommendation by the American Academy of Pediatrics in 1983 did not suggest that all infants born through thick MSAF necessarily require tracheal suction. The second edition of these guidelines noted the absence of additional studies to support or refute the practice of tracheal suction for MSAF and recommended that "in the presence of thick or particulate meconium, the larynx should be visualized, and if meconium is present, the clinician should intubate the trachea and apply suction." The most recent edition of the guidelines published in 1992, is less dogmatic and recommended that depressed infants with meconium in the hypopharynx to have tracheal suction. However, it is further noted that cord visualization and tracheal suction in the vigorous infant with thick meconium may not be necessary. None of the Guidelines have recommended tracheal suction of infants born through thin MSAF.[28],[29]

Meconium aspiration syndrome with gestational age

The overall incidence of MAS and severe MAS increases with GA as reported in recent population-based studies.[5],[6] The overall rates of MAS in the USA[5] and Burgundy are similar: 1.0 versus 1.1 per 1000 live births at 37 weeks; 1.1 versus 1.0% at 38 weeks; 1.5% versus 1.1% at 39 weeks; 2.2% versus 2.4% at 40 weeks; and 3.1% versus 2.6% at 41 weeks. Furthermore, the incidence of severe MAS recorded in Australia[6] at 41 weeks (0.80%) is close to the 0.67% observed at 39-41 weeks in our series. Some studies suggested that prevention of postterm pregnancy prevents severe MAS.[31] This study showed that postterm (OR = 3.50 [CI: 0.39-31.42]) and term (OR = 2.58 [CI: 1.16-5.75]) babies were having more risk of developing MAS compared to preterm (P < 0.01).

Meconium aspiration syndrome with sex

MSAF neonates were found in 78 (9.79%) out of 796 deliveries (live birth) with a male:female ratio 1:1:1.[32] In this study, male (62.4%) showed preponderance as compared to female (37.6%), among which (6.8%) were cases of MAS, making female (10.7%) more prone compared to male (4.4%).

Perinatal asphyxia with gestational age

For more than two decades, postterm pregnancy has been defined as a pregnancy that persists beyond 294 days or 42 weeks of gestation.[33] For the assessment of GA in pregnancy, the last menstrual period in cases with the regular menstrual cycle is the best physiological method. However, a few women are sure of their dates and often cause anxiety when they come with postdates.[34] The cause of postterm pregnancy is unknown. Postterm pregnancies are associated with higher risk of perinatal morbidity and mortality the cause of which is largely unknown. The complications of postdated pregnancy include MAS, asphyxia neonatorum respiratory distress syndrome, jaundice neonatorum, sepsis neonatorum, oligohydramnios, macrosomia, fetal birth injury, fetal distress, and increased rate of cesarean section.[35] This study showed that postterm (OR = 9.15 (CI: 1.91-43.75)) and term (OR = 2.67 [CI: 1.41-5.08]) babies have more risk of developing perinatal asphyxia compared to preterm (P < 0.01).

Perinatal asphyxia with sex

In numerous studies, asphyxia was more prevalent in male than female.[36],[37],[38] In this study, male preponderance is seen. Out of 399 cases, perinatal asphyxia came out to be 11.5%, making male (12%) more prone to female (10.7%).


  Conclusion Top


The present study showed that MAS as an important risk factor for perinatal asphyxia both in term and postterm babies making perinatal asphyxia more common among MAS babies.

There is need of a large randomized controlled trial to study the roles of intrapartum nasopharyngeal and immediate postpartum tracheal suctioning in neonates born through MSAF in developing country setting.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Wiswell TE. Handling the meconium-stained infant. Semin Neonatol 2001;6:225-31.  Back to cited text no. 1
[PUBMED]    
2.
Blackwell SC, Moldenhauer J, Hassan SS, Redman ME, Refuerzo JS, Berry SM, et al. Meconium aspiration syndrome in term neonates with normal acid-base status at delivery: Is it different? Am J Obstet Gynecol 2001;184:1422-5.  Back to cited text no. 2
[PUBMED]    
3.
Liu WF, Harrington T. Delivery room risk factors for meconium aspiration syndrome. Am J Perinatol 2002;19:367-78.  Back to cited text no. 3
[PUBMED]    
4.
Yoder BA, Kirsch EA, Barth WH, Gordon MC. Changing obstetric practices associated with decreasing incidence of meconium aspiration syndrome. Obstet Gynecol 2002;99(5 Pt 1):731-9.  Back to cited text no. 4
    
5.
Zhang X, Kramer MS. Variations in mortality and morbidity by gestational age among infants born at term. J Pediatr 2009;154:358-62.  Back to cited text no. 5
[PUBMED]    
6.
Dargaville PA, Copnell B; Australian and New Zealand Neonatal Network. The epidemiology of meconium aspiration syndrome: Incidence, risk factors, therapies, and outcome. Pediatrics 2006;117:1712-21.  Back to cited text no. 6
[PUBMED]    
7.
Nolent P, Hallalel F, Chevalier JY, Flamant C, Renolleau S. Meconium aspiration syndrome requiring mechanical ventilation: Incidence and respiratory management in France (2000-2001). Arch Pediatr 2004;11:417-22.  Back to cited text no. 7
[PUBMED]    
8.
Vidyasagar D, Harris V, Pildes RS. Assisted ventilation in infants with meconium aspiration syndrome. Pediatrics 1975;56:208-13.  Back to cited text no. 8
[PUBMED]    
9.
Singh BS, Clark RH, Powers RJ, Spitzer AR. Meconium aspiration syndrome remains a significant problem in the NICU: Outcomes and treatment patterns in term neonates admitted for intensive care during a ten-year period. J Perinatol 2009;29:497-503.  Back to cited text no. 9
[PUBMED]    
10.
Kattwinkel J, Perlman JM, Aziz K, Colby C, Fairchild K, Gallagher J, et al. Part 15: Neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122 18 Suppl 3:S909-19.  Back to cited text no. 10
    
11.
Cleary GM, Wiswell TE. Meconium-stained amniotic fluid and the meconium aspiration syndrome. An update. Pediatr Clin North Am 1998;45:511-29.  Back to cited text no. 11
[PUBMED]    
12.
Dargaville PA, Mills JF, Headley BM, Chan Y, Coleman L, Loughnan PM, et al. Therapeutic lung lavage in the piglet model of meconium aspiration syndrome. Am J Respir Crit Care Med 2003;168:456-63.  Back to cited text no. 12
[PUBMED]    
13.
Paz Y, Solt I, Zimmer EZ. Variables associated with meconium aspiration syndrome in labors with thick meconium. Eur J Obstet Gynecol Reprod Biol 2001;94:27-30.  Back to cited text no. 13
[PUBMED]    
14.
Katz VL, Bowes WA Jr. Meconium aspiration syndrome: Reflections on a murky subject. Am J Obstet Gynecol 1992;166 (1 Pt 1):171-83.  Back to cited text no. 14
    
15.
Ghidini A, Spong CY. Severe meconium aspiration syndrome is not caused by aspiration of meconium. Am J Obstet Gynecol 2001;185:931-8.  Back to cited text no. 15
[PUBMED]    
16.
Vidyasagar D, Lukkarinen H, Kaapa P, Zagariya A. Inflammatory response and apoptosis in newborn lungs after meconium aspiration. Biotechnol Prog 2005;21:192-7.  Back to cited text no. 16
[PUBMED]    
17.
Zagariya A, Bhat R, Navale S, Vidyasagar D. Cytokine expression in meconium-induced lungs. Indian J Pediatr 2004;71:195-201.  Back to cited text no. 17
[PUBMED]    
18.
Davey AM, Becker JD, Davis JM. Meconium aspiration syndrome: Physiological and inflammatory changes in a newborn piglet model. Pediatr Pulmonol 1993;16:101-8.  Back to cited text no. 18
[PUBMED]    
19.
Zagariya A, Bhat R, Chari G, Uhal B, Navale S, Vidyasagar D. Apoptosis of airway epithelial cells in response to meconium. Life Sci 2005;76:1849-58.  Back to cited text no. 19
[PUBMED]    
20.
Holopainen R, Aho H, Laine J, Peuravuori H, Soukka H, Kääpä P. Human meconium has high phospholipase A2 activity and induces cellular injury and apoptosis in piglet lungs. Pediatr Res 1999;46:626-32.  Back to cited text no. 20
    
21.
Cleary GM, Wiswell TE. Meconium-stained amniotic fluid and the meconium aspiration syndrome: An update. Pediatr Clin North Am 1998;45:511-29.  Back to cited text no. 21
[PUBMED]    
22.
Wiswell TE, Bent RC. Meconium staining and the meconium aspiration syndrome. Unresolved issues. Pediatr Clin North Am 1993;40:955-81.  Back to cited text no. 22
[PUBMED]    
23.
Coltart TM, Byrne DL, Bates SA. Meconium aspiration syndrome: A 6-year retrospective study. Br J Obstet Gynaecol 1989;96:411-4.  Back to cited text no. 23
[PUBMED]    
24.
Wiswell TE, Tuggle JM, Turner BS. Meconium aspiration syndrome: Have we made a difference? Pediatrics 1990;85:715-21.  Back to cited text no. 24
[PUBMED]    
25.
Bhutani VK, Chima R, Sivieri EM. Innovative neonatal ventilation and meconium aspiration syndrome. Indian J Pediatr 2003;70:421-7.  Back to cited text no. 25
[PUBMED]    
26.
Wiswell TE. Advances in the treatment of the meconium aspiration syndrome. Acta Paediatr Suppl 2001;90:28-30.  Back to cited text no. 26
[PUBMED]    
27.
Sriram S, Wall SN, Khoshnood B, Singh JK, Hsieh HL, Lee KS. Racial disparity in meconium-stained amniotic fluid and meconium aspiration syndrome in the United States, 1989-2000. Obstet Gynecol 2003;102:1262-8.  Back to cited text no. 27
[PUBMED]    
28.
Yoder BA. Meconium-stained amniotic fluid and respiratory complications: Impact of selective tracheal suction. Obstet Gynecol 1994;83:77-84.  Back to cited text no. 28
[PUBMED]    
29.
Liu WF, Harrington T. The need for delivery room intubation of thin meconium in the low-risk newborn: A clinical trial. Am J Perinatol 1998;15:675-82.  Back to cited text no. 29
[PUBMED]    
30.
Fuloria M, Wiswell TE. Resuscitation of the meconium-stained infant and prevention of meconium aspiration syndrome. J Perinatol 1999;19:234-41.  Back to cited text no. 30
[PUBMED]    
31.
Manganaro R, Mamì C, Palmara A, Paolata A, Gemelli M. Incidence of meconium aspiration syndrome in term meconium-stained babies managed at birth with selective tracheal intubation. J Perinat Med 2001;29:465-8.  Back to cited text no. 31
    
32.
Sharma LM. A Study of New Born Infant with Meconium Stained Amniotic Fluid. XXX Congress of the Association for Paediatric Education in Europe (A.P.E.E.); September, 2000. Available from: http://www.aeep.asso.fr/index.php/en/congress/55?task=view. [Last cited on 2012 Sep 29].  Back to cited text no. 32
    
33.
Mary Hannah M. The Maternal-Fetal Medicine Committee of the Society of Obstetricians and Gynaecologists of Canada. Post-Term Pregnancy. SOGC Clinical Practice Guideline No. 15; March, 1997. Available from: http://www.sogc.org/members/guide/library_e.asp. [Last assessed on 2015 Nov 16].  Back to cited text no. 33
    
34.
Bennett KA, Crane JM, O′shea P, Lacelle J, Hutchens D, Copel JA. First trimester ultrasound screening is effective in reducing postterm labor induction rates: A randomized controlled trial. Am J Obstet Gynecol 2004;190:1077-81.  Back to cited text no. 34
[PUBMED]    
35.
Cleary-Goldman J, Bettes B, Robinson JN, Norwitz E, D′Alton ME, Schulkin J. Postterm pregnancy: Practice patterns of contemporary obstetricians and gynecologists. Am J Perinatol 2006;23:15-20.  Back to cited text no. 35
[PUBMED]    
36.
Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O′Sullivan F, Burton PR, et al. Antepartum risk factors for newborn encephalopathy: The Western Australian case-control study. BMJ 1998;317:1549-53.  Back to cited text no. 36
[PUBMED]    
37.
Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O′Sullivan F, Burton PR, et al. Intrapartum risk factors for newborn encephalopathy: The Western Australian case-control study. BMJ 1998;317:1554-8.  Back to cited text no. 37
    
38.
Futrakul S, Praisuwanna P, Thaitumyanon P. Risk factors for hypoxic-ischemic encephalopathy in asphyxiated newborn infants. J Med Assoc Thai 2006;89:322-8.  Back to cited text no. 38
[PUBMED]    



 
 
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