Handling the meconium-stained infant

doi:10.1053/siny.2001.0051

Seminars in Neonatology

Volume 6, Issue 3, June 2001, Pages 225-231

https://doi.org/10.1053/siny.2001.0051 Get rights and content

Abstract

Clinicians who care for infants in the delivery room or afterward must frequently manage many born through meconium-stained amniotic fluid (MSAF). Approximately 5% of infants born through MSAF develop meconium aspiration syndrome (MAS). This disorder can be severe in nature, with half or more of the affected children needing mechanical ventilation. It is frequently associated with pulmonary air leaks and the presence of persistent pulmonary hypertension. MAS is the most common disorder for which babies may be treated with extracorporeal life support. Various possibilities for preventing MAS exist during labor, parturition, and the first minutes of life. Proposed antenatal therapies include amnioinfusion; intrapartum maneuvers include oropharyngeal suctioning prior to delivery of the babies shoulders; the postnatal intervention of intubation for intratracheal suctioning should be reserved for the non-vigorous meconium-stained infant.

References (24)

TE Wiswell et al.
Meconium staining and the meconium aspiration syndrome: Unresolved issues
Pediatric Clinics of North America
(1993)
GM Cleary et al.
Meconium-stained amniotic fluid and the meconium aspiration syndrome: An update
Pediatric Clinics of North America
(1998)
TE Wiswell et al.
Management of meconium-stained amniotic fluid
Clinics in Perinatology
(1999)
HS Falciglia et al.
Does De Lee suction at the perineum prevent meconium aspiration syndrome?
American Journal of Obstetrics and Gynecology
(1992)
P Ting et al.
Tracheal suction in meconium aspiration
American Journal of Obstetrics and Gynecology
(1975)
N Linder et al.
Need for endotracheal intubation and suction in meconium-stained infants
Journal of Pediatrics
(1988)
M Fuloria et al.
Managing meconium aspiration
Contemporary Pediatrics
(2000)
A Lucas et al.
Plasma motilin, gastrin, and enteroglucagon and feeding in the human newborn
Archives of Diseases in Childhood
(1980)
MD Berkus et al.
Meconium-stained amniotic fluid: Increased risk for adverse neonatal outcomes
Obstetrics and Gynecology
(1994)
TE Wiswell et al.
Meconium aspiration syndrome: Have we made a difference?
Pediatrics
(1990)

TE Wiswell et al.

Delivery room management of the apparently vigorous meconium-stained infant: Results of the multicenter, international collaborative trial

Pediatrics

(2000)

A Fleischer et al.

A persistent clinical problem: Profile of the term infant with significant respiratory complications

Obstetrics and Gynecology

(1992)

Cited by (44)

Meconium aspiration syndrome: A role for fetal systemic inflammation
2016, American Journal of Obstetrics and Gynecology
Citation Excerpt :
Whether the male sex is a risk factor for MAS is controversial. Two previous studies have reported that male neonates were at a higher risk of MAS than female neonates,133,134 while another study found no association between the male sex and MAS (odds ratio, 1.0; 95% CI, 0.92–1.2).1 Like all observational studies, causation cannot be inferred from the associations reported herein, and experimental studies would be required to explore this hypothesis.
Meconium aspiration syndrome (MAS) is a leading cause of morbidity and mortality in term infants. Meconium-stained amniotic fluid (MSAF) occurs in approximately 1 of every 7 pregnancies, but only 5% of neonates exposed to MSAF develop MAS. Why some infants exposed to meconium develop MAS while others do not is a fundamental question. Patients with MSAF have a higher frequency of intraamniotic inflammation/infection than those with clear fluid. We propose that fetal systemic inflammation is a risk factor for the development of MAS in patients with MSAF.
We sought to investigate whether intraamniotic inflammation and funisitis, the histopathologic landmark of a fetal inflammatory response, predispose to MAS.
A prospective cohort study was conducted from 1995 through 2009. Amniotic fluid (AF) samples (n = 1281) were collected at the time of cesarean delivery from women who delivered singleton newborns at term (gestational age ≥38 weeks). Intraamniotic inflammation was diagnosed if the AF concentration of matrix metalloproteinase-8 was >23 ng/mL. Funisitis was diagnosed by histologic examination if inflammation was present in the umbilical cord.
The prevalence of MSAF was 9.2% (118/1281), and 10.2% (12/118) of neonates exposed to MSAF developed MAS. There were no significant differences in the median gestational age or umbilical cord arterial pH at birth between neonates who developed MAS and those who did not (each P > .1). Mothers whose newborns developed MAS had a higher median of AF matrix metalloproteinase-8 (456.8 vs 157.2 ng/mL, P < .05). Newborns exposed to intraamniotic inflammation had a higher rate of MAS than those who were not exposed to intraamniotic inflammation [13.0% (10/77) vs 0% (0/32), P = .03], as did those exposed to funisitis [31.3% (5/16) vs 7.3% (6/82); relative risk, 4.3; 95% confidence interval, 1.5–12.3]. Among the 89 newborns for whom both AF and placental histology were available, MAS was more common in patients with both intraamniotic inflammation and funisitis than in those without intraamniotic inflammation and funisitis [28.6% (4/14) vs 0% (0/28), P = .009], while the rate of MAS did not show a significant difference between patients with intraamniotic inflammation alone (without funisitis) and those without intraamniotic inflammation and funisitis [10.9% (5/46) vs 0% (0/28)].
The combination of intraamniotic inflammation with fetal systemic inflammation is an important antecedent of MAS. This concept has implications for the understanding of the mechanisms of disease responsible for MAS and for the development of prognostic models and therapeutic interventions for this disorder.
Evaluation of specific marker CK13 and CK10/13 combined with APM staining for the diagnosis of amniotic fluid embolism and aspiration
2014, Forensic Science International
Citation Excerpt :
However, all 41 live births died within 3 days. Some studies suggested that the incidence of AFA in males is higher than in females [24] and our study showed the same trend, but did not reach statistical significance. It is generally accepted that it is difficult to make a diagnosis of AFE and AFA in forensic autopsy.
To explore the value of CK13 (Rab) and CK10/13(Mab) as objective and specific biomarkers combined with Alcian-Phloxine-Martius yellow (APM) staining for the diagnosis of amniotic fluid embolism (AFE) and amniotic fluid aspiration (AFA).
A retrospective study of forensic autopsy cases of 148 neonatal deaths and 19 maternal deaths in the perinatal stage was conducted at the Institute of Pathology and Forensic Medicine, Zhejiang University. Medical records were reviewed and monoclonal antibody for CK13 (Rab) and CK10/13 (Mab) as immunostaining of amniotic fluid squamous cells, APM staining, and Hematoxylin and Eosin (HE) staining were used to diagnose the AFE and AFA. Descriptive statistics of the patient population were analyzed using SPSS 20.0 software.
Immunoreactivity of CK13 and CK10/13 specifically identified squamous cells of all the AFE and AFA cases. The amniotic fluid squamous cells were stained positive in a deep brown color with the monoclonal antibody to CK 13 and CK10/13 whereas the endothelial cells and alveolar epithelial cells were negative. There was no CK13 or CK10/13 expression in the non-AFE and non-AFA cases. With APM staining keratinized squamous cells were pink and mucus was blue-green in marked contrast with the surrounding tissue, which improved the detection rates of both keratinized squamous cells and mucus.
CK13 (Rab) and CK10/13 (Mab) are valuable and reliable biomarkers of amniotic fluid squamous cells. APM reveals enriched mucus and keratinized squamous cells of amniotic fluid. Immunohistochemical detection of CK13 and CK10/13 combined with APM staining can improve the accuracy and reduce the difficulty in the diagnosis of AFE and AFA.
The Use of Nonnutritive Sucking to Facilitate Oral Feeding in a Term Infant: A Single Case Study
2012, Journal of Pediatric Nursing
Citation Excerpt :
It is also an important factor because it has an association in relation to neurological disability and therefore, an infant is likely to have a higher predisposition to have feeding difficulties (Rutherford et al., 2005). The passage of meconium is thought to be a response to stresses such as hypoxia or infection (Wiswell, 2001). Infants born with meconium aspiration are at greater risk of developing neurological disorders, seizures, and respiratory distress difficulties and frequently have significant problems establishing feeding (Wiswell, 2001).
This individual case study presents an evaluation of and reflection on the use of nonnutritive sucking as a technique to facilitate nutritive sucking with an infant with feeding difficulties. Nonnutritive sucking is used in a variable way with mainly premature or sick infants. However, the rationale underpinning use of such an approach is not clear. The infant participant in this study, Baby H, was born at 37 weeks. This case illustrates the use of nonnutritive sucking as an approach with supported rationales for promoting transition toward oral feeding with infants who have complex needs and who are term infants. The literature focuses on using nonnutritive sucking with premature infants who have no additional difficulties such as hypoxic neonatal encephalopathy, meconium aspiration, sepsis, or severe perinatal asphyxia. The intervention carried out with Baby H demonstrates that nonnutritive sucking can contribute toward the management of an infant's feeding development. Baby H took 23 days to develop a sequential nonnutritive sucking pattern, but her ability to transfer this to nutritive sucking and safe feeding took the first 17 months of this infant's life. This study is unique in that it explored the issues involved with a term infant who had complex needs that impacted on feeding development. It is important because many practitioners use nonnutritive sucking with infants who have complex needs.
L-Arginine pathway in neonates with meconium-stained amniotic fluid
2012, European Journal of Obstetrics and Gynecology and Reproductive Biology
Citation Excerpt :
The events that are most likely responsible for in utero meconium release are not clearly understood. Theories related to the mechanisms underlying meconium passage have been proposed, including intrauterine hypoxia, and some studies have concluded that the in utero passage of meconium is a pathological event caused by fetal hypoxia, which relaxes the anal sphincter and releases the meconium [4–9]. l-Arginine is a semi-essential amino acid [10].
To study the arginase, nitric oxide synthase and nitric oxide pathways associated with passage of meconium.
Cord blood samples were collected from 20 newborns with meconium-stained amniotic fluid (MSAF) and from 23 newborns with clear amniotic fluid. Cord blood pH, arginase, nitric oxide synthase and nitric oxide levels were compared between the groups.
The differences between the arginase and nitric oxide measurements of the newborns with MSAF and those with clear amniotic fluid were significant. In the MSAF group arginase levels were significantly lower (p = 0.007) and nitric oxide levels were significantly higher (p = 0.032) than the clear amniotic fluid group.
Hypoxia may be involved in the pathogenesis of meconium passage due to decreased arginase and increased nitric oxide levels.
Effect of meconium on surface properties of surfactant monolayers and liposomes
2010, Colloids and Surfaces A: Physicochemical and Engineering Aspects
Citation Excerpt :
Meconium aspiration syndrome (MAS) occurs due to meconium staining of the amniotic fluid and its inhalation into the neonatal lungs under conditions of stress like hypoxia [1].
The pathophysiology of meconium aspiration syndrome (MAS) is attributed in part to the development of lung surfactant dysfunction in vivo. Meconium (the first excrement of the newborn) and its components are responsible for development of lung surfactant dysfunction. In this study, the effect of meconium and its components on the surface activity of spread surfactant monolayers was evaluated using Wilhelmy balance at physiological temperature and pH. The effect of meconium on adsorption, airway patency and ultrastructure of liposomes made of various surfactant lipids was also evaluated. Significant inhibition of DPPC monolayer surface activity was observed on addition of meconium, its organic and aqueous phase extracts. All the surfactant lipid mixtures including DPPC attained significantly higher minimum surface tensions (between 12 and 20 mN/m) and lowered monolayer compressibility modulus in presence of meconium suggestive of surfactant monolayer fluidization. Meconium reduced the airway patency and affected the adsorption of DPPC liposomes and was associated with altered ultrastructure of DPPC liposomes. Meconium caused the maximum inhibitory effect on DPPC:PE and DPPC:PG and the least inhibitory effects on DPPC:POPC and DPPC:CHOL in terms of minimum surface tensions. All the surfactants were equally inhibited in terms of airway patency. These findings have implications for the differential inhibition of different surfactants in MAS and for the designing of surfactants that are resistant to meconium inhibition.
Why does meconium cause meconium aspiration syndrome? Current concepts of MAS pathophysiology
2009, Early Human Development
One in every 7 pregnancies ends with meconium-stained amniotic fluid and approximately 5% of these infants develop the meconium aspiration syndrome (MAS). MAS is a severe disease of the (mainly) term neonate, characterized by respiratory distress, pulmonary inflammation, persistent pulmonary hypertension and chronic hypoxia.
The pathophysiology of MAS is multifactorial and complex. In this article, we discuss the mechanical and chemical effects of meconium on a newborn's airway, meconium-induced inflammation, mediated by proinflammatory cytokines and chemokines, the complement system and the proinflammatory enzyme phospholipase A2. Furthermore, we focus on MAS-related apoptotic cell death, causing severe acute lung injury due to damage and detachment of lung airway and alveolar cells.
Finally, risk factors for MAS development to identify those newborns that develop MAS and those who do not are discussed.

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^f1: Correspondence to: Thomas E. Wiswell MD, Professor of Pediatrics, SUNY Stony Brook, Pediatrics, HSC-11-060, Stony Brook, New York 11794-8111, USA. Tel: +1 631 444 7653; Fax: +1 631 444 8968; E-mail:[email protected]

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Regular ArticlesHandling the meconium-stained infant

Abstract

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Pediatric Clinics of North America

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American Journal of Obstetrics and Gynecology

American Journal of Obstetrics and Gynecology

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Delivery room management of the apparently vigorous meconium-stained infant: Results of the multicenter, international collaborative trial

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Regular Articles
Handling the meconium-stained infant