Fatal meconium aspiration in spite of appropriate perinatal airway management: Pulmonary and placental evidence of prenatal disease

Thureen, Patti J.; Hall, Daniel M.; Hoffenberg, Analice; Tyson, R. Weslie

doi:10.1016/s0002-9378(97)70387-9

Cited by 59 publications

(22 citation statements)

References 16 publications

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“…11,17 -20 It is also possible that this did not affect the development of severe MAS, as some studies have suggested that aspiration of meconium occurs in utero and that damage in the lungs has already taken place by the time the baby is born. 1,19,[21][22][23] The high mortality rate of 33% in this study could be related to associated conditions, such as infections and PPHN, and low usage of adjunct respiratory therapies. Among the patients who had their CRP level assessed, 92% had CRP >10 mg l À1 and 78% had CRP >20 mg l À1 , suggesting the presence of infection or inflammation.…”

Section: Discussionmentioning

confidence: 87%

“…This is supported by findings in autopsies from cases dying from severe MAS within 48 h of birth, which revealed muscularization of distal pulmonary arterioles, which requires 3 to 8 days to develop, making it unlikely that PPHN was a complication of MAS. 23,27,28 As PPHN on its own is associated with high mortality rate, one would expect less mortality rate from MAS if infants with PPHN are excluded. In this study, the mortality rate was 73% lower in those with PPHN compared to those without PPHN.…”

Section: Discussionmentioning

confidence: 99%

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Meconium aspiration syndrome requiring assisted ventilation: perspective in a setting with limited resources

Velaphi

Kwawegen

2008

J Perinatol

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To determine characteristics, management, complications and outcome of neonates with meconium aspiration syndrome (MAS) requiring mechanical ventilation (MV). A retrospective review of clinical data of neonates with MAS who were admitted to a public hospital for MV between January 2004 and December 2006. Eighty-eight neonates were ventilated for MAS. Thirtyone percent were postdates and 51% had no electronic fetal monitoring. Postnatal suctioning of meconium was not performed according to protocol in 47% of nonvigorous infants. High-frequency ventilation and surfactant were used in 32 and 14% of cases, respectively. Persistent pulmonary hypertension of the newborn (PPHN) and pneumothorax occurred in 57 and 24% of cases, respectively. Overall mortality rate was 33%. Neonates suffering from MAS with PPHN had higher mortality rate of 48% compared with 13% in those suffering from MAS without PPHN. Factors associated with mortality were peak inspiratory pressure (P<0.001), pneumothorax (P<0.001) and PPHN (P ¼ 0.001). Postdates, inadequate intrapartum monitoring and limited use of adjunct respiratory therapies were common. Severe MAS is associated with adverse outcome.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Meconium aspiration syndrome requiring assisted ventilation: perspective in a setting with limited resources

Velaphi

Kwawegen

2008

J Perinatol

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“…In addition, a severe form of human MAS, which cannot be prevented by these treatments, shows features similar to those of ATF-2 null mutants. Interestingly, the placentas of some severe MAS infants showed significant abnormalities (3), suggesting that at least some type of MAS may be a prenatal rather than a postnatal disease. In addition to the presence of fluid, the level of surfactant protein B in the ATF-2 mutant lungs was decreased to half of the level of the wild type.…”

Section: Discussionmentioning

confidence: 99%

“…Aspiration of meconium may cause mechanical obstruction of the airways, chemical pneumonitis, and surfactant inactivation. Although MAS can be prevented in the majority of infants by appropriate suctioning at birth or by early administration of surfactant, the severe form of MAS is still a neonatal problem that remains to be resolved (3).…”

Section: Meconium Aspiration Syndrome (Mas)mentioning

confidence: 99%

Mouse ATF-2 Null Mutants Display Features of a Severe Type of Meconium Aspiration Syndrome

Maekawa¹,

Bernier²,

Sato³

et al. 1999

Journal of Biological Chemistry

101

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Mouse null mutants of transcription factor ATF-2 were generated by the gene targeting method. They died shortly after birth and displayed symptoms of severe respiratory distress with lungs filled with meconium. These features are similar to those of a severe type of human meconium aspiration syndrome. The increased expression of the hypoxia inducible genes suggests that hypoxia occurs in the mutant embryos and that it may lead to strong gasping respiration with consequent aspiration of the amniotic fluid containing meconium. A reduced number of cytotrophoblast cells in the mutant placenta was found and may be responsible for an insufficient supply of oxygen prior to birth. Using the cDNA subtraction and microarray-based expression monitoring method, the expression level of the platelet-derived growth factor receptor ␣ gene, which plays an important role in the proliferation of trophoblasts, was found to be low in the cytotrophoblasts of the mutant placenta. In addition, ATF-2 can trans-activate the PDGF receptor ␣ gene promoter in the co-transfection assay. These results indicate the important role of ATF-2 in the formation of the placenta and the relationship between placental anomalies and neonatal respiratory distress. The ATF-2 null mutants should enhance our understanding of the mechanism of severe neonatal respiratory distress. Meconium aspiration syndrome (MAS)1 is a common neonatal problem that results in acute and chronic respiratory morbidity (for review, see Refs. 1 and 2). Unfortunately, our understanding of this entity is incomplete. Aspiration of meconium particles may occur before, during, or after delivery and is associated with deep inspiratory movements because of fetal respiratory depression. Aspiration of meconium may cause mechanical obstruction of the airways, chemical pneumonitis, and surfactant inactivation. Although MAS can be prevented in the majority of infants by appropriate suctioning at birth or by early administration of surfactant, the severe form of MAS is still a neonatal problem that remains to be resolved (3).A number of transcription factors of the ATF/CREB family, all of which contain a DNA-binding domain consisting of a cluster of basic amino acids and a leucine zipper region (b-zip), have been identified (for review, see Ref. 4). They bind to the cAMP response element (CRE) as homodimers or heterodimers formed through the leucine zipper. Among the numerous transcription factors of the ATF/CREB family, three factors, ATF-2 (also called CRE-BP1), ATF-a, and CRE-BPa form a subgroup (5-9). These factors are capable of forming homodimers or heterodimers with c-Jun (10). A common characteristic of this group of factors is their activation by the stress-activated protein kinases such as the Jun amino-terminal kinase and p38 (11-13). The stress-activated protein kinases phosphorylate this group of factors at sites close to the NH 2 -terminal transcriptional activation domain containing the metal finger structure and stimulate their trans-activating capacity. Because a group of fac...

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“…46 In addition, these vessels possess a unique ability to undergo rapid changes in architecture, particularly thickening of the media and the adventitia, distal extension of smooth muscle, 47 and increased tortuosity and muscularization of the alveolar septal arterioles. 48 The importance of this abnormal proliferation and excessive collagen synthesis by pulmonary vascular wall cells has been demonstrated by attenuation of the pulmonary hypertensive process by inhibitors of collagen synthesis in a rat model. 49 Similar findings of excessive muscularization of distal pulmonary arterioles in infants with fatal MAS 50 were discounted by Perlman and colleagues 51 who suggested that these findings could be an artifact caused by distortion of the pulmonary vessels during fixation.…”

Section: Pathophysiology Of Meconium Passagementioning

confidence: 99%

Resuscitation of the Meconium-Stained Infant and Prevention of Meconium Aspiration Syndrome

Fuloria

Wiswell

1999

J Perinatol

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The term meconium was originally coined by Aristotle who used the Greek word meconium-arion 1 meaning "opium-like," because he believed meconium induced fetal sleep. It is probable that he recognized the association between the presence of meconium in the amniotic fluid and the occurrence of fetal deaths and neonatal depression.Depending on the population studied, the frequency of meconium-stained amniotic fluid (MSAF) at the time of delivery is variable, ranging between approximately 8% and 19% of all term deliveries. [2][3][4][5][6][7][8] Alexander and colleagues 9 noted a 1.5-fold increased risk for MSAF in black women compared with white women. The authors recommended that maternal ethnicity be viewed as a risk indicator of, and not a causal factor for, MSAF. They also observed an increased likelihood of MSAF with increasing gestational age in both ethnic groups.Regardless of the reason for meconium passage, its presence may be associated with adverse fetal and neonatal outcomes, including death, acute respiratory complications, and long-term pulmonary and neurologic abnormalities. Depending on various factors, including the population studied and the criteria used for making a diagnosis, meconium aspiration syndrome (MAS) will develop in 2% to 33% of infants born through MSAF. 3,4,10,11 As many as 30% or more of infants with MAS require mechanical ventilation. 3,12 Accompanying persistent pulmonary hypertension of the newborn (PPHN) is present in approximately one-third of these infants. 13 The mortality associated with MAS is disturbingly high, ranging from 4% to 19% 3,12,14 ; a large proportion of this mortality is attributable to PPHN.Early-onset neonatal seizures, secondary to hypoxic events, have been reported in infants born through thick MSAF. 15 Berkus et al. 16 observed a sevenfold increased risk of neonatal seizures and a fivefold increased likelihood of hypotonia in infants born through moderate to thick compared with thin meconium-stained or clear amniotic fluid. Some investigators have noted an increased likelihood of cerebral palsy in surviving infants with a low Apgar score who were born through MSAF. 17 In addition, there may be long-term pulmonary sequelae associated with MAS. Yuksel et al. 18 have shown increased functional residual capacity and airway reactivity at 6 months of age in infants with MAS; infants who required more respiratory support in the neonatal period had significantly more symptoms and required bronchodilator therapy more often. MAS has also been implicated in increased airway reactivity and abnormal pulmonary function tests in later childhood. 19,20 PATHOPHYSIOLOGY OF MECONIUM PASSAGEMeconium is a viscous green substance composed primarily of water (72% to 80%). Other components of meconium include gastrointestinal secretions, bile, bile acids, mucus, pancreatic juice, cellular debris, and swallowed amniotic fluid, lanugo, vernix caseosa, and blood. 1,21 The substance may first be noted in the fetal gastrointestinal tract as early as 10 to 16 weeks' gestation. At birt...

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Fatal meconium aspiration in spite of appropriate perinatal airway management: Pulmonary and placental evidence of prenatal disease

Cited by 59 publications

References 16 publications

Meconium aspiration syndrome requiring assisted ventilation: perspective in a setting with limited resources

Meconium aspiration syndrome requiring assisted ventilation: perspective in a setting with limited resources

Mouse ATF-2 Null Mutants Display Features of a Severe Type of Meconium Aspiration Syndrome

Resuscitation of the Meconium-Stained Infant and Prevention of Meconium Aspiration Syndrome

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