Update Article

Meconium Aspiration Syndrome : An Insight

Air Cmde U Raju*, Maj V Sondhi+, Maj SK Patnaik#

Abstract
Meconium aspiration syndrome (MAS) is respiratory distress in a newborn baby caused by the presence of meconium in the
tracheobronchial airways. The aspiration of meconium stained amniotic fluid by the fetus can happen during antepartum or
intrapartum periods and can result in airway obstruction, interference with alveolar gas exchange, chemical pneumonitis as well
as surfactant dysfunction. These pulmonary effects cause gross ventilation-perfusion mismatching. To complicate matters further,
many infants with MAS have primary or secondary persistent pulmonary hypertension of the newborn as a result of chronic in
utero stress and thickening of the pulmonary vessels. Although meconium is sterile, its presence in the air passages can
predispose the infant to pulmonary infection. MAS is essentially a clinical diagnosis and should always be suspected in a child
with respiratory distress and meconium-stained amniotic fluid at delivery. Though a known entity for a long time, its management
still remains contentious. Intubation and direct tracheal suction is performed when meconium is observed in the amniotic fluid
and the infant is not vigorous. Subsequent management involves ventilation, surfactant instillation and lavage, inhaled nitric
oxide and high frequency ventilation. The role of steroids continues to be controversial.
MJAFI 2010; 66 : 152-157
Key Words : Meconium aspiration; Amnioinfusion; Surfactant; Ventilation; Tracheal suction.

Introduction there are encouraging trends of a progressive decline in

S ince when first described by the ancient Greeks to
the present day, meconium and its effect on the
newborn infant, has remained an enigma. The term was
coined by Aristotle from the Greek word meconium
arion meaning opium like as he believed that the
substance induced foetal sleep [1]. In spite of rapid
advances in investigative and management modalities,
meconium and its effects on the foetus and neonate
have over decades remained a cause of worry. To date
debates continue to rage regarding the optimum
obstetrical approach, resuscitation measures at birth and
subsequent management of the critically ill neonate with
meconium aspiration syndrome (MAS).
Definition
The most popularly used definition of MAS is
respiratory distress occurring soon after birth in an infant
born from a meconium stained milieu with compatible
radiological findings which cannot be otherwise
explained.
Incidence
Despite changing strategies, meconium staining of
the amniotic fluid (MSAF) happens in approximately
10-15% of childbirths with incidences ranging from
5-25% [2]. MAS develops in approximately 4-10% of
the infants born from a MSAF milieu. Of late however,
*
AOC, 7 Air Force Hospital, Kanpur, +,#Graded Specialist (Paediatrics), Military Hospital, Ambala.
Received : 10.09.08; Accepted : 08.02.10 E-mail : columaraju@rediffmail.com
the incidence of MAS from Australia and New
Zealand [3]. Of these neonates who develop MAS, one
third require ventilatory support, 10% develop air leaks
and in spite of appropriate management strategies, 5-
10% of them have a fatal outcome. Of the babies who
suffer persistent pulmonary hypertension of the newborn
(PPHN), 5-6 % are related to MAS [2].
Pathophysiology
Meconium which comprises of gastrointestinal,
hepatic and pancreatic secretions, cellular debris,
swallowed amniotic fluid, lanugo, vernix caseosa and
blood begins to appear in the foetal intestines by the
10th week of life gradually increasing in amount to reach
200 gms at birth. However due to lack of strong
peristalsis, good anal sphincter tone, low levels of motilin
and a cap of viscous meconium in the rectum, in utero
passage is uncommon till term. In utero hypoxia and
acidosis lead to a vagal response with resultant increased
peristalsis and a relaxed anal sphincter leading to
meconium passage. Integrity of the parasympathetic
system therefore appears to be pre requisite for
meconium passage making it a maturational event and
rare before term.
It has been seen in animal experiments that when
hypoxia occurs, deep intrauterine gasping ensues placing
the foetus in a MSAF milieu at risk for aspiration [4].
Meconium Aspiration Syndrome
Autopsies have revealed meconium in the terminal
airways of stillborn foetuses. However the relationship
between intrauterine passage of meconium, development
of foetal distress and the pathophysiology of foetal
asphyxia has not been determined precisely. Although
the passage of meconium may be a physiologic event
related to increasing gastrointestinal maturity and
increased motilin levels, it also occurs as a result of
acidosis and hypoxaemia both acute as well as chronic,
its aspiration being more likely in the depressed foetus
and in the one which is post-term.
The clinical features of MAS appear to be related to
the viscosity of meconium; thick meconium being more
associated with complications. This thick particulate
meconium can either block the airways completely
leading to atelectasis and ventilation perfusion mismatch
or partially resulting in ball valve air trapping (Table 1).
These obstructive properties lead to the classical
radiological picture of areas of atelectasis and
consolidation interspersed with hyperexpanded zones
Table 1
Pathophysiology of meconium aspiration syndrome
Meconium aspiration
Large plugs-upper airway obstruction
Acute hypoxia
Mechanical obstruction
Incomplete
Ball valve obstruction
Air leaks
PaCO2
Hypoxemia, Hypercarbia, Acidosis
PPHN
MJAFI, Vol. 66, No. 2, 2010
153
along with air leaks (Figs. 1, 2). Meconium in the airways
initiates an inflammatory reaction which was first
described by Clark et al [5] who showed the effect of
meconium on neutrophil function by inhibiting oxidative
burst and phagocytosis.
Others have found that meconium induces lung injury
by activating alveolar macrophages and generates
increased production of superoxide anions in these cells.
Increased levels of inflammatory cytokines have been
found in broncheoalveolar lavage (BAL) in meconium
aspirated infants suggesting that meconium induces
production of inflammatory cytokines and such an
induction can occur in utero [6]. The contained bile salts
have been implicated in displacing surfactant as well as
damaging type 2 pneumocytes with resultant surfactant
deficiency.
All of these mechanisms lead to hypoxemia, acidosis
and hypercapnea which result in pulmonary
vasoconstriction. Pulmonary hypertension ensues which
Small particles-Diffuse spread
Lower Airway obstruction
Chemical inflammation Infection
Complete
Atelectasis
R L
shunts
PaO2
154
Fig. 1 : Chest X-Ray showing zones of hyper-inflation and
atelectasis.
in turn aggravates the hypoxemia and acidosis creating
a vicious cycle.
The meconium from the airways gets absorbed and
is excreted in urine which may give urine a turbid green
colour in extreme cases (Fig. 3). Meconium aspiration
can occur both by in utero gasping as well as postpartum
aspiration with the initial breaths of the baby, it being
difficult to distinguish which mechanism was responsible
in a given case. However, the babies who follow a more
severe clinical course are likely to have aspirated in utero,
are depressed at birth and develop respiratory distress
early.
Obstetrical management
Foetal Monitoring: The assessment of foetal
condition is a major priority for all birth attendants.
However this assessment is complicated by the high
false positive rate of the indicators. Several workers
have studied the relationship between cardiotocogram
(CTG) abnormality, MSAF, umbilical cord pH and apgar
scores. It has been observed that CTG while picking up
foetal jeopardy does provide a high false positivity [7].
The presence of thick meconium, late decelerations,
tachycardia on CTG, cord pH <7.16, apgar scores of <6
at 1 and 5 minutes and meconium in the trachea correctly
predicted 50% of the infants of MAS. Absence of these
symptoms correctly predicted 97% of the infants who
were healthy. It has been observed that normal CTG
records combined with adequate amniotic fluid volume
have a high predictive accuracy of foetal well being, in
spite of heavy meconium contamination [8]. It has also
been observed that compared with healthy neonates with
MSAF, those with MAS had higher rate of non reassuring
foetal heart record tracing, thick meconium, apgar scores
of < 5 at five minutes and lower birth weights. Thus it
appears that CTG abnormality and MSAF are
insufficiently correlated with apgar scores or cord pH
Raju, Sondhi and Patnaik
Fig. 2 : Chest X-ray showing Fig. 3 : Meconium stained urine in
hyperinflation and Pneumothorax meconium aspiration syndrome.
(Left).
and have more value as predictors of foetal well being
rather than jeopardy. However additional measures such
as foetal ECG, head compression force analysis, CPK-
BB and maternal-foetal temperature difference may
improve our predictive ability [9].
Amnioinfusion: Initial reports indicated that
amnioinfusion by thinning the MSAF would reduce the
incidence and severity of subsequent MAS [10].
However later studies reported that this procedure was
not accompanied by any statistically significant reduction
in adverse foetal outcomes. Moreover this procedure
had fallen into disrepute for its increased association
with foetal heart rate abnormalities, operative/instrument
deliveries and infection. The current consensus is that
in clinical settings with standard perinatal surveillance,
evidence does not support the use of amnioinfusion for
MSAF. However, when there is limited perinatal
surveillance, where complications of MSAF are common,
it appears to reduce the incidence of MAS [11,12].
Neonatal Management
Although meconium staining and the MAS are
common neonatal problems, the appropriate
management in the delivery room and subsequently
remains controversial.
Airway Clearing: There was in the past a universal
agreement that suctioning of the mouth, nose and
posterior pharynx before the delivery of the thorax should
be performed in all cases with MSAF regardless of the
meconium consistency. However the current evidence
suggests that intrapartum suctioning of the oro/
nasopharynx may not reduce the risk of aspiration.
Therefore the present reccomendations no longer advise
routine intrapartum upper airway suctioning in infants
born from a milieu of meconium. Subsequent tracheal
toileting which was earlier advocated has been
challenged on the precincts that it is only the depressed
MJAFI, Vol. 66, No. 2, 2010
Meconium Aspiration Syndrome
neonate who runs the risk of MAS. Therefore the
vigorous infant at low risk should not be subjected to
this potentially risky procedure. It is likely that MAS
will develop in a small minority of apparently healthy
meconium stained infants, but there is no way of
identifying these neonates at risk during childbirth. The
2005 Joint Committee of the American Academy of
Paediatrics and American Heart Association delineated
neonatal resuscitation guidelines recommend that
tracheal toileting be performed on meconium stained
newborns soon after delivery if the neonate is depressed
[13]. The features of foetal depression delineated are
absent/depressed respiration, heart rate < 100/minute
and hypotonia. It is further recommended that the initial
suctioning should not exceed five seconds. If no
meconium is retrieved, repetitive suctioning is not
required. However if meconium is retrieved and no
bradycardia is present, it is recommended to reintubate
and perform suction under oxygen cover. In case of
bradycardia, positive pressure ventilation is to be
administered and airway toileting considered later.
Because moderate amounts of meconium may remain
in the stomach and be aspirated later, it is advisable to
perform a gastric lavage after the baby has stabilized.
Saline lavage and chest physiotherapy performed with
due caution in the stabilized baby may assist the removal
of tenacious secretions [14].
Ventilatory Support: One third of the infants with
MAS require ventilatory support. Because air leaks are
a major problem in this condition, high concentrations of
oxygen are necessary initially. Continuous Positive
Airway Pressure (CPAP) / Bubble CPAP could be
beneficial if air trapping is not a major problem. If CPAP
does not suffice, mechanical ventilation using low
inspiratory pressures, short inspiratory and long
expiratory times and rapid rates have been advocated
to maintain blood gases within normal limits. Elevation
of positive end expiratory pressure (PEEP) while
improving oxygenation may worsen air trapping and the
risk of pneumothorax. Hence low PEEP appears to be
a more beneficial option. This strategy while preventing
air leaks also limits pulmonary hypertension, a major
problem with MAS. Sedation and neuromuscular
blockade aid mechanical ventilation.
High Frequency Ventilation (HFV) by providing
effective gas exchange at low tidal volumes has been
found advantageous in treating MAS. Its benefits include
less barotraumas, increased mobilization of airway
secretions, quicker attainment of respiratory alkalosis
and fewer histopathological changes. In a large
retrospective study, it was observed that HFV was being
increasingly utilized in treating babies with MAS (12.2%
in 1996 to 25.2% in 2003). It was also observed that
MJAFI, Vol. 66, No. 2, 2010
155
infants on HFV spent longer on respiratory support and
there was an increased mortality rate albeit a declining
one, as compared to infants who were provided other
ventilation modalities. This increased morbidity and
mortality was perhaps because HFV was being applied
to infants at the greatest risk of serious adverse
outcomes, more as a rescue therapy [15].
Liquid Ventilation with perfluorocarbons has been
found to be beneficial in lamb models of MAS with
improved survival, gas exchange and haemodynamic
stability. Quality scientific proof of human trials is eagerly
awaited.
Surfactant Therapy: Surfactant deficiency in MAS
is a consequence of altered function rather than a
deficiency state. Meconium displaces surfactant from
the alveolar surface and inhibits its surface tension
lowering function. In high concentrations, it has a direct
cytotoxic effect on the type 2 pneumocytes. Human
trials have shown varying results from marked
improvement to a marginal one in oxygenation when
used in this condition. It has also been observed that
surfactant therapy in MAS restored the distended
terminal airspaces of the lungs and kept the spaces from
irregular overdistension [16]. Surfactant replacement by
bolus or slow infusion in infants with severe meconium
aspiration syndrome improved oxygenation and reduced
the severity of respiratory failure, air leaks and need for
extracorporeal membrane oxygenation (RR: 0.64; 95%
CI: 0.460.91; NNT:6). Doses from 100-200mg/kg of
phospholipid have been used in various studies with
repeat dosages being provided 6-8 hourly till oxygenation
improves. However no clear consensus on the optimal
dosage or the number of doses to be provided exists as
yet [17,18]. Although there was no increase in acute
morbidity in these infants, transient oxygen desaturation
and endotracheal tube obstruction occurred during bolus
administration in nearly one third of the surfactant
treated infants. A review of randomised control trials
(RCTs) evaluating its effects in infants with MAS
suggested that surfactant administration may reduce the
severity of respiratory illness and decrease the number
of infants with progressive respiratory failure requiring
support with Extra corporeal membrane oxygenation
(ECMO). The relative efficacy of surfactant therapy
including KL-4 surfactant compared to, or in conjunction
with, other approaches to treatment including nitric oxide,
liquid ventilation, surfactant lavage and high frequency
ventilation remains to be tested [19,20]. There are
reports which suggest that surfactant when combined
with an adjuvant-PEG/dextran is more efficacious.
Broncho Alveolar Lavage (BAL) : The efficacy of
lung lavage by bronchoscopy in removing large quantities
of meconium and improving lung functions is increasingly
156
being documented. Surfactant lavage for meconium
aspiration was evaluated in a small, randomized trial.
Trends toward lower duration of ventilation and severity
of illness were reported [17]. The recent reports suggest
that surfactant is more effective than saline as a lavage
fluid [21-22]. The use of surfactant/dextran mixture has
been reported to aid the meconium clearance ability of
surfactant [23]. There are reports of perfluorocarbon
lavage followed by partial liquid ventilation being a more
efficacious method as compared to surfactant lavage
alone [24].
Inhaled Nitric Oxide (INO) is currently considered
the most effective therapy in the management of PPHN
which often accompanies MAS. The recommended
dosage of INO is 20 parts per million (PPM). Effective
use of INO requires adequate lung expansion to optimize
its delivery within the lungs. Hence effective ventilation
is required to achieve the full benefits of INO when
there is significant parenchymal disease of the lungs as
occurs in MAS [25].
Steroid Therapy : Meconium in the airway evokes
an inflammatory response characterized by the presence
of elevated cell counts and pro inflammatory cytokines
viz. interleukin (IL-1B), IL-6, tumour necrosis factor
(TNF-). [26]. Reduction in the levels of these cytokines
has been found to correlate with improved lung function
[27]. Steroids provided by both the intravenous as well
as inhaled routes have been observed to suppress this
inflammatory response and thus improve pulmonary
functions in babies with MAS [28]. Given its easy
availability and inexpensive nature, this form of therapy
holds promise in its application in the neonatal intensive
care unit (NICUs) of the developing nations.
Extra corporeal membrane oxygenation (ECMO):
In the 1990s, substantial work has been done assessing
the usefulness of ECMO in neonates with MAS wherein
it has been proved effective in reducing both death and
severe disability in neonates. Further studies have
indicated that MAS patients had a significantly lower
number of complications vs no MAS patients on ECMO.
These data support the consideration of relaxed ECMO
entry criteria for MAS [29].
Antibiotics : Meconium is almost always sterile. Yet
several workers routinely administer antibiotics to the
babies with MAS, the rationale being:-
(a) Meconium produces a chemical pneumonitis with
segmental atelectasis mimicking bacterial
pneumonitis.
(b) There is the possibility that infection may be the
stimulation for in utero meconium passage.
(c) In vitro enhancement of bacterial growth by
meconium suggests the increased risk of
Raju, Sondhi and Patnaik
superimposed bacterial infection in MAS.
However the consensus opinion does not favour the
routine use of antibiotics in babies with MAS [30].
Supportive Care: It is necessary to maintain an
optimal thermal environment and minimal handling
because these infants are agitated easily and become
hypoxemic and acidotic quickly. Careful attention should
be paid to systemic blood pressure and blood volume.
Volume expansion, transfusion therapy and systemic
vasopressors are critical in maintaining systemic blood
pressure greater than pulmonary blood pressure, thereby
decreasing the right to left shunt through the patent ductus
arteriosus.
Newer Therapies: INO as a pulmonary vascular
relaxing agent has been used to treat PPHN, a common
accompaniment of MAS. Studies suggest that though
mortality statistics did not alter significantly, sustained
improvement in oxygenation with nitric oxide and better
oxygenation at initiation with ECMO may have important
clinical benefits. It has been speculated that adopting
specific lung expansion strategies with nitric oxide may
lead to reduced use of the more invasive ECMO. Novel
pharmacologic interventions like pentoxiphylline by
antiinflamatory property of preventing meconium
induced polymorph degranulation, CC10 and tezosentan
are awaiting trials with sufficient power before they come
to be used regularly in this scenario [31,32].
Medicolegal Implications
With increasing consumer awareness, there is an
enhanced risk of lawsuits when a baby born from a
meconium stained milieu is found to develop long term
sequelae. It is as yet not clear if MSAF per se indicates
foetal jeopardy. There is no quality proof to suggest that
MAS leads to sequelae. An accurate calendar for timing
the passage of meconium to delivery time does not exist.
It is known however that many of the infants who have
experienced MAS have suffered pre and postnatal
periods of hypoxia and acidosis which are risk factors
for CNS damage. Though the delivering obstetrician is
the primary focus of such lawsuits, the neonatologist
also gets involved..
Conclusions
Though well recognised and common problems,
MSAF and MAS continue to occur with the same
frequency over the years. The management of the
afflicted neonate with MAS is a daunting task requiring
critical care support. Several modalities of monitoring
and treatment are available, but these are yet to be
substantiated with quality scientific investigation. Our
understanding of this rather complex though common
entity is as yet incomplete, making it a fertile ground for
research.
MJAFI, Vol. 66, No. 2, 2010
Meconium Aspiration Syndrome
MSAF though a sign of foetal maturity, could in the
presence of abnormal CTG and acidemia suggest foetal
jeopardy. Oropharyngeal suctioning at birth, followed
by tracheal toileting in depressed and hypotonic babies
limits the occurrence and severity of MAS.
Management modalities in MAS include mechanical
ventilation, surfactant therapy and supportive care.
Steroid therapy is as yet controversial. Early and
appropriate respiratory support limits PPHN, treatment
of which can be challenging.
Conflicts of Interest
None identified
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