Transcript Meconium-stained amniotic fluid (MSAF)

Meconium-stained
amniotic fluid (MSAF)
Pediatrics point of view
M&M Presentation
Darinka Shaw MD
Pediatrics Resident
February 2009
Objectives
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Definition
Epidemiology
Etiology
Pathophysiology
Clinical features
Management
Morbidity&Mortality
Definition
Meconium aspiration syndrome (MAS)
is a respiratory disorder in an infant
born through
Meconium stained amniotic fluid
whose symptoms cannot be
otherwise explained.
MAS
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Cleary&Wiswell proposed severity criteria
to define MAS:
Mild: requires <40%O2 for <48hrs
Moderate: >40%O2 for >48hrs, no air
leak.
Severe: assisted ventilation for >48hrs
often with PPH.
Epidemiology
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MSAF observed in 13% of all live births.
MAS occurs in 5% of newborns delivered
through MSAF.
25,000 to 30,000 cases and 1,000 deaths
related to MAS annually in US.
Epidemiology
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More frequently in infants who are
postmature and small for gestational age.
Decline from 5.8% to 1.5% (1990–1997),
attributed to a 33% reduction in the
incidence of births >41 weeks gestation.
Physiology
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The passage of meconium from the fetus into
amnion is prevented by lack of peristalsis (low
motilin level), tonic contraction of the anal
sphincter, terminal cap of viscous meconium.
MSAF may be a natural phenomenon that
doesn’t indicate fetal distress but mature GI
tract in post term fetus with increased motilin
level.
Vagal stimulation by cord or head compression
may be associated with passage of meconium in
the absence of fetal distress.
Risk factors for MSAF
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Maternal HT
Maternal DM
Maternal heavy cigarette smoking
Maternal chronic respiratory or CV Dx
Post term pregnancy
Pre-eclampsia/eclampsia
Oligohydramnios
IUGR
Poor biophysical profile
Abnormal fetal HR pattern
Pathophysiology
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The pathophysiology of MAS is complex.
Intrauterine fetal gasping, mechanical airway
obstruction, pneumonitis, surfactant inactivation,
and damage of umbilical vessels: all play roles in
the pathophysiology of meconium aspiration.
There is also a strong association between MAS
and persistent pulmonary hypertension of the
newborn (PPHN).
Pathophysiology
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The timing of the initial insult resulting in
MAS remains controversial.
Chronic in-utero insult may be responsible
for most cases of severe MAS.
In contrast to these severe cases, the
vigorous infant who aspirates meconiumstained fluid from the nasopharynx at birth
usually develops mild to moderate
disease.
Pathophysiology
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The traditional belief was that meconium
aspiration occurs immediately after birth.
Aspirated particulate or thick meconium can be
carried rapidly by the first breaths to the distal
airways.
Studies of neonatal puppies with tantalumlabeled meconium instilled into the trachea
before the first breath have confirmed that the
distal migration of particulate matter can occur
within 1 hour of birth.
Pathophysiology
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Several investigators have suggested that most
cases of meconium aspiration occur in utero
when fetal gasping is initiated before delivery.
Meconium has been found distally as far as the
alveoli in some stillborn infants and in some
infants that die within hours of delivery.
There is currently no way to distinguish
between the infant who has developed MAS by
intrauterine respiration or gasping and the infant
who has developed MAS by inhalation of
meconium at the first breaths after delivery.
Mechanism of injury
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1.Mechanical Obstruction of the Airway
It is commonly thought that the initial and most
important problem of the infant with MAS is
obstruction caused by meconium in the airways.
Complete obstruction of large airways by thick
meconium is an uncommon occurrence.
The exact incidence of large-airway obstruction
is unknown, though Thureen et al, in an autopsy
study of infants who died of MAS, found no
evidence of such obstruction.
Pathophysiology
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Usually, small amounts of meconium migrate
slowly to the peripheral airways.
This mechanism can create a ball valve
phenomenon, in which air flows past the
meconium during inspiration but is trapped
distally during expiration, leading to increases in
expiratory lung resistance, functional residual
capacity, and anterior posterior diameter of the
chest.
Pathophysiology
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Regional atelectasis and V/P mismatches can be
developed from total obstruction of the small
airways.
Adjacent areas often are partially obstructed and
over expanded, leading to pneumothorax and
pneumomediastinum air leaks.
Pulmonary air leaks are 10x more likely to
develop in infants with MAS than those without,
and leaks often develop during resuscitation.
Pathophysiology
2. Pneumonitis
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Pneumonitis is a usual feature of MAS,
occurring in about ½ of the cases.
Meconium has a direct toxic effect
mediated by inflammation.
An intense inflammatory response in the
bronchi and alveoli can occur within hours
of aspiration of meconium.
Pathophysiology
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The airways and lung parenchyma become
infiltrated with large numbers of
polymorphonuclear leukocytes and
macrophages.
Produce direct local injury by release of
inflammatory mediators-cytokines (TNF-α, IL-1β,
IL-8) and reactive oxygen species.
Lead to vascular leakage, which may cause toxic
pneumonitis with hemorrhagic pulmonary
edema.
Pathophysiology
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Meconium contains substances such as bile acids
that also can cause direct injury.
Clinicians should maintain a high index of
suspicion for bacterial pneumonia in infants
with MAS.
Presence of fever, an abnormal WBC or a
decline in respiratory function are indications of
bacterial pneumonia and/or sepsis and should
prompt the clinician to obtain relevant cultures
and initiate antimicrobial therapy.
Pathophysiology
3.Pulmonary vasoconstriction
 The release of vasoactive mediators, such as
eicosanoids, endothelin-1 and prostaglandin E2
as a result of injury from meconium seems to
play role in the development of persistent PH.
 The pulmonary vasoconstriction is, in part, the
result of the underlying in utero stressors.
Pathophysiology
4. Surfactant inactivation
 Recognized in the early 1990.
 Meconium displaces surfactant from the alveolar
surface and inhibits its surface tension lowering
ability.
 A full term baby born with a sufficient quantity
of surfactant may develop surfactant deficiency
by inactivation that leads to atelectasis,
decreased lung compliance/volume and poor
oxygenation.
Pathophysiology
CLINICAL FEATURES
History
Infants with MAS have a history of
MSAF.
 They often are postmature or small
for gestational age.
 Many are depressed at birth.
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CLINICAL FEATURES
Physical examination
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Evidence of postmaturity: peeling skin, long
fingernails, and decreased vernix.
The vernix, umbilical cord, and nails may be
meconium-stained, depending upon how long
the infant has been exposed in utero.
In general, nails will become stained after 6
hours and vernix after 12 to 14 hours of
exposure.
CLINICAL FEATURES
Physical examination
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Affected patients typically have respiratory
distress with marked tachypnea and cyanosis.
Reduced pulmonary compliance and use of
accessory muscles of respiration are evidenced
by intercostal and subcostal retractions and
abdominal (paradoxical) breathing, often with
grunting and nasal flaring.
CLINICAL FEATURES
Physical examination
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The chest typically appears barrel-shaped, with
an increased anterior-posterior diameter caused
by overinflation.
Auscultation reveals rales and rhonchi immediately after birth.
Some patients are asymptomatic at birth and
develop worsening signs of respiratory distress
as the meconium moves from the large airways
into the lower tracheobronchial tree.
Diagnosis
MAS must be considered in any infant
born through MSAF who develops
symptoms of RD.
Diagnosis
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The diagnosis of MAS is confirmed by chest
radiograph.
The initial CXR may show streaky, linear
densities similar in appearance to transient
tachypnea of the newborn (TTN).
As the disease progresses, the lungs typically
appear hyperinflated with flattening of the
diaphragms.
Diffuse patchy densities may alternate with
areas of expansion.
Coarse focal consolidation with emphysema.
Hyperinflation and patchy asymmetric
airspace disease that is typical of MAS.
Coarse interstitial infiltrates +L side pneumothorax
Areas of opacification due to atelectasis
bilaterally.
Close up of left lung demonstrating the streaky lucencies of
the air in the interstitium (red arrows) complicated by a
pneumothorax (yellow arrow).
Diagnosis
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In infants with severe disease who require high
concentrations of supplemental oxygen and
mechanical ventilation, the lungs may develop
an appearance of homogeneous density similar
to respiratory distress syndrome (RDS).
Radiographic changes resolve over the course of
7 to 10 days but sometimes persist for several
weeks.
Air leak occurs in 10 to 30 percent of infants
with MAS.
Homogeneous density similar to respiratory
distress syndrome (RDS).
Diagnosis
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Arterial blood gas measurements typically
show hypoxemia and hypercarbia.
Infants with pulmonary hypertension and
right-to-left shunting may have a gradient
in oxygenation between preductal and
postductal samples.
2D Echocardiogram for evaluation of PPH.
Management
Management
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Sept 2007 the ACOG revised recommendations
and recommended that “all infants with MSAF
should not longer receive intrapartum
suctioning. If meconium present and the
newborn depressed, the clinician should intubate
the trachea and suction meconium from beneath
the glottis”.
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Intrapartum suctioning not effective in removing
meconium aspirated by the fetus into the lungs
prior delivery.
Management
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Skilled resuscitation team should be present at
all deliveries that involve MSAF.
Pediatric intervention depends on whether the
infant is vigorous.
Vigorous infant is if has:
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Strong resp. efforts
Good muscle tone
Heart rate >100b/m
When this is a case-no need for tracheal
suctioning, only routine management.
Management
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When the infant is not vigorous:
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Clear airways as quickly as possible.
Free flow 02.
Radiant warmer but drying and stimulation should be
delayed.
Direct laryngoscopy with suction of the mouth and
hypopharynx under direct visualization, followed by
intubation and then suction directly to the ET tube as it
slowly withdrawn.
The process is repeated until either ‘‘little additional
meconium is recovered, or until the baby’s heart rate
indicates that resuscitation must proceed without
delay’’.
Postnatal Management
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Apparently well child born through MSAF
Most of them do not require any
interventions besides close monitoring for
RD.
Most infants who develop symptoms will
do so in the first 12 hours of life.
Postnatal Management
Approach to the ill newborns:
 Transfer to NICU.
 Monitor closely.
 Full range of respiratory support should be
available.
 Sepsis w/up and ABx indicated.
 Transfer to ECMO center may be
necessary.
Treatment in NICU
Goals:
 Increased oxygenation while minimizing the
barotrauma (may lead to air leak) by minimal
MAP and as short IT as possible.
 Prevent pulmonary hypertension.
 Successful transition from intrauterine to
extrauterine life with a drop in pulmonary
arterial resistance and an increase in pulmonary
blood flow.
Treatment in NICU
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Severe MAS can spiral into vicious cycle of
hypoxemia that leads to acidosis, which together
cause pulmonary vein constriction.
May lead to persistent pulmonary hypertension.
The resultant right-to-left shunting at the level
of the ductus arteriosus, the atrial level, or both
causes further cyanosis and hypoxemia, which
perpetuate the cycle.
Treatment in NICU
Ventilatory support depends on the amount of
respiratory distress:
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O2 hood
Mechanical ventilation (40%).
CPAP (10%).
Observational study showed worse outcome for infants
treated with hyperventilation.
High-frequency ventilators should reduce air leak
syndromes in MAS, but animal and clinical models have
yielded conflicting results.
High-frequency ventilators may slow the progression of
meconium down the tracheobronchial tree and allow
more time for meconium removal.
Treatment in NICU
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Surfactant
Two randomized controlled studies have evaluated the
efficacy of exogenous surfactant administration. Results
showed decreased number of infants requiring ECMO
and possible reduction of pneumothorax, but no
difference in mortality.
A Cochrane meta-analysis of 4 randomized trials
confirmed that surfactant replacement showed no effect
on mortality but reduce the use of ECMO (RR 0.64, 95% CI,
0.46-0.91).
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Lavage with dilute surfactant-increases oxygenation and
decrease the need of MV (need additional trials).
Treatment in NICU
Inhaled NO
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NO causes selective pulmonary vasodilation by acting
directly on the vascular smooth muscle-activates
guanylate cyclase and increases cGMP.
By dilating blood vessels in well ventilated areas of lung,
NO decreases the V/P mismatch and improved
oxygenation in infants with PPH.
Decreases need for ECMO (RR 0.61, 95%CI 0.51, 0.72)
but no difference in mortality.
In a large randomized multicenter trial infants with MAS
responded well to the combination of inhaled nitric oxide
and HFOV, likely because of improved lung inflation and
better delivery of the drug.
ECMO
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40% of infants with MAS treated with
inhaled NO fail to respond and require
bypass.
35% of ECMO patients are with MAS.
Survival rate after ECMO 93-100%.
Morbidity & Mortality
Pulmonary morbidity
 Pulmonary outcome evaluated in 35 infants with
MAS and 70 controls.
 During the first 6mo after birth, the infants with
MAS were significantly more likely to have one
or more episodes of wheezing and/or coughing
lasting ≥3 days (49% vs. 20%) and receive
bronchodilator therapy (23% vs. 3%) compared to
controls.
Morbidity & Mortality
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Pulmonary function testing was performed at 8y
of age in 11 children who had MAS and 9
controls.
The MAS group had evidence of mild airway
obstruction, hyperinflation, and increased closing
volumes compared to controls, and had more
exercise-induced bronchospasm (4 vs. 0 children).
However, during graded exercise stress tests,
MAS children had normal maximal oxygen
consumption and anaerobic threshold without
significant hypoxemia or hypercarbia.
Morbidity & Mortality
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Respiratory symptoms, pulmonary function tests, and
chest radiographs evaluated in 18 children age 6-11y
who had MAS.
7 children had recurrent cough and wheezing consistent
with asthma, and 5 of these had exercise-induced
bronchospasm that responded to bronchodilators.
Of the 11 asymptomatic children, 2 had mild expiratory
airflow limitation, 1-exercise-induced bronchospasm, and
8 had normal pulmonary function. Chest radiographs
were normal in all the children.
Morbidity & Mortality
Neurologic outcome
 Outcome is good in uncomplicated MAS
with no underlying disorder.
 Most cases of severe MAS are associated
with intrauterine asphyxia and/or infection
and neurologic outcome depends upon
these conditions.
Morbidity & Mortality
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In retrospective comparison, perinatal mortality
significantly higher in singleton pregnancies
with/ than without MSAF (1.5 vs. 0.3/1000).
The mortality rate for MAS resulting from severe
parenchymal pulmonary disease and pulmonary
hypertension is as high as 20%.
Severe fetal acidemia-cord arterial pH<7.0 was
significantly more common with meconiumstained fluid (7 vs. 3/1000).
Cesarean delivery was doubled in the meconium
group (14 vs. 7%).
Summary
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Optimal care of an infant born through
MSAF involves close collaboration between
OBs and Pediatricians.
Effective communication and anticipation
of potential problems is a corner stone of
the successful partnership.
References:
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Meconium Stained Fluid: Approach to the Mother and the Baby Michele C. Walsh,
MD, MS; Jonathan M. Fanaroff, MD, JD Clin Perinatol 34 (2007) 653–665
The epidemiology of meconium aspiration syndrome: incidence, risk factors,
therapies, and outcome. Dargaville PA; Copnell B Pediatrics. 2006
May;117(5):1712-21.
Delivery room management of the apparently vigorous meconium-stained
neonate: results of the multicenter, international collaborative trial. Wiswell TE;
Gannon CM; Jacob J; Goldsmith L; Szyld E; Weiss K; Schutzman D; Cleary GM;
Filipov P; Kurlat I; Caballero CL; Abassi S; Sprague D; Oltorf C; Padula M
Pediatrics 2000 Jan;105(1 Pt 1):1-7.
Defecation in utero: a physiologic fetal function. Ramon y Cajal CL; Martinez RO
Am J Obstet Gynecol 2003 Jan;188(1):153-6.
Surfactant and surfactant inhibitors in meconium aspiration syndrome. Dargaville
PA; South M; McDougall PN J Pediatr 2001 Jan;138(1):113-5.