Meconium aspiration syndrome

Meconium is the earliest stool that is passed by mammalian infant(newborn) , meconium is

composed of materials ingested during the time the infant is in the uterus which consists of
intestinal epithelial cells, lanugo, mucus, amniotic fluid, bile and water. Meconium is viscous
and sticky like tar, its color usually being a very dark olive green; It should be completely
passed by the end of the first few days after birth, with the stools progressing toward yellow .
1 https://en.wikipedia.org/wiki/Meconium
Meconium aspiration syndrome is a respiratory distress that a newborn baby suffers who has
breathed (aspirated) a dark green, sterile fecal material called meconium into the lungs before
or around the time of birth. This syndrome occurs when stress causes the fetus to take
forceful gasps, so that the amniotic fluid containing meconium is breathed (aspirated) in and
deposited into the lungs while still in the uterus.. After delivery, the aspirated meconium
may block the newborn's airways and cause regions of the lungs to collapse. Sometimes
airways are only partially blocked, allowing air to reach the parts of the lung beyond the
blockage but preventing it from being breathed out. Thus, the involved lung may become
over-expanded. When a portion of the lung continues to over-expand, it can rupture and then
collapses the lung. Usually this stress results from normal labor contractions, but sometimes
it's due to other causes, such as infection and poor blood or low oxygen flow to the fetus.
Although it is generally sterile in nature Meconium aspirated into the lungs also causes
inflammation of the lungs (pneumonitis) and increases the risk of lung infection.
2 https://www.msdmanuals.com/en-in/home/children-s-health-issues/lung-and-breathing-problems-
in-newborns/meconium-aspiration-syndrome

Clinical signs and symptoms

Each baby may experience symptoms of meconium aspiration differently, but the following
are the most common signs:
 Rapid or labored breathing
 Retractions of the chest wall
 Grunting sounds with breathing
 Bluish skin color, called cyanosis
 Low apgar score, a rating of a baby's color, heartbeat, reflexes, muscle tone and respiration
just after birth
 Limp body

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Pathophysiology
The pathophysiology of meconium aspiration and MAS is complex, and the timing of the
initial insult resulting in MAS remains controversial. Intrauterine fetal gasping, mechanical
airway obstruction, pneumonitis, surfactant inactivation, and damage of umbilical vessels all
play roles in the pathophysiology of meconium aspiration. This all can promote towards this
syndrome.

Fetal Gasping
The meconium aspiration occurs immediately after birth.When the newborn exposed to
meconium begins respiration outside the womb, aspirated particulate or thick meconium can
be carried rapidly by the first breaths to the distal airways.

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. 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, increased lung
resistance,decreased lungcompliance,acute hypoxemia, hypercapnia,atelectasis and respiratoy
acidosis.ventilation-perfusion mismatches develop from total obstruction of the small
airways. Adjacent areas often are partially obstructed and overexpanded, leading to
pneumothorax and pneumomediastinum . Pulmonary air leaks are ten times more likely to
develop in infants with meconium aspiration than those without, and leaks often develop
during resuscitation .

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Pneumonitis
Pneumonitis is a usual feature of MAS, occurring in about one half of the cases. An intense
inflammatory response in the bronchi and alveoli can occur within hours of aspiration of
meconium. The airways and lung parenchyma become infiltrated with large numbers of
polymorphonuclear leukocytes and macrophages, which produce local injury by release of
inflammatory mediators and reactive oxygen species. Depending upon the degree of hypoxia,
hyaline membranes, pulmonary hemorrhage, and vascular necrosis can occur.
Antiinflammatory treatments, such as systemic steroids, can become important in the
prevention of serious lung injury in cases of meconium aspiration.

Umbilical Vessel Damage .

The effect of meconium on the various fetal tissues differs greatly. Meconium exposure to
tile placental membranes and chorionic plate results in only slight inflammation.
Inflammation and focal injury of the umbilical vessels, however, may be quite severe.
Meconium-induced cord vessel wall injury adversely affects vessel function by inducing
spasm and necrosis, with potential fetal hypoperfusion.

Complement activation
A recent hypothesis suggests that meconium activates the two main recognition systems of
innate immunity, toll-like receptors and complement system, leading not only to lung
dysfunction but also to a systemic inflammatory response. Despite an increasing focus on
lung inflammation in MAS, the cellular mechanisms initiating this inflammatory cascade
remain to be clarified.

Surfactant inhibition
Proteins and fatty acids in aspirated meconium can interfere with surfactant function.
Meconium aspiration syndrome in humans is mediated, in part, by inactivation of endogenous
surfactant. Atelectasis, decreased lung compliance, intrapulmonary shunting, and
hypoventilation are aggravated by inhibition of surfactant function. Though it greatly depends
on the thickness of the meconium. The extent of surfactant inhibition depends on both the
concentration of surfactant and meconium. If the surfactant concentration is low, even very
highly diluted meconium can inhibit surfactant function whereas, in high surfactant
concentrations, the effects of meconium are limited. Meconium may impact surfactant
mechanisms by preventing surfactant from spreading over the alveolar surface, decreasing the
concentration of surfactant proteins, and by changing the viscosity and structure of surfactant.

Persistent Pulmonary Hypertension

Newborn PPHN is common in neonates with fatal MAS. Indeed, a majority of cases of
PPHN are associated with MAS and this condition could be the final common pathway for
the severe morbidity and mortality seen in infants with MAS. acute pulmonary arterial
vasoconstriction play a vital role in the pathophysiology of PPHN. Chronic hypoxia caused
by other factors can also lead to PPHN through tile development of abnormal pulmonary
arterial muscularization, hypoxemia, and acidosis can lead to further pulmonary
hypertension that may be difficult or impossible to successfully treat.

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3 https://www.jabfm.org/content/jabfp/12/6/450.full.pdf

Management

Treatment according to the consistency of the meconium

A. Thin Meconium -

1. The infant's oro- and nasopharynx should be suctioned by the obstetrician prior to delivery
.

2. In a clinically well-appearing newborn, visualization of the larynx and intubation should

not be necessary.

3. In a depressed newborn, intubate and suction first, then proceed with the resuscitation.

B. Thick Meconium -

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1. The infant's oro- and nasopharynx should be suctioned by the obstetrician prior to delivery
.

2. Following suctioning of the oro- and nasopharynx by the obstetrician, the infant's oro- and
nasopharynx should be immediately suctioned by the pediatrician followed by endotracheal
intubation and suctioning of any meconium that is present below the cords. In a clinically
well-appearing, vigorously crying newborn without meconium at the level of the vocal cords,
intubation may not be necessary.

3. Visualize the cords via direct laryngoscopy and remove as much of the meconium from
below the cords as possible. Do not apply suction to the tube by your mouth. Use an adapter
connecting the endotracheal tube directly to wall suction, with the pressure set at 40 to 60
TORR. Repeat the intubation as often as necessary to clear the lower airway of meconium,
even if the infant has cried.

4. Following suctioning, ventilate the infant as necessary.

5. Keep the infant warm and dry to prevent hypothermia and shunting. Continue to monitor
(the infant's heart and respiratory rates.

6. After the infant has been stable for a least five minutes, the stomach can be aspirated to
remove as much of the meconium-stained fluid as possible.

7. If warranted by the clinical history (fetal distress, depressed infant, etc.), intubation should
be performed even if meconium is not seen on the cords.

Treatment in the paediatric/ neonatal ICU

A. The infant should be monitored and observed carefully for signs of respiratory distress,
i.e., cyanosis, tachypnea, retractions, and grunting.

B. Arterial blood gases and pH should be monitored for evidence of either metabolic or
respiratory acidosis.

C. Obtain a chest x-ray to rule out air leak (pneumothorax, pneumomediastinum, or

pneumopericardium), secondary to air trapping from ball-valve obstruction.

D. An infant with a history of meconium aspiration who develops respiratory distressshould

be placed in a hood to maintain O2 saturations greater or equal to 99% to prevent episodes of
hypoxia and shunting.

E. Postural drainage should be done as clinically indicated.

F. Consider intubation and suctioning below the cords in the nursery, since meconium can be
removed from the upper airways even after the infant has initiated spontaneous respirations.

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G. If the infant experiences persistent respiratory distress after one-half hour of life,
antibiotics should be started after first obtaining blood, tracheal aspirate, and CSF cultures.
Urine, for Group B Strep Latex, should also be obtained, but antibiotics should not be
withheld while waiting for urine.

Management

General management
All infants should be monitored using noninvasive monitors and blood gas sampling through
an indwelling central arterial catheter. Minimal handling, maintaining a noise-free
environment, sedation, and analgesia (using opioids) are used frequently to prevent pain-and
stress-induced hypoxia and right-to-left shunting in ventilated patients with MAS. Other
effective steps in management include maintenance of normothermia, correction of metabolic
abnormalities (hypoglycemia, hypocalcemia, acidosis, and polycythemia), and maintenance
of systemic blood pressure greater than pulmonary blood pressure by volume expansion,
transfusion or vasopressors.

Nasogastric aspiration
Prophylactic nasogastric lavage before first feed has been advocated to prevent feed
intolerance and secondary MAS due to postnatal aspiration of gastric contents.

Respiratory support
The requirement of respiratory support varies according to the severity of MAS, with a
majority of neonates responding to only supplemental oxygen administration by hood or
nasal prongs. The target oxygen saturation is maintained between 90% and 95%, given the
high incidence of right-to-left shunting. About 10% of those with severe MAS are treated by
CPAP alone, delivered by binasal or single nasal prongs at a pressure of 5–8 cm
H2O.8 However, tolerance to CPAP device is often limited due to the relative maturity of
infants and chances of resulting agitation worsening pulmonary hypertension, thereby
becoming an indication of intubation.29
Approximately 40% of neonates with MAS require intubation and mechanical ventilation.
The indications for intubation include high oxygen requirement (fraction of inspired oxygen
[FiO2] >0.8), respiratory acidosis (arterial pH persistently <7.25), pulmonary hypertension,
and circulatory compromise. the optimal ventilatory management remains controversial with
very few clinical trials upon which to base definite recommendations. This ensues because of
complex pathophysiology involving areas of atelectasis coexisting with hyperinflation along
with ventilation perfusion mismatch and airway compromise. The goal for assisted

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ventilation is to achieve optimal gas exchange with minimal lung barotrauma. Though trials
regarding the appropriate mode of ventilation are lacking, synchronized intermittent
mandatory ventilation is the most commonly used mode in conventional ventilation.
Ventilator settings and target blood gas depend upon the presence or absence of PPHN and
predominant lung abnormality. In cases with marked regional or global atelectasis, high-peak
inspiratory pressure (PIP) (up to maximum 30 cm) and high positive-end expiratory pressure
(PEEP) (4–7 cm) with longer inspiratory time helps in the recruitment of alveoli. If there is
obvious gas trapping, PEEP should be decreased (3–4 cm) with optimal expiratory time (0.5–
0.7) and rapid ventilator rates.54 In infants with associated PPHN, higher rates (50–70) with
higher FiO2 (80%–100%) should be considered to maintain PaO2 between 70 and 100 mm Hg
and PaCO2 between 35 and 45 mm Hg along with volume expansion, vasopressors, and other
supportive measures.Hyperventilation-induced alkalosis should be avoided due to risk of
cerebral vasoconstriction-induced neurologic injury and sensorineural hearing loss. In such
situations, other modalities like inhaled nitric oxide and high-frequency ventilation should be
considered early.

High-frequency ventilation
Despite a dearth of trial-based evidence, high-frequency ventilation (HFV) has been found
beneficial in treating patients with severe MAS failing conventional ventilation. It provides
effective gas exchange at low tidal volume, thus decreasing barotrauma and air leaks. High
frequency oscillatory ventilation is the more commonly used mode, especially in those with
significant atelectasis, where application of higher mean airway pressures (around 25 cm)
with recruitment maneuvers at moderate frequency (6–8 Hz) has been found to be
beneficial.54 It also lends a clinical advantage in MAS with associated severe PPHN, as the
response to inhaled NO is better with HFOV than conventional ventilation, High frequency
jet ventilation has also been found to be beneficial in optimizing oxygenation and prevention
of ECMO in severe MAS especially with an underlying combination of atelectasis and gas
trapping.Hence, high-frequency ventilation should be considered over conventional
pneumothorax in settings of severe MAS with intractable hypoxemia, persistent respiratory
acidosis, or high risk of pneumothorax.

Surfactant therapy
The detrimental effect of meconium on surfactant production and function has been well
known and forms the basis of the use of exogenous surfactant in severe MAS. Surfactant can

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be given either as a bolus or in the form of bronchoalveolar lavage. bolus surfactant therapy
is currently used in 30%–50% of ventilated infants with MAS. Clinical trials of surfactant
lung lavage have suggested that lavage therapy may improve oxygenation and shorten the
duration of ventilation.

Corticosteroids
Pulmonary and systemic inflammation is a key feature of MAS pathophysiology providing
the rationale behind the use of steroids in cases of severe MAS to improve pulmonary
function. inhaled budesonide has shown a promising response when instilled intratracheally
alone or with surfactant, thus providing a promising future therapy.More evidence-based
studies to evaluate the potential benefits and harms of steroid therapy in MAS are the need of
the hour.

Antibiotics
The association between meconium and sepsis has been evaluated extensively, but the role of
antibiotics in the routine management of MAS still remains controversial.

Inhaled nitric oxide (iNO)

Being a selective pulmonary vasodilator, it is an ideal treatment for moderate to severe PPHN
persisting despite ventilatory maneuvers. In severe PPHN improvement in oxygenation
occurs with the use of HFV with iNO owing to decreased pulmonary shunting and increased
delivery of iNO to its site of action. A significant proportion of neonates with PPHN do not
respond to iNO. Moreover, the high cost of therapy preludes its routine use in developing
countries. Other pulmonary vasodilators like phosphodiesterase 5 inhibitors (sildenafil,
dipyridamole, and zaprinast) have been tried in newborns, but the number treated is few.

Extracorporeal membrane oxygenation (ECMO)

MAS has been the leading diagnosis of neonates being referred for this therapy, with the
usual indication being intractable hypoxemia (persistent oxygenation index >40) despite
optimal ventilation.With the advent of newer therapies, the number of infants requiring
ECMO has reduced drastically, but survival in MAS cases remains high (up to 95%).

4 https://www.dovepress.com/meconium-aspiration-syndrome-challenges-and-solutions-peer-
reviewed-fulltext-article-RRN

By : Subhadeep Pal (Bsc . medical technology RT)