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Meconium Aspiration Syndrome
(MAS)
Mohd. Arif Khan
2nd year PG Student
Department Of Pediatrics
Definition
Meconium aspiration syndrome (MAS)
 Respiratory distress in an infant born through
meconium stained amniotic fluid(MSAF) with
characteristic radiological changes & whose
symptoms cannot be otherwise explained.
 Presence of meconium below vocal cord (Avery 6th ed)
Epidemiology
• MSAF observed in approx. 8 to 25% of all live births.
• MAS occurs in approx. 5-35% of newborns delivered
through MSAF
• 50% of them require mechanical ventilation.
• Incidence of MSAF is more in Term or Post-term
newborn.
• Rare before 38 weeks of gestation
Risk factors for MAS
• Pre-eclampsia /eclampsia
• Oligohydramnios
• Maternal Hypertension
• Maternal Diabetes
• Maternal chronic respiratory or Cardio vascular
disease
• Post term pregnancy
• IUGR
• Abnormal fetal HR pattern
Components of meconium
• Meconium is a sterile, viscous, dark green,
odorless material starts accumulating in fetal
intestine in 3rd month of gestation.
• Components of meconium are :
- 72% to 80% water
- desquamated cells from the intestine and
epithelial cell
- Lanugo hair
- Fatty material from vernix caseosa
- Amniotic fluid
- Bile & drug metabolites
• Meconium passage in utero is uncommon before
38 wks of gestational age due to:
- lack of strong peristalsis (low motilin level)
- tonic contraction of anal sphincter
- a cap of viscous meconium in the rectum
• It occurs > 30% beyond 42 wks due to:
- Post term fetal maturation (high motilin level)
- Vagal stimulation by cord or head compression
in absence of fetal distress.
Physiology of MSAF
Pathogenesis of MSAF
 Intestinal ischemia
• Hyperperistalsis
• Relaxation of anal sphincter
 In utero stress (hypoxia or acidosis) producing
relaxation of anal sphincter.
 Perinatal asphyxia
• Intestinal ischemia (diving reflex)
• Acidosis
• Gasping respiration
Pathophysiology
MAS leads to hypoxia / respiratory distress
Mechanism
1. Acute airway obstruction.
2. Surfactant dysfunction or inactivation.
3. Chemical pneumonitis with release of vasoconstrictive
and proinflammatory mediators.
4. PPHN with right-to-left extrapulmonary shunting.
 Aspiration of meconium: During fetal distress,
gasping by fetus results in aspiration of meconium
before or during delivery.
 Mechanical obstruction of airways:
• Thick and viscous meconium complete or
partial airway obstruction.
• Complete obstruction atelectasis.
• Partial Obstruction ball valve effect air trapping
air leak syndromes such as pneumothorax &
pneumomediastinum.
• Chemical pneumonitis: Meconium a source of
proinflammatory mediators (such as interleukins 1,6 &
8, tumor necrosis factors) induces inflammation
directly or indirectly through stimulation of oxidative
bursts in neutrophils & alveolar macrophages that
injure lung parenchyma vascular leakage toxic
pneumonitis & hemorrhagic pulmonary edema.
• Surfactant inactivation:
• Bilirubin,
• fatty acid,
• triglycerides,
• cholesterol content of meconium leads to endogenous
surfactant inactivation.
• Persistent Pulmonary hypertension
(PPHN)
• in infants with MAS caused by
– Pulmonary vasoconstriction secondary to
• hypoxia, hypercarbia & acidosis
• pulmonary inflammation.
– Hypertrophy of the postacinar capillaries as a
result of chronic intrauterine hypoxia
CLINICAL FEATURES
Physical examination:
• Evidence of postmaturity +/-
• Meconium-stained vernix, hairs, umbilical cord &
nails.
• Nails generally become stained after 6 hours and
vernix after 12 to 14 hours of exposure .
Meconium stained umbilical cord
CLINICAL FEATURES
Physical examination:
• Some patients are asymptomatic at birth
• Some develop worsening signs of respiratory distress
– meconium moves from the large airways into the lower
tracheobronchial tree.
• Signs of respiratory distress like
– Tachypnea and cyanosis
– Subcostal & intercostal retractions
– Grunting and nasal flaring.
• Chest typically appears barrel-shaped.
• Auscultation reveals rales and rhonchi immediately
after birth.
Cleary and Wiswell (severity criteria):
1. Mild MAS that requires >40% oxygen for <48 hours
2. Moderate MAS that requires >40% oxygen for >48
hours with no air leak.
3. Severe MAS that requires assisted ventilation for >48
hours and often associated with PPHN.
Differential Diagnosis
• Perinatal Asphyxia
• Bacterial Pneumonia
• Respiratory Distress Syndrome
• Transient Tachypnea Of Newborn
• Congenital Heart Disease
Diagnosis
• Monitor infants born through MSAF for any signs of
respiratory distress for at least 24 hours.
• Diagnosis of MAS based on the presence of
respiratory distress in an infant born through MSAF
with no alternate cause for respiratory distress.
Diagnosis
• Investigations:
-Chest X-ray AP view
- Complete Hemogram
- ABG
- CRP
- Blood culture
- Serum calcium
- Random blood sugar
- Echocardiography
Diagnosis
• Classic chest x-ray findings in MAS-
– Hyperinflation of the lung field
– Widespread consolidations
– Coarse irregular patchy infiltrates
– Flattening of diaphragms
– Pneumothorax & pneumomediastinum may be present
• Severity of chest radiographic abnormality does not
correlate with severity of clinical features
•Chest X-ray showing bilateral coarse irregular patchy
infiltrate with emphysema.
Chest X-ray showing areas of opacification due to
atelectasis bilaterally.
Diagnosis
• ABG 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.
• Echocardiography for evaluation of persistent
pulmonary hypertension (PPHN).
Management
1. Management consists of-
1. Prevention of MAS –
1. Aggressive management of abnormal fetal heart rate(FHS)
monitoring .
2. Reduction in post term delivery decreases the incidence of MAS.
2. Treatment of MAS –
1. Management is primarily supportive.
2. Maintenance of
1. Optimal thermal environment
2. Minimal handling
3. Adequate oxygenation
4. Optimal blood pressure
5. Correction of acidosis, hypoglycemia & other
metabolic disorders is the mainstay of treatment.
Prevention of MAS
• Antenatal management:
• Identification of high risk pregnancies & close monitoring.
• Pregnancy that continue past due date, induction as early as 41
wks prevents MAS.
• Corrective measures should be taken for fetal distress or infant
should be delivered in timely manner.
• Intrapartum Fetal Monitoring:
•Fetal scalp pH determination & fetal pulse oximetry
improve decision making in timing of delivery.
• Amnioinfusion:
•Amnioinfusion helps in diluting meconium & reduces its
mechanical and inflammatory effects.
•It also helps by cushioning umbilical cord that prevents
recurrent umbilical compressions that causes fetal
distress.
• Data regarding efficacy has not supported widespread use
•Postpartum Endotracheal Suctioning:
•Previous NRP recommended intubation & direct
endotracheal suction soon after delivery for non-vigorous
newborn and Routine care in vigorous newborn.
•Postpartum Endotracheal Suctioning:
•NRP (2015)
•resuscitation should follow the same principles for infants
with meconium-stained fluid as for those with clear fluid;
•if poor muscle tone and inadequate breathing effort are
present, the initial steps of resuscitation should be
completed under an overbed warmer.
•PPV should be initiated if the infant is not breathing or the
heart rate is less than 100/min
•Postpartum Endotracheal Suctioning:
•Greater value on harm avoidance (i.e. delays in providing
bag & mask ventilation, potential harm of the procedure)
over the unknown benefit of the intervention of routine
tracheal intubation and suctioning.
•Appropriate intervention to support ventilation and
oxygenation as indicated
•This may include intubation and suction if the airway is
obstructed
Treatment of MAS
• Care of the MAS newborn:
• Infant should be maintained in neutral thermal environment
with minimum handling.
• Assess for hypoglycemia, hypocalcemia and metabolic
acidosis and should be corrected.
• Fluids should be restricted to prevent cerebral and
pulmonary edema.
• Infants may require inotropes for poor cardiac output and
hypotension.
• Maintain hemoglobin concentration above 15 gm/dl (PCV
above 40%) in infants with substantial oxygen and on
mechanical ventilator.
•Adjunctive Therapies:
•Infants with MAS should be monitored using
noninvasive monitors
•pulse oximeter, transcutaneous O2 & CO2 methods.
•Sedation and analgesia
•to alleviate pain and discomfort that may lead to hypoxia
and right-to-left shunting.
•Morphine or fentanyl
•To optimize gas exchange
•avoid asynchrony, reflex catecholamine release, and
aggravation of pulmonary vascular resistance.
• Assisted Ventilation: Ventilation should be aimed at
increasing oxygenation while minimizing the barotrauma that
lead to air leak syndromes.
• Amount of ventilator support depends on severity of
respiratory distress.
• Some newborn needs Oxygen by hood only.
• CPAP-
– CPAP use is contentious in MAS as they have hyperinflated lung field,
CPAP further aggravate it.
– It is rarely indicated in infants with predominantly collapse or
atelectasis.
•Mechanical ventilation:
Conventional Ventilation
•Required in 30-50 % babies with severe MAS
• Indications of mechanical ventilation -
• Excessive CO2 retention (PaCO2 >60 mm hg).
• Persistent hypoxemia (PaO2 <50 mm hg).
• Metabolic acidosis (pH > 7.25) with FiO2 > 60%.
Conventional Ventilation-
• Strategy includes
•Low PEEP (4-5 cm of H2O)
•High resistance high with normal compliance
•Slow rate, moderate pressure
•Pneumonitis prominent
•Rate high with short inspiratory time
•Patient triggered mode preferred
•Adequate sedation and/or muscle relaxant
•High frequency ventilation
•Indications are-
•Conventional ventilation failure
•Air leak syndrome
•May slow the progression of meconium down the airway
•Includes
•High frequency jet ventilation
•High frequency oscillatory ventilation(HFO)
•HFO ventilation has been studied & strategy includes
•MAP 8-9 mm Hg
•Frequency 8-10 Hz
•FiO2 as per oxygen levels(40 – 100%)
• Surfactant therapy in MAS shows promising results
with decrease in number of infants requiring
extracorporeal membrane oxygenation (ECMO) &
reduction of pneumothorax.
• Usually require multiple doses at an interval of 6
hours
• Usually improvement is observed after 2nd / 3rd dose
• Optimum strategy not yet been defined
•Role of Antibiotics- The presence of meconium increases
the chances of positive cultures from amniotic fluid
in preterm and term infants. If antibiotics started for
suspected infection due to perinatal risk factors
consider discontinuing antibiotics once blood culture
results are negative.
Inhaled Nitric oxide (iNO)
– Selective pulmonary vasodilator.
– Activate guanylate cyclase and increases cyclic GMP and
acting directly on the vascular smooth muscle.
– Decreased need for ECMO but no difference in mortality.
– Pretreatment with surfactant improves in delivery of iNO
to the alveoli.
ECMO
• 40% of infants with MAS treated with inhaled NO fail
to respond and require ECMO.
• 35% of ECMO patients are with MAS.
• Survival rate after ECMO 93-100%.
Progonosis
• Mortality reduced to <5% with new modalities of
therapy such as administration of surfactant, HFV,
iNO & ECMO.
• Chronic lung disease may result from prolong
mechanical ventilation.
• Those with significant asphyxial insult may
demonstrate neurological sequelae.
THANK YOU

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Mas ppt arif

  • 1. Meconium Aspiration Syndrome (MAS) Mohd. Arif Khan 2nd year PG Student Department Of Pediatrics
  • 2. Definition Meconium aspiration syndrome (MAS)  Respiratory distress in an infant born through meconium stained amniotic fluid(MSAF) with characteristic radiological changes & whose symptoms cannot be otherwise explained.  Presence of meconium below vocal cord (Avery 6th ed)
  • 3. Epidemiology • MSAF observed in approx. 8 to 25% of all live births. • MAS occurs in approx. 5-35% of newborns delivered through MSAF • 50% of them require mechanical ventilation. • Incidence of MSAF is more in Term or Post-term newborn. • Rare before 38 weeks of gestation
  • 4. Risk factors for MAS • Pre-eclampsia /eclampsia • Oligohydramnios • Maternal Hypertension • Maternal Diabetes • Maternal chronic respiratory or Cardio vascular disease • Post term pregnancy • IUGR • Abnormal fetal HR pattern
  • 5. Components of meconium • Meconium is a sterile, viscous, dark green, odorless material starts accumulating in fetal intestine in 3rd month of gestation. • Components of meconium are : - 72% to 80% water - desquamated cells from the intestine and epithelial cell - Lanugo hair - Fatty material from vernix caseosa - Amniotic fluid - Bile & drug metabolites
  • 6. • Meconium passage in utero is uncommon before 38 wks of gestational age due to: - lack of strong peristalsis (low motilin level) - tonic contraction of anal sphincter - a cap of viscous meconium in the rectum • It occurs > 30% beyond 42 wks due to: - Post term fetal maturation (high motilin level) - Vagal stimulation by cord or head compression in absence of fetal distress. Physiology of MSAF
  • 7. Pathogenesis of MSAF  Intestinal ischemia • Hyperperistalsis • Relaxation of anal sphincter  In utero stress (hypoxia or acidosis) producing relaxation of anal sphincter.  Perinatal asphyxia • Intestinal ischemia (diving reflex) • Acidosis • Gasping respiration
  • 8. Pathophysiology MAS leads to hypoxia / respiratory distress Mechanism 1. Acute airway obstruction. 2. Surfactant dysfunction or inactivation. 3. Chemical pneumonitis with release of vasoconstrictive and proinflammatory mediators. 4. PPHN with right-to-left extrapulmonary shunting.
  • 9.  Aspiration of meconium: During fetal distress, gasping by fetus results in aspiration of meconium before or during delivery.  Mechanical obstruction of airways: • Thick and viscous meconium complete or partial airway obstruction. • Complete obstruction atelectasis. • Partial Obstruction ball valve effect air trapping air leak syndromes such as pneumothorax & pneumomediastinum.
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  • 11. • Chemical pneumonitis: Meconium a source of proinflammatory mediators (such as interleukins 1,6 & 8, tumor necrosis factors) induces inflammation directly or indirectly through stimulation of oxidative bursts in neutrophils & alveolar macrophages that injure lung parenchyma vascular leakage toxic pneumonitis & hemorrhagic pulmonary edema.
  • 12. • Surfactant inactivation: • Bilirubin, • fatty acid, • triglycerides, • cholesterol content of meconium leads to endogenous surfactant inactivation.
  • 13. • Persistent Pulmonary hypertension (PPHN) • in infants with MAS caused by – Pulmonary vasoconstriction secondary to • hypoxia, hypercarbia & acidosis • pulmonary inflammation. – Hypertrophy of the postacinar capillaries as a result of chronic intrauterine hypoxia
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  • 15. CLINICAL FEATURES Physical examination: • Evidence of postmaturity +/- • Meconium-stained vernix, hairs, umbilical cord & nails. • Nails generally become stained after 6 hours and vernix after 12 to 14 hours of exposure .
  • 17. CLINICAL FEATURES Physical examination: • Some patients are asymptomatic at birth • Some develop worsening signs of respiratory distress – meconium moves from the large airways into the lower tracheobronchial tree.
  • 18. • Signs of respiratory distress like – Tachypnea and cyanosis – Subcostal & intercostal retractions – Grunting and nasal flaring. • Chest typically appears barrel-shaped. • Auscultation reveals rales and rhonchi immediately after birth.
  • 19. Cleary and Wiswell (severity criteria): 1. Mild MAS that requires >40% oxygen for <48 hours 2. Moderate MAS that requires >40% oxygen for >48 hours with no air leak. 3. Severe MAS that requires assisted ventilation for >48 hours and often associated with PPHN.
  • 20. Differential Diagnosis • Perinatal Asphyxia • Bacterial Pneumonia • Respiratory Distress Syndrome • Transient Tachypnea Of Newborn • Congenital Heart Disease
  • 21. Diagnosis • Monitor infants born through MSAF for any signs of respiratory distress for at least 24 hours. • Diagnosis of MAS based on the presence of respiratory distress in an infant born through MSAF with no alternate cause for respiratory distress.
  • 22. Diagnosis • Investigations: -Chest X-ray AP view - Complete Hemogram - ABG - CRP - Blood culture - Serum calcium - Random blood sugar - Echocardiography
  • 23. Diagnosis • Classic chest x-ray findings in MAS- – Hyperinflation of the lung field – Widespread consolidations – Coarse irregular patchy infiltrates – Flattening of diaphragms – Pneumothorax & pneumomediastinum may be present • Severity of chest radiographic abnormality does not correlate with severity of clinical features
  • 24. •Chest X-ray showing bilateral coarse irregular patchy infiltrate with emphysema.
  • 25. Chest X-ray showing areas of opacification due to atelectasis bilaterally.
  • 26. Diagnosis • ABG 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. • Echocardiography for evaluation of persistent pulmonary hypertension (PPHN).
  • 27. Management 1. Management consists of- 1. Prevention of MAS – 1. Aggressive management of abnormal fetal heart rate(FHS) monitoring . 2. Reduction in post term delivery decreases the incidence of MAS. 2. Treatment of MAS – 1. Management is primarily supportive. 2. Maintenance of 1. Optimal thermal environment 2. Minimal handling 3. Adequate oxygenation 4. Optimal blood pressure 5. Correction of acidosis, hypoglycemia & other metabolic disorders is the mainstay of treatment.
  • 28. Prevention of MAS • Antenatal management: • Identification of high risk pregnancies & close monitoring. • Pregnancy that continue past due date, induction as early as 41 wks prevents MAS. • Corrective measures should be taken for fetal distress or infant should be delivered in timely manner.
  • 29. • Intrapartum Fetal Monitoring: •Fetal scalp pH determination & fetal pulse oximetry improve decision making in timing of delivery. • Amnioinfusion: •Amnioinfusion helps in diluting meconium & reduces its mechanical and inflammatory effects. •It also helps by cushioning umbilical cord that prevents recurrent umbilical compressions that causes fetal distress. • Data regarding efficacy has not supported widespread use
  • 30. •Postpartum Endotracheal Suctioning: •Previous NRP recommended intubation & direct endotracheal suction soon after delivery for non-vigorous newborn and Routine care in vigorous newborn.
  • 31. •Postpartum Endotracheal Suctioning: •NRP (2015) •resuscitation should follow the same principles for infants with meconium-stained fluid as for those with clear fluid; •if poor muscle tone and inadequate breathing effort are present, the initial steps of resuscitation should be completed under an overbed warmer. •PPV should be initiated if the infant is not breathing or the heart rate is less than 100/min
  • 32. •Postpartum Endotracheal Suctioning: •Greater value on harm avoidance (i.e. delays in providing bag & mask ventilation, potential harm of the procedure) over the unknown benefit of the intervention of routine tracheal intubation and suctioning. •Appropriate intervention to support ventilation and oxygenation as indicated •This may include intubation and suction if the airway is obstructed
  • 33. Treatment of MAS • Care of the MAS newborn: • Infant should be maintained in neutral thermal environment with minimum handling. • Assess for hypoglycemia, hypocalcemia and metabolic acidosis and should be corrected. • Fluids should be restricted to prevent cerebral and pulmonary edema. • Infants may require inotropes for poor cardiac output and hypotension. • Maintain hemoglobin concentration above 15 gm/dl (PCV above 40%) in infants with substantial oxygen and on mechanical ventilator.
  • 34. •Adjunctive Therapies: •Infants with MAS should be monitored using noninvasive monitors •pulse oximeter, transcutaneous O2 & CO2 methods. •Sedation and analgesia •to alleviate pain and discomfort that may lead to hypoxia and right-to-left shunting. •Morphine or fentanyl •To optimize gas exchange •avoid asynchrony, reflex catecholamine release, and aggravation of pulmonary vascular resistance.
  • 35. • Assisted Ventilation: Ventilation should be aimed at increasing oxygenation while minimizing the barotrauma that lead to air leak syndromes. • Amount of ventilator support depends on severity of respiratory distress. • Some newborn needs Oxygen by hood only. • CPAP- – CPAP use is contentious in MAS as they have hyperinflated lung field, CPAP further aggravate it. – It is rarely indicated in infants with predominantly collapse or atelectasis.
  • 36. •Mechanical ventilation: Conventional Ventilation •Required in 30-50 % babies with severe MAS • Indications of mechanical ventilation - • Excessive CO2 retention (PaCO2 >60 mm hg). • Persistent hypoxemia (PaO2 <50 mm hg). • Metabolic acidosis (pH > 7.25) with FiO2 > 60%.
  • 37. Conventional Ventilation- • Strategy includes •Low PEEP (4-5 cm of H2O) •High resistance high with normal compliance •Slow rate, moderate pressure •Pneumonitis prominent •Rate high with short inspiratory time •Patient triggered mode preferred •Adequate sedation and/or muscle relaxant
  • 38. •High frequency ventilation •Indications are- •Conventional ventilation failure •Air leak syndrome •May slow the progression of meconium down the airway •Includes •High frequency jet ventilation •High frequency oscillatory ventilation(HFO) •HFO ventilation has been studied & strategy includes •MAP 8-9 mm Hg •Frequency 8-10 Hz •FiO2 as per oxygen levels(40 – 100%)
  • 39. • Surfactant therapy in MAS shows promising results with decrease in number of infants requiring extracorporeal membrane oxygenation (ECMO) & reduction of pneumothorax. • Usually require multiple doses at an interval of 6 hours • Usually improvement is observed after 2nd / 3rd dose • Optimum strategy not yet been defined
  • 40. •Role of Antibiotics- The presence of meconium increases the chances of positive cultures from amniotic fluid in preterm and term infants. If antibiotics started for suspected infection due to perinatal risk factors consider discontinuing antibiotics once blood culture results are negative.
  • 41. Inhaled Nitric oxide (iNO) – Selective pulmonary vasodilator. – Activate guanylate cyclase and increases cyclic GMP and acting directly on the vascular smooth muscle. – Decreased need for ECMO but no difference in mortality. – Pretreatment with surfactant improves in delivery of iNO to the alveoli.
  • 42. ECMO • 40% of infants with MAS treated with inhaled NO fail to respond and require ECMO. • 35% of ECMO patients are with MAS. • Survival rate after ECMO 93-100%.
  • 43. Progonosis • Mortality reduced to <5% with new modalities of therapy such as administration of surfactant, HFV, iNO & ECMO. • Chronic lung disease may result from prolong mechanical ventilation. • Those with significant asphyxial insult may demonstrate neurological sequelae.