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*WELCOME
TO
SEMINAR
PRESENTED BY-
DR. SYED KAMRUL HASAN
IMO, DEPARTMENT OF NICU
SWMCH, SYLHET
*Meconium Aspiration
Syndrome (MAS)
*
*Aspiration of meconium
contaminated aminotic fluid by a
fetus, or a term or post term
newborn during birth is termed as
meconium aspiration.
*The typical clinical manifestations
produced by the meconium
aspiration pneumonia is termed as
meconium aspiration syndrome.
*
*Meconium Stain Amniotic Fluid observed in
(8-20)% of all births.
*The incidence of MSAF increase from 1.6% at
34-37 weeks to 30% at > 42 weeks
*Meconium Aspiration Syndrome occurs in 5%
of newborns delivered through MSAF.
*MAS primarily affects Term or Post-term
Infants.
Composition of meconium :
Meconium is the first intestinal discharge of the
newborn infants. Which is greenish black in
colour & contains:
*Water (75%)
*Mucopolysaccharides
*Proteins
*Cholesterol, lipids
*Bile acids & salts
*Enzymes
*Vernix & squamous cells
*
*Fetal maturation : Usually term or post term
(high motilin level)
*Vagal stimulation by cord or head compression in
absence of fetal distress.
*In utero stress (hypoxia, acidosis) producing
relaxation of anal sphincter.
*
Maternal risk factor includes all which induce
fetal distress & hypoxia :
*Maternal Hypertension
*Maternal DM
*Maternal chronic respiratory or Cardiovascular
disease
*Maternal infection
*Maternal drug use
*Placental insufficiency
*Post term pregnancy
*Pre-eclampsia / eclampsia
*Oligohydramnios
*IUGR
*Abnormal fetal heart rate pattern
*
Fetal meconium passage depends on hormonal &
parasympathetic neural maturation. Fetal
distress & vagal stimulation are 2 probable
factors may stimulate intestinal peristalsis &
relaxation of the anal sphincter to causes
passage of meconium into the amniotic fluid
leads to MSAF. Gasping by the fetus or newborn
infants can cause aspiration of aminotic fluid
contaminated with meconium and causes the
following :
Mechanical obstruction of airways :
Thick and viscous meconium lead to Complete or
partial airway obstruction. With onset of
respiration meconium migrates from central to
peripheral airways.
Complete obstruction may leads to atelectasis
resulting in hypoxia & increase PVR.
Partial obstruction may result in a Ball-valve
phenomenon leading to air trapping & alveolar
hyperexpansion. Increase risk of pneumothorax
15 – 33%.
Chemical pneumonitis: with distal progressing of
meconium chemical pneumonitis develop resulting
bronchiolar edema and narrowing of the small
airways, all leading to increase hypercarbia &
hypoxemia.
Surfactant inactivation: Bilirubin, fattyacid,
triglycerides, cholesterol content of meconium due
to their higher surface tension, leads to surfactant
dysfunction by stripping surfactant from the
surface of the alveoli.
Pulmonary hypertension: meconium in lungs
stimulate release of pro inflammatory
cytokines and vasoactive substance which
cause pulmonary vasoconstriction. Also
hypoxia, acidosis, and hyperinflation
contribute to pulmonary hypertension.
The increase in pulmonary vescular resistant
may lead to atrial & ductal right to left
shunting.
*
*
History :
*Infants with MAS must have a history of MSAF.
*They often are Term or post-term
*Have a history of fetal distress
*Have a low APGAR score at birth
*Many are depressed at birth.
Physical examination :
*Infants with MAS often exhibit signs of
postmaturity : peeling skin, long fingernails,
abundant hair and decreased vernix.
*Affected patients typically have respiratory
distress with marked tachypnea and cyanosis.
*Use of accessory muscles of respiration are
evidenced by intercostal and subcostal
retractions and abdominal (paradoxical)
breathing, often with grunting and nasal flaring.
*The skin, umbilical cord, and nails may be
meconium-stained, depending upon how
long the infant has been exposed to
meconium & concentration of meconium.
• Umbilical cord begin to stain after 15
minute exposure to thick MSAF or 1 hour to
lightly stained fluid.
•Nails will become stained after 4-6 hours
•vernix after 12 to 14 hours of exposure .
*
*Significant perinatal asphyxia, poor
respiratory effort, decrease muscle tone.
*The chest typically appears barrel-shaped,
with an increased anterior-posterior diameter
caused by hyperinflation.
*Auscultation reveals fine crepitations with
rhonchi and reduced air entry 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.
*Most infants who develop symptoms will do so
in the first 12 hours of life.
*
*Perinatal Asphyxia
*Respiratory Distress Syndrome
*Transient Tachypnea Of Newborn
*Congenital Pneumonia
*Congenital Heart Disease
PNA RDS T TN /
Wet Lungs
CHD Congenital
Pneumonia
H/O delayed
crying after
birth or no cry
Pale
Gasping
respiration or
no respiration
Bradycardia
Hypotonia
Convulsion
Shock
Immediate
resuscitation &
Post
resuscitation
management
Respiratory
distress within
1 hr of life
Due to
deficiency of
surfactant
H/O preterm
delivery, IDM,
C/S
CXR : ground
glass
appearance, air
bronchogram,
complete white
out lungs.
Specific
treatment give
surfactant.
Mild self
limited
pulmonary
disorder
Due to
delayed
absorption of
fetal lung fluid
More in
cesarean
delivery
CXR :
Prominent
vascular
markings, fluid
in the interlobar
fissure, flat
diaphragm
Improve by 12-
24 hours
Respiratory
distress with
or without
cyanosis
Murmur on
auscultation
CXR :
Cardiomegaly
Echo. With
color doppler
is diagnostic
Mother has a
blood stream
infection
Mother may
be febrile or
have other sign
of infection
Crepitation
on
Auscultation
CXR :
Homogeneous
or patchy
opacity,
pneumatocele,
pleural effusion
Treat with
broad spectrum
antibiotic
*
*MAS must be considered in any infant born
through MSAF who develops symptoms of RD with
typical chest x ray findings
*A chest radiographs shows hyperinflation of the
lung field and flatten diaphragms.
*There are coarse irregular patchy infiltrates
*A pneumothorax and pneumomediastinum may
be present .
*
*
*
*Arterial blood gas measurements typically
show hypoxemia and hypercarbia.In mild cases
hyperventilation may result in respiratory
alkalosis. Infants with sever disease usually have
a respiratory acidosis due to airway obstruction,
atelectasis & pneumonitis.
* Echocardiography : Infants with pulmonary
hypertension and right-to-left atrial & ductal
shunt is frequently associated finding in infants
with MAS.
*
*Chemical Pneumonitis
*Emphysema
*Pneumothorax
*Persistent pulmonary hypertension
*Respiratory failure
*
*
Prevention :
Prevention of passage of meconium in utero :
*Identification of high risk pregnancies and close
monitoring. Pregnancy that continue past due
date, induction as early as 41 weeks may help
prevent meconium aspiration.
*If there is sign of fetal distress corrective
measure should be undertaken or infant should be
delivered in timely manner.
*Transcervical amnioinfusion with normal
saline solution in case of thick meconium &
oligohydramnios may reduce the incidence
of fetal distress & meconium aspiration.
Prevention of meconium aspiration :
Baby born through thick particulate mecomium:
• At delivery suction the oropharynx before
the shoulders are delivered.
• Intubation & suction under direct
laryngoscopy is mandatory before triggering
the first breath by drying & stimulating the
infant.
• Intubation & suction should be continued
until the meconium has been cleared.
Baby born through thin meconium:
suction of the mouth first who have effective
respiration at the time of delivery.
*
*Apparently well child born through MSAF,
most of them do not require any interventions
besides close monitoring for respiratory
distress.
*Some may be depressed at birth & require
resuscitation. Oxygen by mask should be
administered as soon as the trachea has been
cleared.
*Oropharyngeal suction should be provided to
assist pulmonary toileting.
*Broad spectrum antibiotic should be started if
a radiological infiltrate or documented
infection.
*Monitor temperature , blood gas level, fluid &
electrolyte balance.
*Hypoxia & acidosis may lead to persistent
pulmonary hypertension & should be treated
promptly.
*Mechanical ventilation may be required.
*Those who fail to improve conventional
treatment may benefit from surfactant
therapy, nitrous oxide or ECMO.
Approach to the ill newborns:
*Transfer to NICU.
*Monitor closely.
*Full range of respiratory support should be
given.
*
Goals:
*Increased oxygenation while minimizing the
barotrauma (may lead to air leak).
*Prevent pulmonary hypertension.
*Prevent secondary infection.
Ventilatory support depends on the amount of
respiratory distress:
*O2 hood
*Continuous positive airway pressure (CPAP)
*Mechanical ventilation :
High-frequency ventilation (HFV) should reduce
air leaks & may slow the progression of
meconium down the tracheobronchial tree and
allow more time for meconium removal.
*
*Surfactant therapy in MAS showed promising
results with decrease in the number of
infants requiring ECMO and Possible
reduction of pneumothorax.
*
*Selective pulmonary vasodilation.
*Activate guanylate cyclase and increases cyclic
GMP and acting directly on the vascular smooth
muscle.
*Use of iNO reduces the need for ECMO by 40%.
*Pretreatment with surfactant improves in
delivery of inhaled NO to the alveoli.
*
ECMO is a form of cardiopulmonary bypass that
augments systemic perfusion & provide gas
exchange. Most common venoarterial bypass,
which required carotid artery ligation &
placement of large catheter in the right
internal jugular vein & carotid artery.
ECMO works by removing blood from the person’s
body & artificially removing the CO2 &
oxygenating RBC.
*ECMO required complete heparinization to
prevent clotting in the circuit, so can’t be
use in patient with or at risk of IVH.
*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%.
*
*Infants of MAS who do not require ventilation
recover within 7- 10 days.
*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 asphyxia insult may
demonstrate neurologic sequele.
Meconum aspiration syndrome

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Meconum aspiration syndrome

  • 2. PRESENTED BY- DR. SYED KAMRUL HASAN IMO, DEPARTMENT OF NICU SWMCH, SYLHET *Meconium Aspiration Syndrome (MAS)
  • 3. * *Aspiration of meconium contaminated aminotic fluid by a fetus, or a term or post term newborn during birth is termed as meconium aspiration. *The typical clinical manifestations produced by the meconium aspiration pneumonia is termed as meconium aspiration syndrome.
  • 4. * *Meconium Stain Amniotic Fluid observed in (8-20)% of all births. *The incidence of MSAF increase from 1.6% at 34-37 weeks to 30% at > 42 weeks *Meconium Aspiration Syndrome occurs in 5% of newborns delivered through MSAF. *MAS primarily affects Term or Post-term Infants.
  • 5. Composition of meconium : Meconium is the first intestinal discharge of the newborn infants. Which is greenish black in colour & contains: *Water (75%) *Mucopolysaccharides *Proteins *Cholesterol, lipids *Bile acids & salts *Enzymes *Vernix & squamous cells
  • 6. * *Fetal maturation : Usually term or post term (high motilin level) *Vagal stimulation by cord or head compression in absence of fetal distress. *In utero stress (hypoxia, acidosis) producing relaxation of anal sphincter.
  • 7. * Maternal risk factor includes all which induce fetal distress & hypoxia : *Maternal Hypertension *Maternal DM *Maternal chronic respiratory or Cardiovascular disease *Maternal infection *Maternal drug use
  • 8. *Placental insufficiency *Post term pregnancy *Pre-eclampsia / eclampsia *Oligohydramnios *IUGR *Abnormal fetal heart rate pattern
  • 9. * Fetal meconium passage depends on hormonal & parasympathetic neural maturation. Fetal distress & vagal stimulation are 2 probable factors may stimulate intestinal peristalsis & relaxation of the anal sphincter to causes passage of meconium into the amniotic fluid leads to MSAF. Gasping by the fetus or newborn infants can cause aspiration of aminotic fluid contaminated with meconium and causes the following :
  • 10. Mechanical obstruction of airways : Thick and viscous meconium lead to Complete or partial airway obstruction. With onset of respiration meconium migrates from central to peripheral airways. Complete obstruction may leads to atelectasis resulting in hypoxia & increase PVR. Partial obstruction may result in a Ball-valve phenomenon leading to air trapping & alveolar hyperexpansion. Increase risk of pneumothorax 15 – 33%.
  • 11. Chemical pneumonitis: with distal progressing of meconium chemical pneumonitis develop resulting bronchiolar edema and narrowing of the small airways, all leading to increase hypercarbia & hypoxemia. Surfactant inactivation: Bilirubin, fattyacid, triglycerides, cholesterol content of meconium due to their higher surface tension, leads to surfactant dysfunction by stripping surfactant from the surface of the alveoli.
  • 12. Pulmonary hypertension: meconium in lungs stimulate release of pro inflammatory cytokines and vasoactive substance which cause pulmonary vasoconstriction. Also hypoxia, acidosis, and hyperinflation contribute to pulmonary hypertension. The increase in pulmonary vescular resistant may lead to atrial & ductal right to left shunting.
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  • 14. * History : *Infants with MAS must have a history of MSAF. *They often are Term or post-term *Have a history of fetal distress *Have a low APGAR score at birth *Many are depressed at birth.
  • 15. Physical examination : *Infants with MAS often exhibit signs of postmaturity : peeling skin, long fingernails, abundant hair and decreased vernix. *Affected patients typically have respiratory distress with marked tachypnea and cyanosis. *Use of accessory muscles of respiration are evidenced by intercostal and subcostal retractions and abdominal (paradoxical) breathing, often with grunting and nasal flaring.
  • 16. *The skin, umbilical cord, and nails may be meconium-stained, depending upon how long the infant has been exposed to meconium & concentration of meconium. • Umbilical cord begin to stain after 15 minute exposure to thick MSAF or 1 hour to lightly stained fluid. •Nails will become stained after 4-6 hours •vernix after 12 to 14 hours of exposure .
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  • 18. *Significant perinatal asphyxia, poor respiratory effort, decrease muscle tone. *The chest typically appears barrel-shaped, with an increased anterior-posterior diameter caused by hyperinflation. *Auscultation reveals fine crepitations with rhonchi and reduced air entry immediately after birth.
  • 19. *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. *Most infants who develop symptoms will do so in the first 12 hours of life.
  • 20. * *Perinatal Asphyxia *Respiratory Distress Syndrome *Transient Tachypnea Of Newborn *Congenital Pneumonia *Congenital Heart Disease
  • 21. PNA RDS T TN / Wet Lungs CHD Congenital Pneumonia H/O delayed crying after birth or no cry Pale Gasping respiration or no respiration Bradycardia Hypotonia Convulsion Shock Immediate resuscitation & Post resuscitation management Respiratory distress within 1 hr of life Due to deficiency of surfactant H/O preterm delivery, IDM, C/S CXR : ground glass appearance, air bronchogram, complete white out lungs. Specific treatment give surfactant. Mild self limited pulmonary disorder Due to delayed absorption of fetal lung fluid More in cesarean delivery CXR : Prominent vascular markings, fluid in the interlobar fissure, flat diaphragm Improve by 12- 24 hours Respiratory distress with or without cyanosis Murmur on auscultation CXR : Cardiomegaly Echo. With color doppler is diagnostic Mother has a blood stream infection Mother may be febrile or have other sign of infection Crepitation on Auscultation CXR : Homogeneous or patchy opacity, pneumatocele, pleural effusion Treat with broad spectrum antibiotic
  • 22. * *MAS must be considered in any infant born through MSAF who develops symptoms of RD with typical chest x ray findings *A chest radiographs shows hyperinflation of the lung field and flatten diaphragms. *There are coarse irregular patchy infiltrates *A pneumothorax and pneumomediastinum may be present .
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  • 26. *Arterial blood gas measurements typically show hypoxemia and hypercarbia.In mild cases hyperventilation may result in respiratory alkalosis. Infants with sever disease usually have a respiratory acidosis due to airway obstruction, atelectasis & pneumonitis. * Echocardiography : Infants with pulmonary hypertension and right-to-left atrial & ductal shunt is frequently associated finding in infants with MAS.
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  • 29. * Prevention : Prevention of passage of meconium in utero : *Identification of high risk pregnancies and close monitoring. Pregnancy that continue past due date, induction as early as 41 weeks may help prevent meconium aspiration. *If there is sign of fetal distress corrective measure should be undertaken or infant should be delivered in timely manner.
  • 30. *Transcervical amnioinfusion with normal saline solution in case of thick meconium & oligohydramnios may reduce the incidence of fetal distress & meconium aspiration.
  • 31. Prevention of meconium aspiration : Baby born through thick particulate mecomium: • At delivery suction the oropharynx before the shoulders are delivered. • Intubation & suction under direct laryngoscopy is mandatory before triggering the first breath by drying & stimulating the infant. • Intubation & suction should be continued until the meconium has been cleared. Baby born through thin meconium: suction of the mouth first who have effective respiration at the time of delivery.
  • 32. * *Apparently well child born through MSAF, most of them do not require any interventions besides close monitoring for respiratory distress. *Some may be depressed at birth & require resuscitation. Oxygen by mask should be administered as soon as the trachea has been cleared. *Oropharyngeal suction should be provided to assist pulmonary toileting.
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  • 34. *Broad spectrum antibiotic should be started if a radiological infiltrate or documented infection. *Monitor temperature , blood gas level, fluid & electrolyte balance. *Hypoxia & acidosis may lead to persistent pulmonary hypertension & should be treated promptly. *Mechanical ventilation may be required. *Those who fail to improve conventional treatment may benefit from surfactant therapy, nitrous oxide or ECMO.
  • 35. Approach to the ill newborns: *Transfer to NICU. *Monitor closely. *Full range of respiratory support should be given.
  • 36. * Goals: *Increased oxygenation while minimizing the barotrauma (may lead to air leak). *Prevent pulmonary hypertension. *Prevent secondary infection.
  • 37. Ventilatory support depends on the amount of respiratory distress: *O2 hood *Continuous positive airway pressure (CPAP) *Mechanical ventilation : High-frequency ventilation (HFV) should reduce air leaks & may slow the progression of meconium down the tracheobronchial tree and allow more time for meconium removal.
  • 38. * *Surfactant therapy in MAS showed promising results with decrease in the number of infants requiring ECMO and Possible reduction of pneumothorax.
  • 39. * *Selective pulmonary vasodilation. *Activate guanylate cyclase and increases cyclic GMP and acting directly on the vascular smooth muscle. *Use of iNO reduces the need for ECMO by 40%. *Pretreatment with surfactant improves in delivery of inhaled NO to the alveoli.
  • 40. * ECMO is a form of cardiopulmonary bypass that augments systemic perfusion & provide gas exchange. Most common venoarterial bypass, which required carotid artery ligation & placement of large catheter in the right internal jugular vein & carotid artery.
  • 41. ECMO works by removing blood from the person’s body & artificially removing the CO2 & oxygenating RBC.
  • 42. *ECMO required complete heparinization to prevent clotting in the circuit, so can’t be use in patient with or at risk of IVH. *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. * *Infants of MAS who do not require ventilation recover within 7- 10 days. *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 asphyxia insult may demonstrate neurologic sequele.