MECONIUM ASPIRATION SYNDROME By Dr. Needa Shrestha Prasuti Griha, PBU
Epidemiology Out of the 130 million annual births worldwide it is estimated that aproximately 15 million newborn infants aspirate meconium and 750000 to 1.8 million of these develop MAS.  Saugstad et al, Pediatrics 1998  It occurs more frequently in infants who are postmature and small for gestational age. Mortality rates vary between 4-12% representing approximately 30,000 to 200,000 deaths annually.  MAS occurs in approx. 35% of live births with MSAF 4% of all live birth  (Gordon and Avery)
Meconium pH of meconium: 5.5 to 7.0 a sterile, viscous, dark green, odorless substance  Components include Water 72-80% Desquamated cells from the intestine and skin Gastrointestinal mucin Lanugo hair Pancreatic juice Fatty material from the vernix caseosa Amniotic fluid and intestinal secretions Blood group specific glycoproteins and bile
Description of Meconium Watery Amniotic fluid that is thinly stained Moderately stained Opaque fluid without particles Pea Soup Fluid with thick meconium with particles
Definition Meconium aspiration syndrome (MAS) is a respiratory disorder caused by inhalation of meconium in amniotic fluid into the tracheobronchial tree.
Physiology Meconium is 1 st  found in the fetal ileum between the 10 th  and 16 th  week of gestation  In utero passage of meconium is uncommon due to  lack of strong peristalsis,  good anal sphincter tone A cap of viscous meconium in the rectum  Meconium passage uncommon before 36 wks but occurs in more than 30% of pregnancy beyond 42 wks
Factors that promote the passage of meconium in utero Placental insufficiency Maternal hypertension Preeclampsia Oligohydramnios Maternal drug abuse, especially of tobacco and cocaine Maternal infection/chorioamnionitis Fetal gasping secondary to hypoxia
Causes of Meconium Passage intrauterine stress causing: fetal hypoxia: Hypoxia causes increased gastrointestinal peristalsis and relaxed anal sphincter tone.  asphyxia, and  acidosis Mature fetus (post dated babies): facilitated by myelination of nerve fibers, an increase in parasympathetic tone,  increases in the concentration of motilin (a peptide that stimulates the contraction of the intestinal muscle). Vagal stimulation produced by cord or head compression leading to in utero fetal stress.
Causes of Meconium Passage Other factors: Increased maternal age Previous reproductive casualties Prenatal complications Prolonged gestation, Obesity, Toxaemia Hypertension Anaemia
Post partum aspiration Inadequate removal of meconium from the airway prior to the first breath Use of PPV prior to clearing the airway of meconium
Pathophysiology Aspiration induces hypoxia via 3 major pulmonary effects,  airway obstruction (ball-valve phenomenon),  chemical pneumonitis, PPHN, surfactant dysfunction.  Resulting in Acidosis, Hypoxaemia and Hypercapnea and infection.
Pathophysiology
History Presence of meconium in amniotic fluid is required to cause MAS, but not all neonates with meconium-stained fluid develop MAS. Green urine may be observed in newborns with MAS less than 24 hours after birth. Meconium pigments can be absorbed by the lung and excreted in urine.
Physical Severe respiratory distress may be present. Symptoms include the following: Cyanosis End-expiratory grunting (prolonged expiratory phase) Alar flaring Intercostal retractions Tachypnea Barrel chest in the presence of air trapping Auscultated rales and rhonchi (in some cases) Yellow-green staining of fingernails, umbilical cord, and skin Meconium found below vocal cord defines MAS.
Physical Pulmonary Hypertension is observed with severe MAS (50%) Signs of cerebral irritation resulting from cerebral edema or hypoxia may appear soon after birth or later.  Jitteriness seizures
Classification of Respiratory Disease Mild MAS Disease requiring <40% O 2  for < 48 hours Moderate MAS Disease requiring >40% O 2  for > 48 hours without air leak Severe MAS Disease requiring assisted ventilation for >48 hours, often associated with PPHN
Differentials Aspiration Syndromes Congenital Diaphragmatic Hernia Congenital Pneumonia Idiopathic Pulmonary Hypertension Persistent Pulmonary Hypertension of Newborn (PPHN) Transient Tachypnea of Newborn (TTN) Transposition of the Great Arteries (TGA)
Lab investigations Acid-base status V-Q mismatch and perinatal stress are prevalent and assessment of acid-base status is crucial. Metabolic acidosis from perinatal stress is complicated by respiratory acidosis from parenchymal disease and PPHN. Arterial blood gases  Continuous measurement of oxygenation by pulse oximetry is necessary for appropriate management.
Lab investigations Serum electrolytes:  sodium, potassium, and calcium concentrations at 24 hours to detect SIADH and ARF due to perinatal stress.
Lab investigations CBC In utero or perinatal blood loss, as well as infection, contributes to postnatal stress. Hemoglobin and hematocrit levels must be sufficient to ensure adequate oxygen-carrying capacity. Thrombocytopenia increases the risk for neonatal hemorrhage. Neutropenia or neutrophilia with left shift of the differential may indicate perinatal bacterial infection. Polycythemia may be present secondary to chronic and/or acute fetal hypoxia. Polycythemia is associated with decreased pulmonary blood flow and may exacerbate the hypoxia associated with MAS and PPHN.
iMAGiNG A chest radiograph is essential to do the following: Determine the extent of intrathoracic pathology Identify areas of atelectasis and air block syndromes Assure appropriate positioning of the endotracheal tube and umbilical catheters.
Radiological findings of MAS B/L diffuse grossly patchy opacities or coarse infiltrates Hyperinflation with areas of emphysema Spontaneous pneumothorax or pneumomediastinum (25%) Small Pleural effusion (20%) No air bronchogram  Rapid clearing usually within 48 hrs
Air trapping and hyperexpansion due to airway obstruction Classic radiographic findings : Diffuse, asymmetric patchy infiltrates, Areas of consolidation Hyperinflation
Diffuse chemical pneumonitis from constituents of meconium
atelectasis
iMAGiNG Later in the course of MAS when the infant is stable, imaging procedures of the brain, such as MRI, CT scan, or cranial ultrasound, are indicated if the infant's neurologic examination is abnormal.
Echocardiogram To ensure normal cardiac structure,  To assess cardiac function,  To assess the severity of pulmonary hypertension and right-to-left shunting.
Complications Severe Parenchymal Pulmonary Disease Pulmonary Hypertension  Air Block Syndromes  pneumothorax,  pneumomediastinum,  pneumopericardium pulmonary interstitial emphysema  Pulmonary Interstitial Emphysema
Sequelae Increased risk of perinatal and neonatal mortality Severe acidemia Need for CS delivery Need for Intensive Care and O 2  administration Adverse neurologic outcome In preterms,  increased incidence of Gr 3 to 4 IVH Cystic periventricular leukomalacia Cerebral palsy
Prevention Obstetricians should  monitor  mothers at risk for uteroplacental insufficiency and fetal status in an attempt to identify fetal stress with repeated CTG and Biophysical Profile. When meconium is detected, administering  amnioinfusion  with warm sterile saline may be beneficial. This procedure dilutes meconium in the amniotic fluid; therefore, the severity of aspiration may be minimized. However studies have failed to show benefit.  Timing of delivery: In pregnancies that continue past due date, induction as early as 41 wks may help prevent MAS. Upon delivery of the head of the baby, careful suctioning of the posterior pharynx decreases the potential for aspiration of meconium.
Anticipate the worst Be prepared
American Academy of Pediatrics Neonatal Resuscitation Program Steering Committee guidelines: If the baby is not vigorous:  Suction the trachea immediately after delivery.  Suction for no longer than 5 seconds.  If no meconium is retrieved, do not repeat intubation and suction.  If meconium is retrieved and no bradycardia is present, reintubate and suction.  If the heart rate is low, administer positive pressure ventilation and consider suctioning again later. If the baby is vigorous:  Clear secretions and meconium from the mouth and nose with a bulb syringe or a large-bore suction catheter.  Dry, stimulate, reposition, and administer oxygen as necessary.
Suctioning technique
Note: many cases of MAS are related only to chronic hypoxia and its sequelae and cannot be prevented by efforts to clear the fetal nasopharynx of meconium.  a substantial proportion of MAS is directly caused by the meconium itself, and  recommended measures to clear meconium from the fetal nasopharynx should not be abandoned on the basis of pathophysiologic considerations.
General management Maintain an optimal thermal environment.  Minimal handling to prevent right-to-left shunting, leading to hypoxia and acidosis. Continue respiratory care.  Oxygen therapy via hood or positive pressure Mechanical ventilation  Minimize the mean airway pressure  Use as short an inspiratory time as possible.  Oscillatory, high-frequency, and jet ventilation are alternative effective therapies.  Hyperventilation to induce hypocapnia and respiratory alkalosis is not recommended. Broad Spectrum Antibiotics according to sensitivity pattern.
Supportive Treatment i.v. dextrose,  Fluids restricted as much as possible to prevent cerebral and pulmonary edema Electrolytes incl. calcium and correction of severe metabolic acidosis Protein, lipids, and vitamins to ensure adequate nutrition and prevent essential amino acid and essential fatty acid deficiencies.
Ventilatory Support Provide sufficient O 2  to prevent PAH. CPAP: if FiO 2   requirements >0.40, a trial of CPAP with pressures of 2-6 cm of H 2 O before mechanical ventilation. Indication for Conventional Mechanical Ventilation PaO2 < 50mmHg PaCO2 > 60 mmHg Persistent Acidosis with pH < 7.25 Apnea Clinical Deterioration with increasing RD
Conventional Mechanical Ventilation High flow rate Short inspiratory time  Adequate expiratory time to prevent air trapping  PEEP 2-6cm of H2o Inspiratory time 0.4-0.5 sec
Volume and Pressure support Inhaled nitric oxide has replaced the use of most intravenous pulmonary vasodilators. Maintain systemic BP greater than pulmonary BP, thereby decreasing the right-to-left shunt through the patent ductus arteriosus by Volume expansion,  Transfusion therapy, and  Systemic vasopressors incl. dopamine
Surfactant therapy Surfactant therapy is now commonly used to replace displaced or inactivated surfactant and as a detergent to remove meconium.  May decrease resp. failure with MAS within 6 hrs with 3 doses. Pulmonary lavage with surfactant. Albumin/Bile acid blocker administration. Ongoing studies
Albumin/Bile acid blockers Meconium contains a high concentration of free fatty acids, lipids and bile acids which may have toxic effects on the lung.  Bile acid blockers such as cholestyramine and Albumin (serum bovine albumin) that binds to lipids and free fatty acids are administered into the trachea of the newborn infant, thereby reducing the pulmonary toxicity. Administration may be coupled to surfactant administration.
ECMO Extracorporeal membrane oxygenation (ECMO) is employed if all other therapeutic options have been exhausted. Effective in treating MAS but associated with poor neurological outcomes.  ECMO is a lung bypass system that allows for oxygenation of blood while the lung recovers.
References Manual of neonatal care 6 th  edition John P. Cloherty Essential Pediatrics 6 th  edition, O.P. Ghai Neonatal Resuscitation Manual www.emedicine.com
Thank you

Meconium aspiration syndrome

  • 1.
    MECONIUM ASPIRATION SYNDROMEBy Dr. Needa Shrestha Prasuti Griha, PBU
  • 2.
    Epidemiology Out ofthe 130 million annual births worldwide it is estimated that aproximately 15 million newborn infants aspirate meconium and 750000 to 1.8 million of these develop MAS. Saugstad et al, Pediatrics 1998 It occurs more frequently in infants who are postmature and small for gestational age. Mortality rates vary between 4-12% representing approximately 30,000 to 200,000 deaths annually. MAS occurs in approx. 35% of live births with MSAF 4% of all live birth (Gordon and Avery)
  • 3.
    Meconium pH ofmeconium: 5.5 to 7.0 a sterile, viscous, dark green, odorless substance Components include Water 72-80% Desquamated cells from the intestine and skin Gastrointestinal mucin Lanugo hair Pancreatic juice Fatty material from the vernix caseosa Amniotic fluid and intestinal secretions Blood group specific glycoproteins and bile
  • 4.
    Description of MeconiumWatery Amniotic fluid that is thinly stained Moderately stained Opaque fluid without particles Pea Soup Fluid with thick meconium with particles
  • 5.
    Definition Meconium aspirationsyndrome (MAS) is a respiratory disorder caused by inhalation of meconium in amniotic fluid into the tracheobronchial tree.
  • 6.
    Physiology Meconium is1 st found in the fetal ileum between the 10 th and 16 th week of gestation In utero passage of meconium is uncommon due to lack of strong peristalsis, good anal sphincter tone A cap of viscous meconium in the rectum Meconium passage uncommon before 36 wks but occurs in more than 30% of pregnancy beyond 42 wks
  • 7.
    Factors that promotethe passage of meconium in utero Placental insufficiency Maternal hypertension Preeclampsia Oligohydramnios Maternal drug abuse, especially of tobacco and cocaine Maternal infection/chorioamnionitis Fetal gasping secondary to hypoxia
  • 8.
    Causes of MeconiumPassage intrauterine stress causing: fetal hypoxia: Hypoxia causes increased gastrointestinal peristalsis and relaxed anal sphincter tone. asphyxia, and acidosis Mature fetus (post dated babies): facilitated by myelination of nerve fibers, an increase in parasympathetic tone, increases in the concentration of motilin (a peptide that stimulates the contraction of the intestinal muscle). Vagal stimulation produced by cord or head compression leading to in utero fetal stress.
  • 9.
    Causes of MeconiumPassage Other factors: Increased maternal age Previous reproductive casualties Prenatal complications Prolonged gestation, Obesity, Toxaemia Hypertension Anaemia
  • 10.
    Post partum aspirationInadequate removal of meconium from the airway prior to the first breath Use of PPV prior to clearing the airway of meconium
  • 11.
    Pathophysiology Aspiration induceshypoxia via 3 major pulmonary effects, airway obstruction (ball-valve phenomenon), chemical pneumonitis, PPHN, surfactant dysfunction. Resulting in Acidosis, Hypoxaemia and Hypercapnea and infection.
  • 12.
  • 13.
    History Presence ofmeconium in amniotic fluid is required to cause MAS, but not all neonates with meconium-stained fluid develop MAS. Green urine may be observed in newborns with MAS less than 24 hours after birth. Meconium pigments can be absorbed by the lung and excreted in urine.
  • 14.
    Physical Severe respiratorydistress may be present. Symptoms include the following: Cyanosis End-expiratory grunting (prolonged expiratory phase) Alar flaring Intercostal retractions Tachypnea Barrel chest in the presence of air trapping Auscultated rales and rhonchi (in some cases) Yellow-green staining of fingernails, umbilical cord, and skin Meconium found below vocal cord defines MAS.
  • 15.
    Physical Pulmonary Hypertensionis observed with severe MAS (50%) Signs of cerebral irritation resulting from cerebral edema or hypoxia may appear soon after birth or later. Jitteriness seizures
  • 16.
    Classification of RespiratoryDisease Mild MAS Disease requiring <40% O 2 for < 48 hours Moderate MAS Disease requiring >40% O 2 for > 48 hours without air leak Severe MAS Disease requiring assisted ventilation for >48 hours, often associated with PPHN
  • 17.
    Differentials Aspiration SyndromesCongenital Diaphragmatic Hernia Congenital Pneumonia Idiopathic Pulmonary Hypertension Persistent Pulmonary Hypertension of Newborn (PPHN) Transient Tachypnea of Newborn (TTN) Transposition of the Great Arteries (TGA)
  • 18.
    Lab investigations Acid-basestatus V-Q mismatch and perinatal stress are prevalent and assessment of acid-base status is crucial. Metabolic acidosis from perinatal stress is complicated by respiratory acidosis from parenchymal disease and PPHN. Arterial blood gases Continuous measurement of oxygenation by pulse oximetry is necessary for appropriate management.
  • 19.
    Lab investigations Serumelectrolytes: sodium, potassium, and calcium concentrations at 24 hours to detect SIADH and ARF due to perinatal stress.
  • 20.
    Lab investigations CBCIn utero or perinatal blood loss, as well as infection, contributes to postnatal stress. Hemoglobin and hematocrit levels must be sufficient to ensure adequate oxygen-carrying capacity. Thrombocytopenia increases the risk for neonatal hemorrhage. Neutropenia or neutrophilia with left shift of the differential may indicate perinatal bacterial infection. Polycythemia may be present secondary to chronic and/or acute fetal hypoxia. Polycythemia is associated with decreased pulmonary blood flow and may exacerbate the hypoxia associated with MAS and PPHN.
  • 21.
    iMAGiNG A chestradiograph is essential to do the following: Determine the extent of intrathoracic pathology Identify areas of atelectasis and air block syndromes Assure appropriate positioning of the endotracheal tube and umbilical catheters.
  • 22.
    Radiological findings ofMAS B/L diffuse grossly patchy opacities or coarse infiltrates Hyperinflation with areas of emphysema Spontaneous pneumothorax or pneumomediastinum (25%) Small Pleural effusion (20%) No air bronchogram Rapid clearing usually within 48 hrs
  • 23.
    Air trapping andhyperexpansion due to airway obstruction Classic radiographic findings : Diffuse, asymmetric patchy infiltrates, Areas of consolidation Hyperinflation
  • 24.
    Diffuse chemical pneumonitisfrom constituents of meconium
  • 25.
  • 26.
    iMAGiNG Later inthe course of MAS when the infant is stable, imaging procedures of the brain, such as MRI, CT scan, or cranial ultrasound, are indicated if the infant's neurologic examination is abnormal.
  • 27.
    Echocardiogram To ensurenormal cardiac structure, To assess cardiac function, To assess the severity of pulmonary hypertension and right-to-left shunting.
  • 28.
    Complications Severe ParenchymalPulmonary Disease Pulmonary Hypertension Air Block Syndromes pneumothorax, pneumomediastinum, pneumopericardium pulmonary interstitial emphysema Pulmonary Interstitial Emphysema
  • 29.
    Sequelae Increased riskof perinatal and neonatal mortality Severe acidemia Need for CS delivery Need for Intensive Care and O 2 administration Adverse neurologic outcome In preterms, increased incidence of Gr 3 to 4 IVH Cystic periventricular leukomalacia Cerebral palsy
  • 30.
    Prevention Obstetricians should monitor mothers at risk for uteroplacental insufficiency and fetal status in an attempt to identify fetal stress with repeated CTG and Biophysical Profile. When meconium is detected, administering amnioinfusion with warm sterile saline may be beneficial. This procedure dilutes meconium in the amniotic fluid; therefore, the severity of aspiration may be minimized. However studies have failed to show benefit. Timing of delivery: In pregnancies that continue past due date, induction as early as 41 wks may help prevent MAS. Upon delivery of the head of the baby, careful suctioning of the posterior pharynx decreases the potential for aspiration of meconium.
  • 31.
  • 32.
    American Academy ofPediatrics Neonatal Resuscitation Program Steering Committee guidelines: If the baby is not vigorous: Suction the trachea immediately after delivery. Suction for no longer than 5 seconds. If no meconium is retrieved, do not repeat intubation and suction. If meconium is retrieved and no bradycardia is present, reintubate and suction. If the heart rate is low, administer positive pressure ventilation and consider suctioning again later. If the baby is vigorous: Clear secretions and meconium from the mouth and nose with a bulb syringe or a large-bore suction catheter. Dry, stimulate, reposition, and administer oxygen as necessary.
  • 33.
  • 34.
    Note: many casesof MAS are related only to chronic hypoxia and its sequelae and cannot be prevented by efforts to clear the fetal nasopharynx of meconium. a substantial proportion of MAS is directly caused by the meconium itself, and recommended measures to clear meconium from the fetal nasopharynx should not be abandoned on the basis of pathophysiologic considerations.
  • 35.
    General management Maintainan optimal thermal environment. Minimal handling to prevent right-to-left shunting, leading to hypoxia and acidosis. Continue respiratory care. Oxygen therapy via hood or positive pressure Mechanical ventilation Minimize the mean airway pressure Use as short an inspiratory time as possible. Oscillatory, high-frequency, and jet ventilation are alternative effective therapies. Hyperventilation to induce hypocapnia and respiratory alkalosis is not recommended. Broad Spectrum Antibiotics according to sensitivity pattern.
  • 36.
    Supportive Treatment i.v.dextrose, Fluids restricted as much as possible to prevent cerebral and pulmonary edema Electrolytes incl. calcium and correction of severe metabolic acidosis Protein, lipids, and vitamins to ensure adequate nutrition and prevent essential amino acid and essential fatty acid deficiencies.
  • 37.
    Ventilatory Support Providesufficient O 2 to prevent PAH. CPAP: if FiO 2 requirements >0.40, a trial of CPAP with pressures of 2-6 cm of H 2 O before mechanical ventilation. Indication for Conventional Mechanical Ventilation PaO2 < 50mmHg PaCO2 > 60 mmHg Persistent Acidosis with pH < 7.25 Apnea Clinical Deterioration with increasing RD
  • 38.
    Conventional Mechanical VentilationHigh flow rate Short inspiratory time Adequate expiratory time to prevent air trapping PEEP 2-6cm of H2o Inspiratory time 0.4-0.5 sec
  • 39.
    Volume and Pressuresupport Inhaled nitric oxide has replaced the use of most intravenous pulmonary vasodilators. Maintain systemic BP greater than pulmonary BP, thereby decreasing the right-to-left shunt through the patent ductus arteriosus by Volume expansion, Transfusion therapy, and Systemic vasopressors incl. dopamine
  • 40.
    Surfactant therapy Surfactanttherapy is now commonly used to replace displaced or inactivated surfactant and as a detergent to remove meconium. May decrease resp. failure with MAS within 6 hrs with 3 doses. Pulmonary lavage with surfactant. Albumin/Bile acid blocker administration. Ongoing studies
  • 41.
    Albumin/Bile acid blockersMeconium contains a high concentration of free fatty acids, lipids and bile acids which may have toxic effects on the lung. Bile acid blockers such as cholestyramine and Albumin (serum bovine albumin) that binds to lipids and free fatty acids are administered into the trachea of the newborn infant, thereby reducing the pulmonary toxicity. Administration may be coupled to surfactant administration.
  • 42.
    ECMO Extracorporeal membraneoxygenation (ECMO) is employed if all other therapeutic options have been exhausted. Effective in treating MAS but associated with poor neurological outcomes. ECMO is a lung bypass system that allows for oxygenation of blood while the lung recovers.
  • 43.
    References Manual ofneonatal care 6 th edition John P. Cloherty Essential Pediatrics 6 th edition, O.P. Ghai Neonatal Resuscitation Manual www.emedicine.com
  • 44.