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Meconium Aspiration syndrome.pptx

  1. Meconium Aspiration syndrome Moderator Assoc. Prof. Dr. Sunil Kumar Yadav Department of Pediatrics and Adolescent Medicine Nobel Medical College & Teaching Hospital Presenter: Dr Subodh Kumar Shah 2nd year Resident Pediatric
  2. Defination: • Meconium is a sterile, thick, black-green, odorless material that results from the accumulation of debris in the fetal intestine starting in the third month of gestation. (Cloherty-and-Starks-Manual-of-Neonatal-Care-2021) • Meconium is sterile and does not contain bacteria, which is the primary factor that differentiates it from stool. Intrauterine distress can cause passage of meconium into the amniotic fluid.
  3. • In the fetus, passage of meconium first occurs physiologically in the 10th-16th week of gestation, when it contributes to alkaline phosphatase in amniotic fluid. • Fetal defecation reduces after 16 weeks and stops by 20 weeks, concurrent with innervation of the anal sphincter. • In-utero meconium passage is uncommon till term due to: o lack of strong peristalsis o good anal sphincter tone o low levels of motilin o cap of viscous meconium in the rectum • Because meconium is rarely found in the amniotic fluid before 34 weeks gestation, MAS mainly affects infants at term and post-term beyond 42 weeks.
  4. Incidence: • Meconium-stained amniotic fluid (MSAF) complicates approximately 10% to 15% of deliveries. • The incidence of MSAF in preterm infants is very low. Most babies with MSAF are 37 weeks or older, and many meconium-stained infants are post mature and small for gestational age. • Approximately 3% to 4% of neonates born through MSAF develop meconium aspiration syndrome (MAS), and • Approximately 30% to 50% of these infants require continuous positive airway pressure (CPAP) or mechanical ventilation.
  5. Meconium Aspiration Syndrome: “Respiratory distress in newborn infants from inhalation of meconium stained amniotic fluid into the tracheobronchial tree with compatible radiological findings which cannot be otherwise explained.”
  6. Causes:
  7. Etiology: IN MOTHER IN FETUS -Maternal hypertension/ DM -Heavy cigarette smoking -Chronic Respiratory or CVS disease -Post-term pregnancy -Pre-eclampsia/eclampsia -Oligohydramnios -Intrauterine growth retardation -Poor biophysical profile -Abnormal fetal heart rate patterns
  8. 1.Mechanical obstruction • Thick and viscous meconium lead to Complete or partial airway obstruction. With onset of respiration – meconium migrates from central to peripheral airways. • Complete obstruction – atelectasis • Partial obstruction –Ball-valve – air trapping. Risk of pneumothorax - 15 – 33% PATHOPHYSIOLOGY
  9. • Aspiration of meconium causes airway irritation. • The enzymes and bile salts of meconium may cause a release of cytokines (eg, tumor necrosis factor-1-alpha and interleukins-1B, -6, -8, -13), which can result in diffuse toxic pneumonitis. • With distal progressing of meconium, chemical pneumonitis develop resulting bronchiolar edema and narrowing of the small airway. 2. Chemical pneumonitis:
  10. 3. Surfactant inactivation: • Meconium has cytotoxic effect on type II pneumocytes and decreased levels of surfactant protein A and B (SP-A and SP-B). • Bilirubin, fatty acid, triglycerides, cholesterol content of meconium causes alterations in phospholipid structure. • Bile salts in meconium may inhibit surfactant synthesis.
  11. Contd… • Several constituents of meconium, especially the free fatty acids (eg, palmitic, stearic, and oleic acid), have a higher minimal surface tension than surfactant. • These may displace it from the alveolar surface, resulting in diffuse atelectasis, with decreased lung volume, compliance, and oxygenation. • The effect of MAS on surfactant dysfunction usually occurs in the subacute and late phase of the disease.
  12. 4. Persistent pulmonary hypertension (PPHN) • Persistent pulmonary hypertension of the newborn (PPHN) frequently accompanies MAS, with right-to-left shunting caused by increased pulmonary vascular resistance. • PPHN usually presents in the subacute phase and as persistent hypoxemia at 6 to 24 hours after birth. • Significant pulmonary hypertension with right-to-left shunting occurs in about 20% to 40% of infants who have MAS.
  13. • PPHN in infants who have MAS could be due to: 1) hypertrophy or neomuscularization of post-acinar capillaries as a result of chronic intrauterine hypoxia. 2) pulmonary vasoconstriction as a result of hypoxia, hypercarbia, or acidosis. 3) pulmonary vasoconstriction as a result of lung inflammation
  14. (Wiswell)
  15. Physical Examination Symptoms include the following: o Cyanosis o End-expiratory grunting o Alar nasal flaring o Intercostal retractions o Tachypnea o Barrel chest (increased anteroposterior diameter) due to the presence of air trapping o Auscultated rales and rhonchi (in some cases)  Yellow-green staining of fingernails, umbilical cord, skin or under the vocal cords. Signs of cerebral irritation resulting from cerebral edema and hypoxia may appear later after birth i.e. seizures or jitteriness
  16. Thank you……..
  17. Reference: • Wiswell, T.E.; Tuggle, J.M.; Turner, B.S. Meconium aspiration syndrome: Have we made a difference?Pediatrics1990,85,715–721.[PubMed] • Clearly, G.M.; Wiswell, T.E. Meconium-stained amniotic fluid and the meconium aspiration syndrome: An update.Pediatr.Clin.N. Am. 1998, 45, 511–529. [CrossRef] • Manual of Neonatal Care 8th edition John P. Cloherty • Essential Pediatrics 8th edition, O.P Ghai • Neonatal Resuscitation Manual • Clarke, M.B. and Rosenkrantz, T. (2016) Meconium aspiration syndrome: Background, Pathophysiology, prognosis. Available at: (Accessed: 5 July 2016)