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syndrome

syndrome. איילת שלז מחלקת ילודים ופגים. “ mekonionarion ” – “ opium like ” (Aristotle) Meconium stained amniotic fluid – 8-15 % of all deliveries. 5% of them – meconium aspiration syndrome 5% mortality. Origin and composition. Meconium is recognized – 70-85 d of gestation

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syndrome

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  1. syndrome איילת שלז מחלקת ילודים ופגים

  2. “mekonionarion”–“opium like” (Aristotle) • Meconium stained amniotic fluid – 8-15 % of all deliveries. • 5% of them – meconium aspiration syndrome • 5% mortality

  3. Origin and composition • Meconium is recognized – 70-85 d of gestation • Composition: • Water, Mucopolysaccharides, Cholesterol and sterol precursos, Protein, Lipid, Bile acids and salts, Enzymes, Blood group substances, Squamous cell, Vernix caseosa • No bacteria!

  4. In utero passage • Risk factors associated with in utero passage of meconium: • Postterm pregnancy • Little/no amniotic fluid at amniotomy • Oligohydramnion by US • IUGR/ placental insufficiency • Maternal HTN • Preeclampsia • Maternal drug abuse (tobacco, cocaine). • Gestational age > 34w – increasingly present with advancing gestational age.

  5. Pathophysiology • As the GI tract matures: vagal stimulation peristalsis+ rectal sphincter relaxation  meconium • Etiology not well understood: • Fetal response to intra-uterine stress: hypoxia  increased vagal tone • Transient compression of umbilical cord/head  increased vagal tone • Maturation of of fetal intestinal function

  6. Timing of the initial insult: • Traditional belief: immediately after birth • Several investigations: Most cases occur in utero when fetal gasping is initiated before delivery.

  7. Effects of meconium: • Reduce antibacterial activity (perinatal bacterial infection) • Irritating to fetal skin ( erythema toxicum) • The most severe complication of meconium passage in utrro is aspiration of stained amniotic fluid before, during, and after birth

  8. Meconium aspiration syndrome - pathophysiology • Airway obstruction: • Chemical pneumonitis: • Surfactant dysfunction: • Umbilical vessel damage • Persistent pulmonary hypertension of the newborn

  9. Airway obstruction: • Immediate : obstruction of large airways: (volume dependent ): hypoventilation => hypoxemia, hypercapnea, acidosis • Central clearing–obstruction of small airways: • Complete athelectasis • Partial  air trapping (ball valve phenomenon)  hyperdistention of alveoli  increaesed lung resistance during exhalation • pneumothorax, pneumomediastinum , pneumopericardium.

  10. Chemical pneummonitis: • 50% of cases • Enzemes, bile salts, fats – irritants PMN, MQ, inflammatory mediators. • Chemical pneumonitis, edema (6h)  inflamation (24h) • Hyalin membranes, hemorrhage, vascular necrosis can occur. • Bacterial superinfection. • Activated Vasoactive mediators play a role in the develipment of PPHN.

  11. Surfactant dysfunction • Free fatty acids (paimitic, stearic, oleic) – higher minimal surface tention than surfactant (striping effect) • decreased lung compliance • concentration dependent

  12. Umbilical vessel damage • Umbilical vessels exposed to meconium  may cause severe focal inflammation injury. • Spasm and necrosis  fetal hypoperfusion • 1% meconium induced umbilical vascular necrosis among meconium stained placentas.

  13. Persistent pulmonary hypertension of the newborn • Final common pathway for the severe morbidity and mortality in infants with MAS. • Hypoxia  Pulmonary arterial vasoconstriction. • Abnormal pulmonary arterial muscularization  m/p chronic change • Association between MAS and PPHN : • Direct pathogenic cause of lung damage • Simple marker of chronic intrauterine hypoxia

  14. Risk factors of MAS developing into PPHN • “Risk factors of meconium aspiration syndrome developing into persistent pulmonary hypertension of newborn.Acta Paediatr Taiwan. 2004 Jul-Aug;45(4):203-7”– 362 cases of MAS (17% with PPHN). • Pneumothorax, change in FHR base line, asphyxia  most important risk factors

  15. Risk and severety of MAS: • Degree of contamination of the amniotic fluid and Presence of meconium in the airway at delivery is meconium itself a direct primary cause of morbidity mortality? • MAS is commonly associated with chronic hypoxia is meconium a marker of fetal maturation of chronic fetal hypoxia? • Asphyxia, pneumothorax, PPHN – the most important risk factors of mortality in MAS.

  16. Clinical presentation: • Depressed at birth • Early onset of respiratory distress (within 2 h) • Mild tachypnea • cyanosis • Dyspnea: granting, ala nazi, intercostal retraction • Barral chest (presence of air trapping) • respiratory failure • Auscultayion: “wet” inspiratory crackles, occasional expiratory noises • Severe Mas: • Hypoxemia – RL shant • Persistant fetal circulation • PPHN – hypoxic pulmonary arterial vasoconstriction – acidosis, hypercapnea, hypoxemia (prenatal & perinatal maladaptation) • Cardiopulmonary failure • acidosis

  17. Complication: • PPHN • AIR LEAK • PULMONARY HEMORRAGE • ASPHYXIA COMPLICATIONS

  18. Laboratory: • Hypoxemia (RL shunt) • Hypercarbia (in significant obstruction) • Respiratory alkalosis (hyperventilation) • Combined respiratory and metabolic acidosis (severe disease – respiratory failure)

  19. Chest x-ray • 73% - positive x-ray findings • Global atelectasis – early • Patchy dense opacifications (decreased vantilation) accompanied by areas of hyperinflation • Widespread infiltrates • Consolidations • Small pleural effusion (30%) • Pneumothorax/ pneumomediastinum (25%)

  20. Prenatal diagnosis and prevention: • Diagnosis of fetus “at risk”– monitoring fetal status. • Thick VS thin meconium • Meconium and FHR abnormalities • Amnioinfusion during labor • Nasopharyngeal suctioning

  21. Upon delivery intervention: • “combined approach” : nasopharengeal suctioning + neonatal trachea suction. • Thick meconium + depressed infant  tracheal suction - marked reduction in morbidity and mortality. • The American Academy of pediatrics Neonatal Resuscitation Program Steering Guidelines

  22. management • Minimize agitation (prevent additional acidosis and hypoxemia) – optimal thermal environment, minimal handling, muscle relaxation. • NGT • Respiratory care • Maintain systemic blood pressure (RL shunt) • Antibiotics.

  23. MAS treatment – ventilation support: • Main target: oxigenation! – PaO2 60-90mmHg • difficulty with oxigenation positive airway pressure (CPAP) –improves ventilation, stabilizes small airways. • Respiratory acidosis/severe respiratory distress  mechanical ventilation –sPO2> 50 mm Hg with FiO2 – 100% & pH< 7.2 . sedation! Relaxation! • Surfactant • iNO • failed conventional ventilation – HFJV, HFO • ECMO

  24. SURFACTANT • Lung lavage using sufractant in MAS is currently being investigated “Treatment of severe meconium aspiration syndrome with porcine surfactant: a multicentre, randomized, controlled trial”Acta Paediatr. 2005 Jul;94(7):896-902. “ Pulmonary function after surfactant lung lavage followed by surfactant administration in infants with severe meconium aspiration syndrome”.J Matern Fetal Neonatal Med. 2004 Aug;16(2):125-30.

  25. Steroids • Pathophysiology: anti-infalammatory properties. • Corticosteroid treatment, started early, show some improvement in oxigenation and pulmonary hemodynamics durind acute phase. • Effect on morbidity and mortality  Cochrane Database Syst Rev, 2003  insufficient evidence. • Further research: clinucal significant, optimal timing, dosing.

  26. גמרתי!!!

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