MECONIUM ASPIRATION SYNDROME

DefinitionEpidemiologyPhysiologyRisk factorsPathophysiologyClinical featuresDifferential diagnosisLab investigationsManagementPrognosis

DefinitionMeconium aspiration syndrome

( MAS ) is a respiratory distress of an infant born through meconium stained amniotic fluid

Meconium found below vocal cord

Epidemiology MSAF observed in (8-20%) of all

births.MAS occurs in 5% of newborns

delivered through MSAF. It is a disease of Term or Post-

term Infant.

MeconiumpH of meconium : 5.5-7A sterile, viscous, dark green, odorless substanceComponent : - 75-80% water - desquamated cells from the intestine and epithelial cell - Lanugo hair - Fattry material from vernix caseosa - Mucus - BileDescription : Light – amniotic fluid thinly stained Moderate – opaque without patricles Thick – pea soup particles

PhysiologyMeconium 1st found in the fetal ileum between the 10th and 16th

week of gestationIn utero passage of meconium uncommon due to : - lack of strong peristalsis (low motilin level) - good anal sphinter - a cap of viscious meconium in the rectum Meconium passage uncommon before 36 weeks but occurs

more than 30% beyond 42 weeks due to : - Fetal maturation post term (high motilin level). - In utero stress (hypoxia, acidosis) producing relaxation of anal sphincter.

Risk factors for MASMaternal HPTMaternal DMMaternal heavy cigarette smokingMaternal chronic respiratory or

cardiovascular diseasePost date pregnancyPre-eclampsia/eclampsiaOligohydromnionsIUGRAbnormal fetal HR pattern

Pathophysiology 1. 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 -> atelectasis Partial Obstruction -> ball valve –air trapping (risk of

penumothorax 15-33%)

2. Chemical pneumonitis Distal progressing of meconium chemical pneumonitis -> bronchiolar edema and narrowing of the small airway.

3. Surfactant inactivation Bilirubin, fatty acid, triglycerides,

cholestrol content of meconium inhibit surfactant function and inactivation.

4. Pulmonary hypertension Meconium in lung stimulate - >

proinflammatory cytokines and vasoactive substance which cause pulmonary vasoconstriction

Hypoxia, acidosis, hyperinflation -> pulmonary hypertension

CLINICAL FEATURESHistory Infant with MAS must have a history of MSAF Often are term or post-term IUGR Many are depressed at birth

Physical Examination Evidence of postmaturity ; peeling skin, long fingernails, reduced

vernix Vernix, umbilical cord and nails may be meconium-stained,

depending how long the infant has been exposed in utero

Generally nails stained after 6 hrs vernix after 12-14 hrs umbilical cord staining thick 15 min, thin 1 hour

Respiratory distress with marked tachypnea and cyanosis Use of accessory muscles of respiration (ICR, SCR and

abdominal breathing) , grunting and nasal flaring. Chest : appears barreal shape with increase AP diameter

due to overinflation Auscultation : rhonchi immmediately after birth Sign of cerebral irritation from cerebral edema or hypoxia :

jitteriness, seizures Some patient are asymptomatic at birth and develop

worsening signs of respiratory distress as the meconium moves from large airways into the lower tracheobronchial tree.

Meconium found below vocal cord defines MAS

Differential diagnosisPerinatal AsphyxiaBacterial PneumoniaRespiratory Distress SyndromeTransient Tachypnea Of NewbornCongenital Heart Disease

Lab Investigations Arterial blood gas (Acid-base status) - VQ mismatch - Metabolic acidosis - Hypoxia - Hypercarbia - ABG tds in 2 hour

Chest radiograph - hyperinflated lung and flatten diapghram- B/L diffuse grossly irregular patchy infiltrates- Pneumothorax and pneumomediastinum- Small pleural effusion- No air bronchogram

Air trapping and hyperexpansion due to

airway obstruction

Diffuse, asymmetric patchy infiltrates

Areas of concolidationHyperinflation

a

Atelectasis

Diffuse chemical pneumonitis

MANAGEMENTPrenatal1. Identification of high risk pregnancies - recognition of predisposing maternal factors - post dates pregnancy inductionas as early as 41 weeks2. Monitoring - careful observation and fetal monitoring during labour - corrective measures should be undertaken in identifies compromised fetus.3. Amnioinfusion - relieved umbilical cord compression during labor ->

reducing occurrence of variable fetal heart rate decelerations

- efficiency not well demonstrated.

Delivery room management Anticipate the worst….

Be prepared…

American Academy of Paediatrics NRP guidelines: If the baby is not vigorous : - direct suction immediately after delivery - suction for no longer than 5 sec - If no meconium retrieved, do not repeat

intubation and suction - If meconium is retrieved and no bradycardia

present, re-intubate and suction. - If HR low, administer IPPV and consider

suctioning again later. If baby is vigorous : - Clear secretions and meconium from the mouth

and nose with a bulb syringe or a large bore suction catheter.

Management of newborn with MAS1. General management Maintain a neutral thermal environment Minimal handling protocol to avoid agitation Maintain adequate BP and perfusion Correct any abnormalities Sedation2. Respiratory management Pulmonary toilet - from the ETT + chest physiotherapy every

30 min to 1 hr Arterial blood gas level - to assess infant ventilatory

compromise Frequent blood taking -> UAC + UVC3. Oxygen monitoring Severity of infant’s respiratory status and to prevent

hypoxemia Compare pre ductal and post ductal o2 saturation identifies

infant with right to left ductal shunting secondary to MAS associated pulmonary hypertension

4. Antibiotic coverage Start on broad spectrum antibiotic5. Supplemental OxygenTo prevent episodes of alveolar hypoxia leading to

hypoxic pulmonary vasoconstriction and PPHN.maintain arterial oxygen tension 80-90mmHg6. CPAPTo improved oxygenation if the Fio2 exceeds 40-50%7.Mechanical ventilation In MAS with impending respiratory failure with

hypercapnia and persistent hypoxemiaVolume targeted ventilation decreased lung

overdistentionUse of relatively short inspiratory time limit potential

air trappingRequires high pressure and faster rate

8. Surfactant RCT show infant with severe MAS

who require mechanical ventilation and radiologic findings of parenchymal lung disease benefit from early surfactant therapy

9. Inhaled nitric oxideMAS with pulmonary hypertensionIn setting without iNO, sildenafil

reduced PVR and improves oxygenation and decrease mortality

PrognosisComplications are common and

associated with significant mortality

In patient surviving due to severe MAS, BPD, CLD may result from prolonged ventilation

Neurodevelopmental sequelae including GDD, CP, and autism –long term follow up