Meconium Stained Amniotic Fluid Aspiration Syndrome

Rusila TikoitogaMBBS 42016

OBJECTIVES• Background• Epidemiology• Etiology• Pathophysiology• Clinical Features• Differential Diagnosis• Diagnosis• Management • Prognosis

History• Greek philosopher Aristotle (350-370 BC) first described the condition

meconium stained amniotic fluid derived from the Greek word “meconium-arion” literally meaning “opium-like”.

• He believed that MSAF induced fetal sleep and that it was also associated with fetal deaths and neonatal depression, or because meconium resembled the black, tarry consistency of processed opium.

• Several publications from the 1600s reported MSAF as a sign of fetal death.

• The first description of in-utero aspiration of meconium and MAS was published in 1918.

Meconium• sterile, thick, black-green, odorless matter that is first found in the fetal ileum by the

10th-16th week of gestation gradually increasing to reach about 200g at birth as the first intestinal discharge within 24-48hrs after birth.

• Composition:o 72-80% water o desquamated cells from skin and intestineo bile and drug metaboliteso gastrointestinal mucino lanugo o vernix caseosao amniotic fluido cholesterol, pancreatic enzymes, blood group specific glycoproteins

• 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 motilino 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.

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.”

Epidemiology• Meconium stained amniotic fluid occurs in about 10-25% of childbirths after 34 weeks of

gestation.• Meconium aspiration syndrome develops in about 4-10% of the infants born with MSAF. • Neonates with MAS, 1/3 will need ventilatory support, 10% develop air leaks and 5-10%

have a definite fatal outcome and 5-6 % develop persistent pulmonary hypertension of the newborn.

• Mortality rate vary 4-12% depending on the severity of the complication and the effectiveness of treatment.

• Changes in obstetrical and neonatal practices appear to be decreasing the incidence of meconium aspiration syndrome.

• In developing countries with less availability of prenatal care and where home births are common, incidence of meconium aspiration syndrome is thought to be higher and is associated with a greater mortality rate.

Etiology• Risk factors that promote meconium passage in-utero:o Placental insufficiencyo Maternal hypertension and diabetes mellituso Pre-eclampsia/Eclampsia o Oligohydramnioso Maternal drug abuse especially tobacco and cocaineo Maternal infection/chorioamnionitiso Fetal gasping secondary to hypoxia

• Causes of meconium passage:o Distressed Fetus-Hypoxia and acidosis

stimulates vagal pathway causing peristalsis and relaxes anal sphincter

o Mature fetus (Post-term)-increased parasympathetic tone, increased motilin, vagal stimulation produced by cord or head compression causing in-utero distress

Pathophysiology

Clinical Features• Historyo The presence of meconium in amniotic fluid but not all

neonates with MSAF develop MAS.o Green urine may be observed in newborns less than 24 hours

after birth. Meconium pigments can be absorbed by the lung and excreted in urine.

o Post term delivery

• Physical Examination Severe respiratory distress may be present. Symptoms include the following:o Cyanosiso End-expiratory gruntingo Alar nasal flaringo Intercostal retractionso Tachypneao Barrel chest (increased anteroposterior diameter) due to the presence of air trappingo 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

Differential Diagnosis• Aspiration Syndromes• Neonatal Pneumonia• Transient Tachypnea of the Newborn• Respiratory Distress Syndrome• Neonatal Congenital Diaphragmatic Hernia• Persistent Pulmonary Hypertension of the

Newborn• Surfactant Deficiency• Transposition of the Great Arteries• Neonatal Sepsis• Congenital Heart Disease with Pulmonary

Hypertension

DiagnosisLab Investigations

Acid-base status• V-Q mismatch and perinatal stress• Arterial Blood Gases• Metabolic acidosis from perinatal stress is

complicated by respiratory acidosis from parenchymal disease and persistent pulmonary hypertension of the newborn.

• Continuous measurement of oxygenation by pulse oximetry are necessary for appropriate management

Serum Electrolytes• Na, Ca, K concentrations at 24 hours of life to

detect MAS because SIADH and ARF are frequent complications of perinatal stress.

Full Blood Count• Low Hemoglobin and Hematocrit

Hypoxia• Thrombocytopenia neonatal

hemorrhage. • Neutropenia or neutrophilia with left shift

of the differential perinatal bacterial infection.

• Polycythemia chronic fetal hypoxia• Polycythemia is associated with decreased

pulmonary blood flow and may worsen the hypoxia associated with MAS and PPHN.

• Imaging Chest X-Rayo Confirm the diagnosis of

MAS and see the extent of intra-thoracic pathology

o Identify atelectasiso Ensure appropriate

positioning of the ETT and umbilical catheters

• Classic CXR Findings:o Diffuse asymmetric patchy infiltration and

consolidationo Air trapping and hyper-expansion from airway

obstruction.o Acute atelectasiso Pneumomediastinum from gas trapping and air leak. o Left pneumothorax with depressed diaphragm and

minimal mediastinal shift because of noncompliant lungs.

o Diffuse chemical pneumonitis from constituents of meconium.

• Echocardiographyo ensure normal cardiac structure and assess cardiac

function, determine the severity of pulmonary hypertension and right-to-left shunting.

• Brain Imagingo Later in the course of meconium aspiration syndrome,

when the infant is stable, imaging studies of the brain (e.g. MRI, CT scanning, cranial ultrasonography) are indicated, if the infant's neurologic examination is abnormal.

• Classification of MAS:o Mild MAS <40% pO2 for <48hrso Moderate MAS >40% pO2 for >48hrs without air

leako Severe MAS Assisted ventilation for >48hrs

often associated with PPHN

• Complications of MASo Severe Parenchymal Pulmonary Diseaseo Pulmonary HTNo Air block syndromes pneumothorax, pneumomediastinum pneumopericardium o Pulmonary interstitial emphysema

Anticipate the worst!

Be prepared!

Immediate Management The American Academy of Pediatrics Neonatal Resuscitation

Program Steering Committee guidelines are as follows 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:• Do not electively intubate• 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. Transfer ill newborns with respiratory distress to NICU

General Management Continued care in the neonatal ICU (NICU) Maintain an optimal thermal environment Minimal handling to reduce agitation thus pulmonary

hypertension and right-to-left shunting causing hypoxia and acidosis

Insert umbilical artery to monitor blood pH and blood gases without agitating the infant.

Continue respiratory care. o Oxygen therapy via hood or positive. o Conventional Mechanical ventilation• High flow rate • minimize mean airway pressure • short inspiratory time (0.4-0.5 secs)• Adequate expiratory time to prevent air trappingo Oxygen saturations should be maintained at 90-95%. Broad spectrum antibiotics

Supportive treatmento IV Dextrose to prevent hypoglycemia. o Fluid restriction (60-70 mL/kg/d) to prevent cerebral and

pulmonary edemao Electrolytes to correct metabolic acidosis o Protein, lipids, and vitamins to prevent deficiencies Conventional Mechanical Ventilation Supporto Continuous Positive Airway Pressure If FiO2 is >0.4 CPAP with pressures 2-6 cm of H20 before mechanical

ventilationo Indications of CMV PaO2 <50 mm of Hg PaC02 >60 mm of Hg pH <7.25 Sleep Apnea

CPAP: ECMO:

Volume and Pressure Supporto Inhaled nitric oxide has replaced the use

of most IV pulmonary vasodilatorso Maintain systemic BP higher than

pulmonary BP by decreasing R-L shunt through the PDA by:

• Volume expansion• Transfusion therapy• Systemic vasopressors e.g. dopamine Albumin/Bile Acid Blockerso Bile acid blockers such as cholestyramine

and serum bovine albumin that binds to lipids and free fatty acids are administered into the trachea and reducing lung toxicity

o Maybe coupled with surfactant administration

• Surfactant Therapy• replace displaced or inactivated surfactant and as a

detergent to remove meconium• may reduce the severity of disease, progression to

extracorporeal membrane oxygenation and decrease length of hospital stay

• May decrease respiratory failure with MAS within 6 hrs of 3 doses

ECMO• Extracorporeal membrane oxygenation is the last

option• focused on the function of oxygenation and CO2

removal• Effective but associated with a high incidence of poor

neurologic outcomes• ECMO is done using only cervical cannulation, which

can be performed under local anesthesia• used for longer-term support ranging from 3-10 days • allow time for intrinsic recovery of the lungs and

heart• Survival rate 93-100%

Prevention of MAS• Obstetricians should monitor mothers at risk

for uro-placental insufficiency and fetal distress with repeated CTG

• Timing of delivery in post due date, induction as early as 41 weeks may help prevent MAS

• Upon delivery of the head of baby careful suctioning of the posterior pharynx decreases potential for MAS

Prognosis• Most complete recovery of pulmonary

function. • Severely affected infants have about a 50%

risk of developing reactive airway disease in the first 6 months of life.

• May cause the infant to have long-term neurologic deficits, including CNS damage, seizures, mental retardation, and cerebral palsy.

References• Manual of Neonatal Care 6th edition John P. Cloherty• Essential Pediatrics 6th edition, O.P Ghai• Neonatal Resuscitation Manual• Clarke, M.B. and Rosenkrantz, T. (2016) Meconium aspiration syndrome: Background,

Pathophysiology, prognosis. Available at: http://emedicine.medscape.com/article/974110-overview#a5 (Accessed: 5 July 2016)

• Fanaroff, A.A. (2008) ‘Meconium aspiration syndrome: Historical aspects’, Journal of Perinatology, 28, pp. S3–S7. doi: 10.1038/jp.2008.162.

• Raju, U., Sondhi, V. and Patnaik, S. (2010) ‘Meconium aspiration syndrome: An insight’, Medical Journal Armed Forces India, 66(2), pp. 152–157. doi: 10.1016/s0377-1237(10)80131-5.