Meconium-Stained Amniotic Fluid MSAF

7/31/2019 Meconium-Stained Amniotic Fluid MSAF

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Meconium-stainedamniotic fluid (MSAF)

Pediatrics point of viewM&M Presentation

Darinka Shaw MDPediatrics Resident

February 2009


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Objectives

Definition

Epidemiology

Etiology Pathophysiology

Clinical features

Management Morbidity&Mortality


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Definition

Meconium aspiration syndrome (MAS)is a respiratory disorder in an infant

born throughMeconium stained amniotic fluid

whose symptoms cannot be

otherwise explained.


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MAS

Cleary&Wiswell proposed severity criteriato define MAS:

Mild: requires 48hrs, no airleak.

Severe: assisted ventilation for >48hrsoften with PPH.


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Epidemiology

MSAF observed in 13% of all live births.

MAS occurs in 5% of newborns delivered

through MSAF. 25,000 to 30,000 cases and 1,000 deaths

related to MAS annually in US.


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Epidemiology

More frequently in infants who arepostmature and small for gestational age.

Decline from 5.8% to 1.5% (19901997),attributed to a 33% reduction in theincidence of births >41 weeks gestation.


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Physiology

The passage of meconium from the fetus intoamnion is prevented by lack of peristalsis (lowmotilin level), tonic contraction of the anal

sphincter, terminal cap of viscous meconium. MSAF may be a natural phenomenon that

doesnt indicate fetal distress but mature GItract in post term fetus with increased motilin

level. Vagal stimulation by cord or head compression

may be associated with passage of meconium inthe absence of fetal distress.


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Risk factors for MSAF

Maternal HT Maternal DM

Maternal heavy cigarette smoking Maternal chronic respiratory or CV Dx Post term pregnancy Pre-eclampsia/eclampsia

Oligohydramnios IUGR Poor biophysical profile Abnormal fetal HR pattern


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Pathophysiology

The pathophysiology of MAS is complex.

Intrauterine fetal gasping, mechanical airway

obstruction, pneumonitis, surfactant inactivation,and damage of umbilical vessels: all play roles inthe pathophysiology of meconium aspiration.

There is also a strong association between MASand persistent pulmonary hypertension of thenewborn (PPHN).


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Pathophysiology

Thetimingof the initial insult resulting inMAS remains controversial.

Chronic in-utero insult may be responsiblefor most cases ofsevere MAS. In contrast to these severe cases, the

vigorous infant who aspirates meconium-

stained fluid from the nasopharynx at birthusually develops mild to moderatedisease.


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Pathophysiology

The traditional belief was that meconiumaspiration occurs immediatelyafter birth.

Aspirated particulate or thick meconium can becarried rapidly by the first breaths to the distalairways.

Studies of neonatal puppies with tantalum-

labeled meconium instilled into the tracheabefore the first breath have confirmed that thedistal migration of particulate matter can occurwithin 1 hour of birth.


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Pathophysiology

Several investigators have suggested that mostcases of meconium aspiration occur in uterowhen fetal gasping is initiated before delivery.

Meconium has been found distally as far as thealveoli in some stillborn infants and in someinfants that die within hours of delivery.

There is currently no way to distinguish

between the infant who has developed MAS byintrauterine respiration or gasping and the infantwho has developed MAS by inhalation ofmeconium at the first breaths after delivery.


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Mechanism of injury

1.Mechanical Obstruction of the Airway It is commonly thought that the initial and most

important problem of the infant with MAS is

obstruction caused by meconium in the airways. Complete obstruction of large airways by thick

meconium is an uncommon occurrence. The exact incidence of large-airway obstruction

is unknown, though Thureen et al, in an autopsystudy of infants who died of MAS, found noevidence of such obstruction.


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Pathophysiology

Usually, small amounts of meconium migrateslowly to the peripheral airways.

This mechanism can create a ball valvephenomenon, in which air flows past themeconium during inspiration but is trappeddistally during expiration, leading to increases in

expiratory lung resistance, functional residualcapacity, and anterior posterior diameter of thechest.


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Pathophysiology

Regional atelectasis and V/P mismatches can bedeveloped from total obstruction of the small

airways. Adjacent areas often are partially obstructed and

over expanded, leading to pneumothorax andpneumomediastinum air leaks.

Pulmonary air leaks are 10x more likely todevelop in infants with MAS than those without,and leaks often develop during resuscitation.


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Pathophysiology

2. Pneumonitis Pneumonitis is a usual feature of MAS,

occurring in about of the cases. Meconium has a direct toxic effect

mediated by inflammation.

An intense inflammatory response in thebronchi and alveoli can occur within hoursof aspiration of meconium.


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The airways and lung parenchyma becomeinfiltrated with large numbers ofpolymorphonuclear leukocytes andmacrophages.

Produce direct local injury by release ofinflammatory mediators-cytokines (TNF-, IL-1,IL-8) and reactive oxygen species.

Lead to vascular leakage, which may cause toxicpneumonitis with hemorrhagic pulmonaryedema.

Pathophysiology


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Pathophysiology

Meconium contains substances such as bile acidsthat also can cause direct injury.

Clinicians should maintain a high index of

suspicion for bacterial pneumonia in infantswith MAS.

Presence of fever, an abnormal WBC or adecline in respiratory function are indications of

bacterial pneumonia and/or sepsis and shouldprompt the clinician to obtain relevant culturesand initiate antimicrobial therapy.


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Pathophysiology

3.Pulmonary vasoconstriction

The release of vasoactive mediators, such as

eicosanoids, endothelin-1 and prostaglandin E2as a result of injury from meconium seems toplay role in the development of persistent PH.

The pulmonary vasoconstriction is, in part, the

result of the underlying in utero stressors.


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Pathophysiology

4. Surfactant inactivation

Recognized in the early 1990.

Meconium displaces surfactant from the alveolarsurface and inhibits its surface tension loweringability.

A full term baby born with a sufficient quantity

of surfactant may develop surfactant deficiencyby inactivation that leads to atelectasis,decreased lung compliance/volume and pooroxygenation.


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Pathophysiology


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CLINICAL FEATURES

History

Infants with MAS have a history of

MSAF. They often are postmature or small

for gestational age.

Many are depressed at birth.


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CLINICAL FEATURES

Physical examination Evidence of postmaturity: peeling skin, long

fingernails, and decreased vernix.

The vernix, umbilical cord, and nails may bemeconium-stained, depending upon how longthe infant has been exposed in utero.

In general, nails will become stained after 6

hours and vernix after 12 to 14 hours ofexposure.


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CLINICAL FEATURES

Physical examination

Affected patients typically have respiratorydistress with marked tachypnea and cyanosis.

Reduced pulmonary compliance and use ofaccessory muscles of respiration are evidencedby intercostal and subcostal retractions and

abdominal (paradoxical) breathing, often withgrunting and nasal flaring.


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CLINICAL FEATURES

Physical examination The chest typically appears barrel-shaped, with

an increased anterior-posterior diameter caused

by overinflation. Auscultation reveals rales and rhonchi -

immediately after birth.

Some patients are asymptomatic at birth and

develop worsening signs of respiratory distressas the meconium moves from the large airwaysinto the lower tracheobronchial tree.


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Diagnosis

MAS must be considered in any infant

born through MSAF who developssymptoms of RD.


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Diagnosis

The diagnosis of MAS is confirmed by chestradiograph.

The initial CXR may show streaky, linear

densities similar in appearance to transienttachypnea of the newborn (TTN).

As the disease progresses, the lungs typicallyappear hyperinflated with flattening of the

diaphragms. Diffuse patchy densities may alternate with

areas of expansion.


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Coarse focal consolidation with emphysema.


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Hyperinflation and patchy asymmetricairspace disease that is typical of MAS.


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Coarse interstitial infiltrates +L side pneumothorax


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Areas of opacification due to atelectasisbilaterally.


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Close up of left lung demonstrating the streaky lucencies ofthe air in the interstitium (red arrows)complicated by a

pneumothorax(yellow arrow).


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Diagnosis

In infants with severe disease who require highconcentrations of supplemental oxygen andmechanical ventilation, the lungs may develop

an appearance of homogeneous density similarto respiratory distress syndrome (RDS).

Radiographic changes resolve over the course of7 to 10 days but sometimes persist for severalweeks.

Air leak occurs in 10 to 30 percent of infantswith MAS.


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Homogeneous density similar to respiratorydistress syndrome (RDS).


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Diagnosis

Arterial blood gas measurements typicallyshow hypoxemia and hypercarbia.

Infants with pulmonary hypertension andright-to-left shunting may have a gradientin oxygenation between preductal and

postductal samples. 2D Echocardiogram for evaluation of PPH.


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Management


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Management

Sept 2007 the ACOG revised recommendationsand recommended that all infants with MSAFshould not longer receive intrapartum

suctioning. If meconium present and thenewborn depressed, the clinician should intubatethe trachea and suction meconium from beneaththe glottis.

Intrapartum suctioning not effective in removingmeconium aspirated by the fetus into the lungsprior delivery.


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Management

Skilled resuscitation team should be present atall deliveries that involve MSAF.

Pediatric intervention depends on whether theinfant is vigorous.

Vigorous infant is if has:1. Strong resp. efforts

2. Good muscle tone

3. Heart rate >100b/m

When this is a case-no need for trachealsuctioning, only routine management.


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Postnatal Management

Apparently well child born through MSAF

Most of them do not require any

interventions besides close monitoring forRD.

Most infants who develop symptoms will

do so in the first 12 hours of life.


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Postnatal Management

Approach to the ill newborns:

Transfer to NICU.

Monitor closely.

Full range of respiratory support should beavailable.

Sepsis w/up and ABx indicated.

Transfer to ECMO center may benecessary.


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Treatment in NICU

Goals:

Increased oxygenation while minimizing thebarotrauma (may lead to air leak) by minimalMAP and as short IT as possible.

Prevent pulmonary hypertension.

Successful transition from intrauterine to

extrauterine life with a drop in pulmonaryarterial resistance and an increase in pulmonaryblood flow.


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Treatment in NICU

Severe MAS can spiral into vicious cycleofhypoxemia that leads to acidosis, which together

cause pulmonary vein constriction. May lead to persistent pulmonary hypertension.

The resultant right-to-left shunting at the levelof the ductus arteriosus, the atrial level, or both

causes further cyanosis and hypoxemia, whichperpetuate the cycle.


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Treatment in NICUVentilatory support depends on the amount of

respiratory distress:

O2 hood

Mechanical ventilation (40%). CPAP (10%). Observational study showed worse outcome for infants

treated with hyperventilation. High-frequency ventilators should reduce air leak

syndromes in MAS, but animal and clinical models haveyielded conflicting results.

High-frequency ventilators may slow the progression ofmeconium down the tracheobronchial tree and allowmore time for meconium removal.


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Treatment in NICU

Surfactant

Two randomized controlled studies have evaluated theefficacy of exogenous surfactant administration. Results

showed decreased number of infants requiring ECMOand possible reduction of pneumothorax, but nodifference in mortality.

A Cochrane meta-analysis of 4 randomized trialsconfirmed that surfactant replacement showed no effect

on mortality but reduce the use of ECMO (RR 0.64, 95% CI,0.46-0.91).

Lavage with dilute surfactant-increases oxygenation anddecrease the need of MV (need additional trials).


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Treatment in NICU

Inhaled NO

NO causes selective pulmonary vasodilation by acting

directly on the vascular smooth muscle-activatesguanylate cyclase and increases cGMP. By dilating blood vessels in well ventilated areas of lung,

NO decreases the V/P mismatch and improvedoxygenation in infants with PPH.

Decreases need for ECMO (RR 0.61, 95%CI 0.51, 0.72)but no difference in mortality. In a large randomized multicenter trial infants with MAS

responded well to the combination of inhaled nitric oxideand HFOV, likely because of improved lung inflation and

better delivery of the drug.


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ECMO

40% of infants with MAS treated withinhaled NO fail to respond and require

bypass. 35% of ECMO patients are with MAS.

Survival rate after ECMO 93-100%.


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Morbidity & Mortality

Pulmonary morbidity

Pulmonary outcome evaluated in 35 infants with

MAS and 70 controls. During the first 6mo after birth, the infants with

MAS were significantly more likely to have oneor more episodes of wheezing and/or coughing

lasting 3 days (49% vs. 20%)and receivebronchodilator therapy (23% vs. 3%)compared tocontrols.


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Pulmonary function testing was performed at 8yof age in 11 children who had MAS and 9controls.

The MAS group had evidence of mild airwayobstruction, hyperinflation, and increased closingvolumes compared to controls, and had moreexercise-induced bronchospasm (4 vs. 0 children).

However, during graded exercise stress tests,MAS children had normal maximal oxygenconsumption and anaerobic threshold withoutsignificant hypoxemia or hypercarbia.


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Respiratory symptoms, pulmonary function tests, andchest radiographs evaluated in 18 children age 6-11ywho had MAS.

7 children had recurrent cough and wheezing consistentwith asthma, and 5 of these had exercise-inducedbronchospasm that responded to bronchodilators.

Of the 11 asymptomatic children, 2 had mild expiratoryairflow limitation, 1-exercise-induced bronchospasm, and

8 had normal pulmonary function. Chest radiographswere normal in all the children.


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Neurologic outcome

Outcome is good in uncomplicated MAS

with no underlying disorder. Most cases of severe MAS are associated

with intrauterine asphyxia and/or infection

and neurologic outcome depends uponthese conditions.


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In retrospective comparison, perinatal mortalitysignificantly higher in singleton pregnancieswith/ than without MSAF (1.5 vs. 0.3/1000).

The mortality rate for MAS resulting from severeparenchymal pulmonary disease and pulmonaryhypertension is as high as 20%.

Severe fetal acidemia-cord arterial pH


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Summary

Optimal care of an infant born throughMSAF involves close collaboration between

OBs and Pediatricians. Effective communication and anticipation

of potential problems is a corner stone of

the successful partnership.


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References:

1. Meconium Stained Fluid: Approach to the Mother and the Baby Michele C. Walsh,MD, MS; Jonathan M. Fanaroff, MD, JD Clin Perinatol 34 (2007) 653665

2. The epidemiology of meconium aspiration syndrome: incidence, risk factors,therapies, and outcome. Dargaville PA; Copnell B Pediatrics. 2006May;117(5):1712-21.

3. Delivery room management of the apparently vigorous meconium-stainedneonate: results of the multicenter, international collaborative trial. Wiswell TE;Gannon CM; Jacob J; Goldsmith L; Szyld E; Weiss K; Schutzman D; Cleary GM;Filipov P; Kurlat I; Caballero CL; Abassi S; Sprague D; Oltorf C; Padula MPediatrics 2000 Jan;105(1 Pt 1):1-7.

4. Defecation in utero: a physiologic fetal function. Ramon y Cajal CL; Martinez RO

Am J Obstet Gynecol 2003 Jan;188(1):153-6.

5. Surfactant and surfactant inhibitors in meconium aspiration syndrome. DargavillePA; South M; McDougall PN J Pediatr 2001 Jan;138(1):113-5.

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Meconium-Stained Amniotic Fluid MSAF

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