NICU CASE

Presented by:

Airamsherlyn P. Natinga, MD

General Data:

A case of B. Bb. Boyadmitted to NICU-BMarch 06, 2012@ 4:32 pm

Maternal History

- Born to a 30 y.o. G2P2 (2002) mother- Regular PNCU - No teratogenic nor radiation exposure- No hypertension, no DM, no BA- No thyroid nor cardiac diseases- With multivitamins intake- Mother’s blood type: “O+”

Had UTI @ 6 mos AOG with Cefalexin 500mg 1 cap TID x 7 days, completed

Admitted @ Catbalogan Provincial Hospital on March 4, 2012 due to labor pains1st HD: Had fever, T= 38.4ºC, lysed with

Paracetamol 500mg tablet q 4H and started with Cefuroxime 750mg IVTT q 8H

2nd HD: Referred to this center as HOC for CS, re: meconium-stained AF with NRFHS

Interpregnancy intervals:

G1 – 2000 – full term, NSVD @ Catbalogan Provincial Hospital

G2 – present pregnancy

BIRTH HISTORY

- delivered term, 39 wks by BS, via NSVD - cephalic presentation- no cyanosis- thickly meconium - stained amniotic fluid- AS 4,6

PHYSICAL EXAMINATION

SIGN 0 1 2Heart rate Absent Below 100 Over 100

Respiratory effort Absent Slow, irregular Good, crying

Muscle tone Limp Some flexion of extremities

Active motion

Response to catheter in nostril (tested after oropharynx is clear)

No response

Grimace Cough or sneeze

Color Blue, pale Body pink, extremities blue

Completely pink

A P G A R1’ 0 1 1 1 15’ 1 2 1 1 1

PHYSICAL EXAMINATION

With irregular cry and activityWith alar flaring, with sl retractions, no

grunting, no apneaSuctioned secretions oropharyngeal, thick

greenish fluid

Vital signs: HR 120’s bpm RR 65 cpm O2 sat 85% at room air

ANTHROPOMETRIC :

BW : 3.39 kg ( p 90)HC : 35 cm ( p 90) CC : 33 cmAC : 32 cmBL : 51 cm (p 10)

AGA

BALLARD SCORE: 39 Weeks

BALLARD SCORE: 39 Weeks

SKIN: pinkish, (-) jaundiceHEAD & NECK: normocephalic,

(+) caput succedaneum,(-) cephalhematoma, open & flat

anterior & posterior fontanelles, with alar flaring

CHEST & LUNGS: SCE, harsh breath sounds, no crackles, no

wheeze, with retractionsHEART: AP, NRRR, no murmur

ABDOMEN: globular, NABS, greenish tinged umbilical cord with 2A 1V, full pulses

BACK : no dimpling, no lumps, no tuffs of hairGENITALIA : grossly male, descended testes

with good rugaeANUS: patentEXTREMITIES: full pulses, no deformitiesNEUROLOGIC EXAM: No neurologic deficit

Admitting Impression:

Live Full Term Baby Boy, 39 weeks AOG by Maturity Aging delivered via NSD to a G2P2 (2002) 30yrs old mother , Cephalic, Thickly

MS Amniotic Fluid, Apgar Score 4,6 BW 3.39kg BL 51cms, AGA

T/C MAS

COURSE IN THE WARD

Admitted to NICU-B: O2 sat 85% @ room air HR 120 bpm RR 65 cpm

- Routine NB care done- TPR q 4h- V/S q hourly until stable- Vit. K 1mg IM- Hepa B vaccine 0.5ml IM ®- IVF: D5W at 60cc/kg/day- Meds:

Ampicillin 100mg/kg/day q12hGentamycin 5mg/kg/dose

COURSE IN THE WARD

- Hook to NCPAP, FiO2 @ 60%, PEEP 6

- pulse oximeter- OGT - HGT monitoring q 8h- NPO temporarily- CBC, Platelet Count- Blood typing- Blood C/S- CXR: APL

Hgb 136Hct . 0.40Rbc 4.49Wbc 21.0Pmn 0.34Lymphocytes 0.33Monocytes 0.10Stabs 0.23Plt ct. 186Bld type “A+”NRBC 21/100WBC

2 HOURS OF LIFE:

S = (+) grunting

(+) subcostal retractions (+) tachypnea

(+) alar flaring ( -) cyanosis

O = O2 sat 90%, HR = 150 bpm RR = 65 cpm, afebrile SCE, harsh BS

CRT 2 sec

A= T/C Meconium Aspiration Syndrome; Sepsis Neonatorum

P = NCPAP : FiO2 = 60%;

PEEP 6d/c Ampicillin, shifted to

Cefuroxime 100mk q 12H

ABG detnReferred to

Neonatologist for further evaluation and co-management

3 HOURS OF LIFE:

S = (+) grunting (+) subcostal

retractions (+) circumoral

cyanosis (-) seizureO = O2 sat 80%

HR 140s bpm RR 70 cpm afebrile SCE, harsh BS CRT 4 secA= MAP; Sepsis

Neonatorum

P = Emergency ET Intubation (3.5cm)

Hook to Mech. Vent : FiO2 = 100%

RR = 60 PIP = 20-30

PEEP 4-5cm H2O IT = 0.5 I:E =1:2

Dopamine 5ug/kg/hr PNSS IV push 20cc/kgABG determination

ABG det’n

CXR: APL

CXR Reading:Haziness is seen in both

lung fields. Lung fields appeared

hyperaerated.The heart is not

enlarged.ET tube seen with tip at

the level of T2.Impression:

Hyaline Membrane Disease is primarily considered. But on review of the film it is more consistent with MAP.

pH = 6.9pCO2 = 102.6pO2 = 30

4 HOURS OF LIFE:

S = (+) desaturation (+) cyanosis (-) seizure O = O2 sat 80% (+) HR 140s (+) tachypnea (-) seizure, afebrile

A = MAS; Sepsis Neonatorum

P= the same mechanical vent set-up

• NaHCO3 2meq/kg IV push• PNSS 10cc/kg IV push• ABGs det’n• Amikacin 15mg/kg OD, IV drip

10HOURS OF LIFE:

S = (+) desaturation (+) bradycardia (+) apnea (+) cyanosis O = O2 sat 80s % rt. hand

O2 sat 60% LL Ext HR 90 bpm; RR 70 cpm

afebrile SCE, (+) crackles all

over LF faint pulses, CRT 4 secA = MAP; t/c PPHN; Sepsis

Neonatorum

P= mech vent RR adjusted up to 150, still no improvement

NaHCO3 2meq/kg IV push

Suction secretionsPNSS 10cc/kg IV pushDopamine increased to

10ug/kg/hrDexamethasone 0.5mg

IVTT q 6H x 4 dosesFurosemide 2mk IV

pushABGs det’n

24 HOURS OF LIFE:

S = (+) desaturation (+) tachynea (+) pallor (-) UO; (+)BM

O = O2 sat 80s%; afebrile

HR 134 bpm; RR 60 Sclerematous SCE, (+) crackles Faint pulses, CRT 4 sec

A= MAP; t/c PPHN; Sepsis Neonatorum

P = • Foley catheter inserted,

(+) tea-colored urine • Rpt cbc, plt ct • For FFP transfusion• Parents requested to

transfer EVRMC• Bld c/s in 24H no growth

A= MAP; PPHN

P = Epinephrine 0.5mg via ET Tube

Continuous CPR and ambubagging

Parents decided DNR

32 HOURS OF LIFE:

S = (+) desaturations (+) bradycardia (+) cyanosis (+) apnea

O = O2 sat 40s% Mottled skin sclerematous Dilated pupils no spontaneous breathing Faint pulses

33 HOURS OF LIFE:

Hr = 0Rr = 0Pr = 0Pupils fixed and

dilatedEcg LLII = flat tracings

Cardiopulmonary Arrest, Secondary

Meconium Aspiration Pneumonia with PPHN

Sepsis NeonatorumTerm Baby Boy,

delivered via NSVD, cephalic, Thickly Meconium-stained Amniotic Fluid, AS 7,8 to a G2P2 (2002) mother, BW 3.39 kg, BL 51 cm, AGA

Salient FeaturesBirth:

Full term NBMaleTMS amniotic fluidAS 4,6

P.E.(+) caput succedaneumGreenish tinged

umbilical cord(+) grunting(+) tachypnea(+) alar flaring(+) apnea(+) subcostal retractions(+) crackles

Thick greenish (ms) secretions

Perinatal Hx - maternal infection (UTI) - maternal fever - NRFHS

Diagnostics:ABG = respiratory

acidosisCXR

- consistent with meconium aspiration pneumonia

Final Diagnosis

Cardiopulmonary Arrest from Severe Hypoxia, secondary to

Persistent Pulmonary Hypertension; Meconium Aspiration Pneumonia

Sepsis Neonatorum; Term Baby Boy delivered via NSVD, Cephalic,

Thickly meconium stained Amniotic Fluid, Apgar Score 4,6 to a G2P2 (2002) Mother,

BW 3.39 kg, BL 51 cm

Differential Diagnosis

Respiratory Distress in Newborn

Pulmonary

Transient Tachypnea of the Newborn

Hyaline Membrane DiseaseMeconium Aspiration SyndromeNeonatal Pneumonia

Behrman’s Pediatric 5th edition

Non-Pulmonary

Cardiac: CHDAnatomical Anomalies: CDHMetabolic Disorders: Galactosemia

Establish degree of Distress

mild moderate severe

Supplemental O2IVFNG feeds if BP stablePulse oximetryMonitoringConsider antibiotics

CPAPBP/ABG monitoringIVF, NG feeds (if BP stable)Cont. Pulse Ox monitoringEmpiric antibiotics

Intubation & ventilationBP/ABG monitoringTPN if BP is unstableNG feeds if BP stableCont. Pulse Ox monitoringTranscutaneous O2/CO2Empiric antibiotics

Worsening resp distress

Worsening resp distress

Hemodynamic instability

Consider surfactant replacementECG if FiO2 >0.6 prior to surfactant in near term and term infants

Follow up Oxygenation and & ventilation

1.Transient Tachypnea of the Newborn

• is a self-limited disease common in infants throughout the world as an early onset of tachypnea, following vaginal or cesarian delivery, normal preterm or term, present within the first few hours of life with retractions, expiratory grunting, or cyanosis, increased oxygen requirement.

• Features:

presents as respiratory distress in full-term or near-term infants that become evident shortly after birth

TachypneaNasal flaringGruntingRetractionsCyanosis in extreme

cases

1.Transient Tachypnea of the Newborn

ABG: do not reflect carbon dioxide retention, resolves over a 24-hour to 72-hour period.×partial carbon

dioxide tensions are usually normal

CXR×prominent perihilar

streaking, which correlates with the engorgement of the lymphatic system with retained lung fluid, and fluid in the fissures

×Small pleural effusions may be seen.

×Patchy infiltrates have also been described.

2.Congenital Diaphragmatic Hernia

Herniation of the abdominal contents into the thoracic cavity through an opening in the diaphragm causing varying degree of pulmonary hypoplasia

2 types:Bochdalek Hernia

(posterolateral location)

Morgagni Hernia retrosternal location)

Symptoms are critical in the 1st 72 hours

Features: Infant sex: higher in

malesSigns of respiratory

distressAlar flaring, grunting,

retractionstachypneaCyanosisABG – dec pO2 shows

evidence of severe hypoxia, pCO2 elevated, decreased pH and HCO3

2. Congenital Diaphragmatic Hernia

Maternal Hx:× underweight women× Smoking during

pregnancy× Epileptic mothers, taking

anticonvulsant drugs× Tachycardia× Scaphoid abdomen× Decreased breath sounds

on the affected side× Hyperresonce to percussion

on the affected side× Asymmetry of the wall× Increased diameter of the

chest wall

Chest Xray× Mediastinal structures

shifted away from the affected side

× Heart shifted away from the affected side

× Decreased lung volume× Loops of bowel in the

thoracic cavity× Ngt tubes inserted inserted

into the stomach seen in the thoracic cavity

× Gasless abdominal bowelPrenatal utz: between 16 &

24 week× Polyhydramnios× Chest mass

3. Congenital Heart Disease

Common Types:Acyanotic Congenital Heart

DiseaseAtrial Septal Defect

(ASD) Ventricular Septal Defect

(VSD) Patent Ductus Arteriosis

(PDA)Coarctation of the Aorta

(CoA)Aortic Valve Stenosis

(AVS)Pulmonary Valve

Stenosis

Cyanotic Congenital Heart DiseaseTetralogy of Fallotd-Transposition of the

Great ArteriesTricuspid AtresiaTotal Anomalous

Pulmonary Venous Connection (TAPVC)

Congenital heart defects are structural problems with the heart present at birth, when a mishap occurs during heart development soon after conception and often before the mother is aware that she is pregnant.

3. Congenital Heart Defects

 the reason defects occur is presumed to be genetic

Environmental exposure: × ingestion of some drugs× Smoking during

pregnancy infections during

PE Signs of respiratory

distress Tachypnea Alar flaring Grunting

cyanosis (skin, lips and fingernails

× Usually in preterm infants× Most commonly with genetic

disorders such as Down syndrome

× O2 sats 75%-85%× Murmur × Rales (VSD)

Diagnostics:Cxr /2D-Echo:

× Cardiomegaly× Engorged pulmonary

vessels (VSD)× RVH× Pulmonary edema

(CAA)

Meconium - Stained Amniotic Fluid

Meconium:

a viscous, sticky, dark green substance composed of: intestinal epithelial cellsSwallowed vernix caseosaLanugoMucusBlood and cellular debris3 major solid constituents of intestinal secretions of

meconium Bilemucosal cellssolid elements of swallowed amniotic fluid

Water is the major liquid constituent, making up 85-95% of meconium.

Medscape Updated July 2011

Meconium-stained amniotic fluid 10-15% of births usually occurs in term or post-term infants

Meconium Aspiration Syndrome

• is a respiratory disorder in a term and or near term infant born through meconium stained amniotic fluid whose symptoms is a serious condition in which a newborn breathes a mixture of meconium and amniotic fluid into the lungs around the time of delivery.

Although meconium is sterile, its passage into amniotic fluid is important because of the risk of meconium aspiration syndrome (MAS) and its sequelae.

Meconium-stained amniotic fluid may be aspirated during labor and delivery, causing neonatal respiratory distress.

Because meconium is rarely found in the amniotic fluid prior to 34 weeks' gestation, meconium aspiration chiefly affects infants at term and postterm.

Medscape Updated July 2011

Meconium Aspiration Pneumonia

develops in 5% of such infants 30% of them require mechanical ventilation3-5% expire

fetal distress and hypoxia occur with passage of meconium into amniotic fluid

infants may be depressed and require resuscitation at birth

Meconium inactivates surfactant

Physiology

The passage of meconium from the fetus into amnion is prevented by: lack of peristalsis (low motilin level)tonic contraction of the anal sphincter terminal cap of viscous meconium

MSAF may be a natural phenomenon that doesn’t indicate fetal distress.

mature GI tract in post term fetus:increased motilin levelvagal stimulation by cord or head compression (may be associated with passage of meconium in

the absence of fetal distress)

Factors that promote the passage in-utero include:

Placental insufficiencyMaternal hypertensionMaternal chronic respiratory or CV DiseasePost term pregnancyOligohydramniosPoor biophysical profileMaternal drug abuse, especially of tobacco and

cocaineAbnormal fetal HR pattern

Incidence:

Passage of meconium is increasingly common in infants >37 weeks' gestation occurs in up to 50 % of post-mature infants

( >42 weeks)

MAS varies between 1 and 5 % of all deliveries where there has been meconium-stained fluid.

Cleary & Wiswell proposed severity criteria to define MAS:

Mild: requires <40%O2 for <48hrsModerate: >40%O2 for >48hrs, no air leak.Severe: assisted ventilation for >48hrs

often with PPH.

International Journal of Pediatrics October 9, 2011

Pathophysiology:

In utero, meconium passage may occur either: in response to fetal hypoxia, with transient

period of hyperperistalsis and relaxation of anal sphincter tone

or as a normal physiologic event in fetal gut maturation

Meconium in the lungs causes:ventilation-perfusion mismatch secondary to ball

valve effect (mechanical obstruction) chemical pneumonitis (surfactant inactivation)

Pathophysiology

The pathophysiology of MAS is complex. Intrauterine fetal gaspingmechanical airway obstructionPneumonitissurfactant inactivationdamage of umbilical vessels

all play roles in the pathophysiology of meconium aspiration

Pathophysiology

There is also a strong association between MAS and persistent pulmonary hypertension of the newborn (PPHN).

The timing of the initial insult resulting in MAS remains controversial.

Chronic in-utero insult may be responsible for most cases of severe MAS.

In contrast to these severe cases, the vigorous infant who aspirates meconium-stained fluid from the nasopharynx at birth usually develops mild to moderate disease.

Mechanism of Injury:

1.Mechanical Obstruction of the Airwaythe initial and most important problem of the

infant with MASthe exact incidence of large-airway obstruction is

unknownmechanism can create:

ball valve phenomenonair flows passed the meconium during

inspiration but is trapped distally during expiration

increases in: expiratory lung resistancefunctional residual capacityanterior posterior diameter of the chest

Mechanism of injury

total obstruction of the small airways: regional atelectasis and ventilation/perfussion

mismatches can be developed

Adjacent areas often are partially obstructed and over expanded, leading to:Pneumothoraxpneumomediastinum air leaks

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

Mechanism of injury

2. Pneumonitisusual feature of MAS, occurring in about ½ of the

casesMeconium has a direct toxic effect mediated by

inflammation.An intense inflammatory response in the bronchi

and alveoli can occur within hours of aspiration of meconium.

airways and lung parenchyma become infiltrated with large numbers of PMNs, leukocytes and macrophages.

Produce direct local injury by release of inflammatory mediators-cytokines:TNF-αIL-1βIL-8and reactive oxygen species.

Lead to vascular leakage, which may cause toxic pneumonitis with hemorrhagic pulmonary edema.

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

Clinicians should maintain a high index of suspicion for bacterial pneumonia in infants with MAS.

Indications of bacterial pneumonia and/or sepsis and should prompt the clinician to obtain relevant cultures and initiate antimicrobial therapy in the presence of:feveran abnormal WBC decline in respiratory function

Mechanism of injury

3.Pulmonary vasoconstriction

the release of vasoactive mediators, such as:eicosanoidsendothelin-1 prostaglandin E2 (as a result of injury from meconium seems to

play role in the development of persistent PHN)The pulmonary vasoconstriction is, in part, the

result of the underlying in utero stressors.

Mechanism of injury

4. Surfactant inactivation

Meconium displaces surfactant from the alveolar surface and inhibits its surface tension lowering ability.

A full term baby born with a sufficient quantity of surfactant may develop surfactant deficiency by inactivation that leads to: Atelectasisdecreased lung compliance/volumepoor oxygenation

http://video.about.com/pregnancy/MAS.htm

Clinical Manifestations

Either in utero

first breath, thick, particulate meconium is aspirated into the lungs.

small airway obstruction respiratory distress within 1st hoursTachypneaRetractionsGruntingcyanosis observed in severely affected infants.

Clinical Manifestations

Partial obstruction of some airways may lead to pneumothorax Pneumomediastinumboth

Overdistention of the chest may be prominentcondition usually improves w/in 72 hrassisted ventilation: may be severe with a high

risk for mortalityTachypnea may persist for many days or even

several weeksassisted ventilation: may be severe with a high

risk for mortality

Clinical Manifestations

typical chest roentgenogram is characterized by :patchy infiltratescoarse streaking of both lung fieldsincreased anteroposterior diameter, and

flattening of the diaphragmNº CXR in an infant with severe hypoxia and no

cardiac malformation suggests the diagnosis of pulmonary hypertension.

ABG Arterial Po2 may be low in either disease, and if

hypoxia has occurred, metabolic acidosis is usually present

Diagnosis

Coarse interstitial infiltrates +L side pneumothorax

Hyperinflation and patchy asymmetric airspace disease that is typical of MAS.

B., BB. BOY CXR

Diagnosis

Coarse interstitial infiltrates +L side pneumothorax

Areas of opacification due to atelectasis bilaterally.

Close up of left lung demonstrating the streaky lucencies of the air in the interstitium (red arrows) complicated by a pneumothorax (yellow arrow).

Homogeneous density similar to respiratory distress syndrome (RDS).

B., BB. BOY CXR

In infants with severe disease who require high concentrations of supplemental oxygen and mechanical ventilation, the lungs may develop an appearance of homogeneous density similar to respiratory distress syndrome (RDS).

Radiographic changes resolve over the course of 7 to 10 days but sometimes persist for several weeks.

Air leak occurs in 10 to 30 percent of infants with MAS.

Arterial blood gas measurements typically show hypoxemia and hypercarbia.

Infants with pulmonary hypertension and right-to-left shunting may have a gradient in oxygenation between preductal and postductal samples.

2D Echocardiogram for evaluation of PPH.

Management

Sept 2007 the ACOG revised recommendations and recommended that:

“all infants with MSAF should not longer receive intrapartum suctioning. If meconium present and the newborn depressed, the clinician should intubate the trachea and suction meconium from beneath the glottis”.

Intrapartum suctioning not effective in removing meconium aspirated by the fetus into the lungs prior delivery.

Skilled resuscitation team should be present at all deliveries that involve MSAF.

Pediatric intervention depends on whether the infant is vigorous.

Vigorous infant is if has:1. Strong resp. efforts2. Good muscle tone3. Heart rate >100b/m

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

When the infant is not vigorous: Clear airways as quickly as possible. Free flow 02.

Radiant warmer but drying and stimulation should be delayed.

Direct laryngoscopy with suction of the mouth and hypopharynx under direct visualization, followed by intubation and then suction directly to the ET tube as it slowly withdrawn.

When the infant is not vigorous: The process is repeated until either ‘‘little

additional meconium is recovered, or until the baby’s heart rate indicates that resuscitation must proceed without delay’’.

Postnatal ManagementApparently well child born through MSAFMost of them do not require any interventions

besides close monitoring for RD. Most infants who develop symptoms will do so in

the first 12 hours of life.Approach to the ill newborns:Transfer to NICU.Monitor closely.Full range of respiratory support should be

available.Sepsis: ABx indicated.Transfer to ECMO center may be necessary.

Treatment in NICUGoals:

Increased oxygenation while minimizing the barotrauma (may lead to air leak) by minimal MAP and as short IT as possible.

Prevent pulmonary hypertension.

Successful transition from intrauterine to extrauterine life with a drop in pulmonary arterial resistance and an increase in pulmonary blood flow.

Severe MAS can spiral into vicious cycle of hypoxemia that leads to acidosis, which together cause pulmonary vein constriction.

May lead to persistent pulmonary hypertension.

The resultant right-to-left shunting at the level of the ductus arteriosus, the atrial level, or both causes further cyanosis and hypoxemia, which perpetuate the cycle.

Ventilatory support depends on the amount of respiratory distress:

O2 hoodCPAP (10%). Mechanical ventilation (40%). Observational study showed worse outcome for

infants treated with hyperventilation.

High-frequency ventilators may slow the progression of meconium down the tracheobronchial tree and allow more time for meconium removal.

Surfactant

Two randomized controlled studies have evaluated the efficacy of exogenous surfactant administration. Results showed decreased number of infants

requiring ECMO and possible reduction of pneumothorax, but no difference in mortality.

A Cochrane meta-analysis of 4 randomized trials confirmed that surfactant replacement showed no effect on mortality but reduce the use of ECMO.

Lavage with dilute surfactant-increases

oxygenation and decrease the need of MV.

Inhaled NO

Randomized clinical trials have demonstrated that iNO therapy decreases the need for ECMO in addition to mortality in full-term and near-term neonates with hypoxic respiratory failure and PPHN

For hypoxic respiratory failure due to MAS, infants responded well to combined iNO and HFV as compared to either treatment alone

The response to combined treatment with HFV and iNO reflects both decreased intrapulmonary shunt and augmented nitric oxide delivery to its site of action.

ECMO

40% of infants with MAS treated with inhaled NO fail to respond and require bypass.

35% of ECMO patients are with MAS.Survival rate after ECMO 93-100%.

Treatment

Routine intubation to aspirate the lungs of vigorous infants born through meconium-stained fluid is not recommended.

Depressed infants (those with hypotonia, bradycardia, fetal acidosis, or apnea) should undergo endotracheal intubation, and suction should be applied directly to the endotracheal tube to remove meconium from the airway.

The risk associated with laryngoscopy and endotracheal intubation: BradycardiaLaryngospasmHypoxiaposterior pharyngeal laceration with

pseudodiverticulum formation

less than the risk of meconium aspiration syndrome in these severe circumstances.

Treatment of meconium aspiration pneumonia includes: supportive carestandard management for respiratory distress.

The oxygenation benefit of PEEP must be weighed against the risk of pneumothorax.

Severe meconium aspiration may be complicated by persistent pulmonary hypertension and requires similar treatment.

Patients who are refractory to conventional mechanical ventilation or HFV may benefit from:surfactant therapy

regardless of gestational ageiNOor extracorporeal membrane oxygenation

(ECMO)

Prevention of MAS

The risk of meconium aspiration may be decreased by: Antepartum Period: elective induction of labor

for pregnancies at or beyond 41 weeksIntrapartum Fetal Monitoring: paying careful

attention to fetal distress Initiating prompt delivery in the presence of

fetal acidosis, late decelerations, or poor beat-to-beat variability.

Amnioinfusion: ACOG 2007, conclude that routine prophylactic amnioinfusion for the dilution of MSAF is not recommended

PreventionRoutine intrapartum oropharyngeal and

nasopharyngeal suctioning for infants born with clear or meconium-stained amniotic fluid is no longer recommended.

Postpartum Endotracheal SuctioningNRP recommends intubation and direct endotracheal

suctioning soon after delivery for non-vigorous infants born through MSAF, depressed respiratory efforts, poor muscle tone, HR less than 100/min

According to Int’l Consensus on CP Resuscitation and Emergency CV Care, available evidence does not support or refute the routine endotracheal suctioning of depressed infants born through MSAF

International Journal of Pediatrics Oct 2011

PrognosisThe mortality rate of meconium-stained infants is

considerably higher than that of non-stained infants.

Meconium aspiration used to account for a significant proportion of neonatal deaths.

Residual lung problems are rare but include symptomatic cough, wheezing, and persistent hyperinflation for up to 5-10 yr.

The ultimate prognosis depends on the extent of CNS injury from asphyxia and the presence of associated problems such as pulmonary hypertension.

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 upon these conditions.

Potential Future Therapy

Currently MAS treatments are all supportive in nature and do not directly affect the injurious actions of meconium on the lung.

There is still no effective and safe treatment or prophylactic measure for MAS once the meconium has passed below the vocal cords into the lungs.

It has been suggested that fetal pancreatic digestive enzymes play an important role in the lung damage after meconium aspiration by causing disruption of intercellular connections and cell detachment from the basement membrane.

Potential Future Therapy

Recent data show that some of the cell death induced by meconium occurs by apoptosis, and therefore has the potential for pharmacologic inhibition through the use of apoptosis blockers or other strategies.

Summary

Optimal care of an infant born through MSAF involves close collaboration between OBs and Pediatricians.

Effective communication and anticipation of potential problems is a corner stone of the successful partnership.

References:

1. Nelson’s Textbook of Pediatrics 18th and 19th Ed; Respiratory Tract Disorders

2. Standards of Newborn Care 3rd Edition; Management of Newborns with Acute Respiratory Disorders; Hernandez. Matias. Santos; Phil. Society of Newborn Medicine 2008

3. Behrman’s Pediatric Decision Making 5th Ed; Neonatal; 20114. Meconium-stained amniotic fluid (MSAF) Pediatrics point of

view . Fostersom / Pediatrics / Neonatology. February 20095. The epidemiology of meconium aspiration syndrome: incidence,

risk factors, therapies, and outcome. Dargaville PA; Copnell B Pediatrics. 2006 May;117(5):1712-21.

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

Persistent Newborn Pulmonary Hypertension Medscape Pediatrics Updated Dec 20, 2011 Robin H Steinhorn, MD  Raymond and Hazel Speck Berry Professor

of Pediatrics, Division Head of Neonatology, Vice Chair of Pediatrics, Northwestern University, The Feinberg School of Medicine Member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Heart Association, American Pediatric Society, American Thoracic Society and Society for Pediatric Research

Meconium Aspiration Syndrome Medscape Pediatrics Updated March 30, 2010  Melinda B Clark, MD  Assistant Professor of Pediatrics, Department of

Pediatrics, Albany Medical College Member of the following medical societies: Alpha Omega Alpha, Ambulatory Pediatric Association, American Academy of Pediatrics, and Medical Society of the State of New York

Transient Tachypnea of the NewbornMedscape Pediatrics updated Jan 13, 2010 KN Siva Subramanian, MD  Professor of Pediatrics and

Obstetrics/Gynecology, Chief of Neonatal Perinatal Medicine, Hospital Ethicist, Georgetown University Hospital Member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Nutrition,American Society for Parenteral and Enteral Nutrition, American Society of Law, Medicine & Ethics,New York Academy of Sciences, and Southern Society for Pediatric Research

“The frequency of meconium-stained amniotic fluid increases as a function of the duration of labor.”

The Journal of Maternal-Fetal & Neonatal Medicine : Official Journal of the European Association of Perinatal Medicine

PubMed Articles, 2009

Journal Updates

Journal Updates

Glucocorticoids in the treatment of neonatal meconium aspiration syndrome

England Journal of Pediatrics 2011 December; 170(12): 1495–1505.

Published online 2011 April 6. doi:  10.1007/s00431-011-1453-2

PMCID: PMC3221844Copyright © The Author(s) 2011

Journal Updates

Meconium-induced lung edema, inflammation and vasoconstriction on the course of the disease, glucocorticoids are increasingly used in the treatment of MAS despite the fact that principal questions on the choice of GCs derivative, mode of delivery and dosing have not been answered yet.

To bring a complex insight into the topic, this article reviews the pathomechanisms of MAS, mechanisms of action of GCs, as well as the advantages and disadvantages of GCs administration in experimental models and newborns with MAS.

Journal Updates

The anti-inflammatory effect of GCs is supplied also through enhancing the activity of lipocortines.

Lipocortines inhibit the activity of PLA2 and thereby decrease the production of arachidonic acid and mediators of lipooxygenase and cyclooxygenase pathway as well as of PAF.

Journal Updates

GCs reduce the penetration of neutrophils into the

lungs, decreasing their adherence to the endothelium thereby increasing secondarily a count of

circulating neutrophilscirculating mononuclearseosinophils basophils as well as the synthesis of cytokines by

Macrophageseosinophils T lymphocytes.

Journal UpdatesGCs stimulate the production of secretion leukocyte

protease inhibitor, an important antiprotease, which may suppress an inflammation in the airways.

GCs facilitate the transcription of β2-receptor gene and reduce the mast cells count and production of mucus in the airways.

By stabilizing the cell membranes and decreasing the production of pro-inflammatory and vasoactive substances, GCs reduce microvascular permeability.

By direct modulation of the pulmonary vasomotoric tone, GCs diminish pulmonary vasoconstriction and inhibit fibrogenesis.

Journal UpdatesGCs may effectively suppress:

pmn’s inflammationlung edema formation pulmonary vasoconstriction.

However, the effect of the treatment depends on: the specific propertiesdose mode of delivery of the individual GCs as well as on the current status of the newborn or

experimental animal with MAS.

Journal UpdatesDexamethasone is a synthetic GC with potent anti-inflammatory and

immunosuppressive action. It is >30 times stronger than hydrocortisone and

about five times stronger than prednisone. is also used for diagnostic procedures (to suppress

the natural pituitary–adrenal axis) in obstetrics to promote the maturation of foetal lungs as well as in a wide spectrum of endocrine, oncological and other diseases.

the action is fast, but of a short term. In newborns, the plasma half-life of dexamethasone

is 150–300 min and the biological half-life is between 36–54 h.

Journal Updates

The half-life of dexamethasone in adults is 110–190 min, with the biological half-life of 36–72 h.

Considering time-related inflammatory changes in MAS, limitations of the treatment efficacy in late administration of GCs may be reduced by repetitive administration, every 2–4 h is recommended (data given by the producer, Dexamed, Medochemie, Cyprus).

Although the acute cardiovascular changes may be critical for neonates with meconium-induced lung injury, the side effects of repetitive GCs administration in MAS have not been investigated yet in a clinical study

Journal Updates

Concluding remarksDespite the increasing number of trials with GCs in

experimental models and newborns with MAS, their administration is still missing in the generally accepted therapeutic protocol of MAS.

However, favourable results from the studies indicate that GCs may be beneficial, particularly in severe forms of MAS with apparent lung edema, pulmonary vasoconstriction and inflammation.

The authors found that the surfactant lung lavage in combination with dexamethasone pretreatment may improve the status of the newborns with MAS more effectively than the surfactant lavage alone.

Journal UpdatesInternational Journal of PediatricsVolume 2012 (2012), Article ID 359571, 7 pagesdoi:10.1155/2012/359571

Review ArticleAdvances in the Management of Meconium Aspiration Syndrome

Kamala Swarnam,1 Amuchou S. Soraisham,1,2,3 and Sindhu Sivanandan1

1Division of Neonatology, Department of Pediatrics, University of Calgary, Calgary, AB, T2N 1N4, Canada2Alberta Children's Hospital Research Institute for Child and Maternal Health, University of Calgary, Calgary, AB, T2N 4N1, Canada3Department of Pediatrics, Foothills Medical Centre, Rm C211 1403-29th Street NW, Calgary, AB, T2N 2T9, CanadaReceived 25 July 2011; Accepted 9 October 2011

Journal UpdatesAbstractMeconium aspiration syndrome (MAS) is a common

cause of severe respiratory distress in term infants, with an associated highly variable morbidity and mortality.

MAS results from aspiration of meconium during intrauterine gasping or during the first few breaths.

The pathophysiology of MAS is multifactorial and includes acute airway obstruction, surfactant dysfunction or inactivation, chemical pneumonitis with release of vasoconstrictive and inflammatory mediators, and persistent pulmonary hypertension of newborn (PPHN).

This disorder can be life threatening, often complicated by respiratory failure, pulmonary air leaks, and PPHN.

Journal UpdatesAbstract

This disorder can be life threatening, often complicated by respiratory failure, pulmonary air leaks, and PPHN

Approaches to the prevention of MAS have changed over time with collaboration between obstetricians and pediatricians forming the foundations for care.

The use of surfactant and inhaled nitric oxide (iNO) has led to the decreased mortality and the need for extracorporeal membrane oxygenation (ECMO) use.

In this paper, we review the current understanding of the pathophysiology and management of MAS.

Journal Updates

ConclusionsDespite improvement in obstetrical and neonatal

care, MAS continues to be a neonatal disorder with high morbidity and mortality.

The lung injury caused by meconium is complex and can be attributed to mechanical obstruction of airways, surfactant inactivation, chemical pneumonitis, and PPHN.

Among preventive strategies, elective induction of labor for pregnancies at or beyond 41 weeks is associated with significant reduction in the incidence of MAS and amnioinfusion reduces the risk of MAS only in clinical settings with limited peripartum surveillance.

Journal Updates

ConclusionsIntrapartum management includes endotracheal

suctioning to clear meconium only in nonvigorous infants born through MSAF.

The management of a symptomatic infant with MAS is primarily supportive.

These infants are at high risk of developing PPHN and air leaks. Invasive ventilation if required should use lower PIP, moderate PEEP, higher rates (40–60/min), and adequate expiratory time and permissive hypercapnea should be tolerated to facilitate gentle ventilation.

Journal Updates

ConclusionsMAS complicated with PPHN and not responsive to

conventional ventilation may require HFV and iNO. iNO therapy has decreased the need for ECMO in

MAS complicated by hypoxic respiratory failure and PPHN.

Surfactant replacement should be considered in ventilated infants requiring more than 50% FiO2.

Unless there is definite risk for infection, prophylactic use of antibiotics in MAS does not reduce infection or alter the clinical course of illness.

Journal Updates

ConclusionsECMO has been used as a final rescue therapy in

infants with severe and refractory hypoxemia associated with MAS.

The role of steroids and other adjuvant pharmacotherapies like magnesium sulfate, free radical scavengers, and protease inhibitors is still experimental and they are not routinely recommended.

As MAS is a major cause of mortality in developing countries, studies focusing on prevention and early treatment should be continued to reduce mortality and morbidity.

CLINICAL REPORT

Surfactant-Replacement Therapy for Respiratory Distress in the Preterm and Term Neonate

By:William A. Engle, MD, and the Committee on Fetus and Newborn

PEDIATRICS Volume 121, Number 2February 2008

ABSTRACT

Respiratory failure secondary to surfactant deficiency is a major cause of morbidity and mortality in preterm infants.

Surfactant therapy substantially reduces mortality and respiratory morbidity for this population.

Secondary surfactant deficiency also contributes to acute respiratory morbidity in late-preterm and term neonates with meconium aspiration syndrome, pneumonia/sepsis, and perhaps pulmonary hemorrhage; surfactant replacement may be beneficial for these infants.

This statement summarizes indications, administration, formulations, and outcomes for surfactant-replacement therapy.

Because respiratory insufficiency may be a component of multiorgan dysfunction, preterm and term infants receiving surfactant-replacement therapy should be managed in facilities with technical and clinical expertise to administer surfactant and provide multisystem support.

CLINICAL IMPLICATIONS

1. Surfactant should be given to infants with respiratory distress syndrome as soon as possible after intubation irrespective of exposure to antenatal steroids or gestational age.

2. Prophylactic surfactant replacement should be considered for extremely preterm infants at high risk of respiratory distress syndrome, especially infants who have not been exposed to antenatal steroids.

3. Rescue surfactant may be considered for infants with hypoxic respiratory failure attributable to secondary surfactant deficiency (eg, meconium aspiration syndrome, sepsis/pneumonia, and pulmonary hemorrhage).

4. Preterm and term neonates who are receiving surfactant should be managed by nursery and transport personnel with the technical and clinical expertise to administer surfactant safely and deal with multisystem illness.

RESEARCH IMPLICATIONS

1. Randomized trials of continuous positive airway pressure, with or without surfactant, during a brief intubation compared with prophylactic or early surfactant replacement in preterm infants are needed.

2. Improved surfactant preparations, surfactant-dosing strategies for infants born to mothers who are receiving antenatal steroids, and noninvasive techniques for surfactant administration need additional study.

3. Surfactant replacement for illnesses other than respiratory distress syndrome needs additional study.

4. It is no longer necessary to include first-generation synthetic surfactants in future studies.

Take Home Points

The initial assessment of a patient in respiratory distress should be rapid and focused on quickly determining the severity of respiratory distress and need for emergent interventions.

Specific causes of respiratory distress can be categorized as pulmonary and non-pulmonary and require specific interventions.

Thank You