2. General Data:
A case of B. Bb. Boy
admitted to NICU-B
March 06, 2012
@ 4:32 pm
3. 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+”
4. 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 pains
1st 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
6. BIRTH HISTORY
- delivered term, 39 wks by BS, via NSVD
- cephalic presentation
- no cyanosis
- thickly meconium - stained amniotic fluid
- AS 4,6
7. PHYSICAL EXAMINATION
SIGN 0 1 2
Heart 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 R
1‟ 0 1 1 1 1
5‟ 1 2 1 1 1
8. PHYSICAL EXAMINATION
With irregular cry and activity
With alar flaring, with sl retractions, no grunting,
no apnea
Suctioned secretions oropharyngeal, thick
greenish fluid
Vital signs:
HR 120‟s bpm
RR 65 cpm
O2 sat 85% at room air
9. ANTHROPOMETRIC :
BW : 3.39 kg ( p 90)
HC : 35 cm ( p 90)
CC : 33 cm
AC : 32 cm
BL : 51 cm (p 10)
AGA
12. SKIN: pinkish, (-) jaundice
HEAD & NECK: normocephalic,
(+) caput succedaneum,
(-) cephalhematoma, open & flat anterior
& posterior fontanelles, with alar
flaring
CHEST & LUNGS: SCE, harsh breath sounds,
no crackles, no wheeze,
with retractions
HEART: AP, NRRR, no murmur
13. ABDOMEN: globular, NABS, greenish tinged
umbilical cord with 2A 1V, full pulses
BACK : no dimpling, no lumps, no tuffs of hair
GENITALIA : grossly male, descended testes with
good rugae
ANUS: patent
EXTREMITIES: full pulses, no deformities
NEUROLOGIC EXAM: No neurologic deficit
14. 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
15. 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 q12h
Gentamycin 5mg/kg/dose
17. 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 6
d/c Ampicillin, shifted to
Cefuroxime 100mk q 12H
ABG detn
Referred to
Neonatologist for further
evaluation and co-
management
18. 3 HOURS OF LIFE:
S = (+) grunting
(+) subcostal
retractions
(+) circumoral
cyanosis
(-) seizure
O = O2 sat 80%
HR 140s bpm
RR 70 cpm
afebrile
SCE, harsh BS
CRT 4 sec
A= 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/kg
ABG determination
19. 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 = 6.9
pCO2 = 102.6
pO2 = 30
20. 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
21. 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 sec
A = MAP; t/c PPHN; Sepsis
Neonatorum
P= mech vent RR adjusted
up to 150, still no
improvement
NaHCO3 2meq/kg IV
push
Suction secretions
PNSS 10cc/kg IV push
Dopamine increased to
10ug/kg/hr
Dexamethasone 0.5mg
IVTT q 6H x 4 doses
Furosemide 2mk IV push
ABGs det‟n
22. 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
23. 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
24. 33 HOURS OF LIFE:
Hr = 0
Rr = 0
Pr = 0
Pupils fixed and dilated
Ecg LLII = flat tracings
Cardiopulmonary
Arrest, Secondary
Meconium Aspiration
Pneumonia with PPHN
Sepsis Neonatorum
Term 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
26. 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
28. Respiratory Distress in Newborn
Pulmonary
Transient Tachypnea of the
Newborn
Hyaline Membrane Disease
Meconium Aspiration
Syndrome
Neonatal Pneumonia
Behrman’s Pediatric 5th edition
Non-Pulmonary
Cardiac: CHD
Anatomical Anomalies: CDH
Metabolic Disorders:
Galactosemia
Establish degree of Distress
29. mild moderate severe
Supplemental O2
IVF
NG feeds if BP stable
Pulse oximetry
Monitoring
Consider antibiotics
CPAP
BP/ABG monitoring
IVF, NG feeds (if BP stable)
Cont. Pulse Ox monitoring
Empiric antibiotics
Intubation & ventilation
BP/ABG monitoring
TPN if BP is unstable
NG feeds if BP stable
Cont. Pulse Ox monitoring
Transcutaneous O2/CO2
Empiric antibiotics
Worsening resp distress Worsening resp distress
Hemodynamic instability
Consider surfactant
replacement
ECG if FiO2 >0.6 prior to
surfactant in near term and term
infants
Follow up Oxygenation and &
ventilation
30. 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
Tachypnea
Nasal flaring
Grunting
Retractions
Cyanosis in extreme
cases
31. 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.
32. 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
males
Signs of respiratory
distress
Alar flaring, grunting,
retractions
tachypnea
Cyanosis
ABG – dec pO2 shows
evidence of severe
hypoxia, pCO2 elevated,
decreased pH and HCO3
33. 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 bowel
Prenatal utz: between 16 & 24
week
× Polyhydramnios
× Chest mass
34. 3. Congenital Heart
Disease
Common Types:
Acyanotic Congenital Heart
Disease
Atrial 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
Disease
Tetralogy of Fallot
d-Transposition of the
Great Arteries
Tricuspid Atresia
Total 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.
35. 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)
37. Meconium:
a viscous, sticky, dark green substance composed
of:
intestinal epithelial cells
Swallowed vernix caseosa
Lanugo
Mucus
Blood and cellular debris
3 major solid constituents of intestinal secretions
of meconium
Bile
mucosal cells
solid elements of swallowed amniotic fluid
Water is the major liquid constituent, making up 85-
95% of meconium.
Medscape Updated July 2011
38. 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.
39. 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
40. Meconium Aspiration Pneumonia
develops in 5% of such infants
30% of them require mechanical ventilation
3-5% 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
41. 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 level
vagal stimulation by cord or head compression
(may be associated with passage of meconium in the
absence of fetal distress)
42. Factors that promote the passage in-utero
include:
Placental insufficiency
Maternal hypertension
Maternal chronic respiratory or CV Disease
Post term pregnancy
Oligohydramnios
Poor biophysical profile
Maternal drug abuse, especially of tobacco and
cocaine
Abnormal fetal HR pattern
43. 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.
44.
45.
46. Cleary & Wiswell proposed severity criteria to
define MAS:
Mild: requires <40%O2 for <48hrs
Moderate: >40%O2 for >48hrs, no air leak.
Severe: assisted ventilation for >48hrs often
with PPH.
International Journal of Pediatrics October 9, 2011
47. 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)
48. Pathophysiology
The pathophysiology of MAS is complex.
Intrauterine fetal gasping
mechanical airway obstruction
Pneumonitis
surfactant inactivation
damage of umbilical vessels
all play roles in the pathophysiology of meconium
aspiration
49. 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.
50. Mechanism of Injury:
1.Mechanical Obstruction of the Airway
the initial and most important problem of the infant
with MAS
the exact incidence of large-airway obstruction is
unknown
mechanism can create:
ball valve phenomenon
air flows passed the meconium during
inspiration but is trapped distally during
expiration
increases in:
expiratory lung resistance
functional residual capacity
anterior posterior diameter of the chest
51. 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:
Pneumothorax
pneumomediastinum air leaks
Pulmonary air leaks are 10x more likely to develop in
infants with MAS than those without, and leaks often
develop during resuscitation.
52. Mechanism of injury
2. Pneumonitis
usual feature of MAS, occurring in about ½ of the
cases
Meconium 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-α
IL-1β
IL-8and reactive oxygen species.
53. 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:
fever
an abnormal WBC
decline in respiratory function
54. Mechanism of injury
3.Pulmonary vasoconstriction
the release of vasoactive mediators, such as:
eicosanoids
endothelin-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.
55. 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:
Atelectasis
decreased lung compliance/volume
poor oxygenation
57. Clinical Manifestations
Either in utero
first breath, thick, particulate meconium is
aspirated into the lungs.
small airway obstruction
respiratory distress within 1st hours
Tachypnea
Retractions
Grunting
cyanosis observed in severely affected infants.
58. Clinical Manifestations
Partial obstruction of some airways may lead to
pneumothorax
Pneumomediastinum
both
Overdistention of the chest may be prominent
condition usually improves w/in 72 hr
assisted ventilation: may be severe with a high risk
for mortality
Tachypnea may persist for many days or even
several weeks
assisted ventilation: may be severe with a high risk
for mortality
59. Clinical Manifestations
typical chest roentgenogram is characterized by :
patchy infiltrates
coarse streaking of both lung fields
increased anteroposterior diameter, and flattening
of the diaphragm
Nº 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
62. Close up of left lung demonstrating
the streaky lucencies of the air in
the interstitium (red arrows)
complicated by a pneumothorax
(yellow arrow).
63. Homogeneous density similar to respiratory
distress syndrome (RDS).
B., BB. BOY CXR
64. 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.
65. 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.
66. 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.
67. 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. efforts
2. Good muscle tone
3. Heart rate >100b/m
When this is a case-no need for tracheal
suctioning, only routine management.
68. 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‟‟.
69. Postnatal Management
Apparently well child born through MSAF
Most 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.
70. Treatment in NICU
Goals:
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.
71. 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.
72. Ventilatory support depends on the amount of
respiratory distress:
O2 hood
CPAP (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.
73. 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.
74. 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.
75. 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%.
76. 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.
77. The risk associated with laryngoscopy and
endotracheal intubation:
Bradycardia
Laryngospasm
Hypoxia
posterior pharyngeal laceration with
pseudodiverticulum formation
less than the risk of meconium aspiration
syndrome in these severe circumstances.
78. Treatment of meconium aspiration pneumonia
includes:
supportive care
standard 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.
79. Patients who are refractory to conventional
mechanical ventilation or HFV may benefit from:
surfactant therapy
regardless of gestational age
iNO
or extracorporeal membrane oxygenation (ECMO)
80. Prevention of MAS
The risk of meconium aspiration may be decreased
by:
Antepartum Period: elective induction of labor for
pregnancies at or beyond 41 weeks
Intrapartum 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
81. Prevention
Routine intrapartum oropharyngeal and
nasopharyngeal suctioning for infants born with
clear or meconium-stained amniotic fluid is no
longer recommended.
Postpartum Endotracheal Suctioning
NRP 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
82. Prognosis
The 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.
83. 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.
84. 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.
85. 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.
86. 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.
87. 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; 2011
4. Meconium-stained amniotic fluid (MSAF) Pediatrics point of view .
Fostersom / Pediatrics / Neonatology. February 2009
5. 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.
88. 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
89. Transient Tachypnea of the Newborn
Medscape 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
92. 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.
93. 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.
94. Journal Updates
GCs
reduce the penetration of neutrophils into the lungs,
decreasing their adherence to the endothelium
thereby increasing secondarily a count of
circulating neutrophils
circulating mononuclears
eosinophils
basophils
as well as the synthesis of cytokines by
Macrophages
eosinophils
T lymphocytes.
95. Journal Updates
GCs 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.
96. Journal Updates
GCs may effectively suppress:
pmn‟s inflammation
lung edema formation
pulmonary vasoconstriction.
However, the effect of the treatment depends on:
the specific properties
dose
mode of delivery of the individual GCs
as well as on the current status of the newborn or
experimental animal with MAS.
97. Journal Updates
Dexamethasone
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.
98. 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
99. Journal Updates
Concluding remarks
Despite 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.
100. Journal Updates
International Journal of Pediatrics
Volume 2012 (2012), Article ID 359571, 7 pages
doi:10.1155/2012/359571
Review Article
Advances 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, Canada
2Alberta Children's Hospital Research Institute for Child and
Maternal Health, University of Calgary, Calgary, AB, T2N 4N1,
Canada
3Department of Pediatrics, Foothills Medical Centre, Rm C211
1403-29th Street NW, Calgary, AB, T2N 2T9, Canada
Received 25 July 2011; Accepted 9 October 2011
101. Journal Updates
Abstract
Meconium 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.
102. Journal Updates
Abstract
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.
103. Journal Updates
Conclusions
Despite 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.
104. Journal Updates
Conclusions
Intrapartum 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.
105. Journal Updates
Conclusions
MAS 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.
106. Journal Updates
Conclusions
ECMO 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.
107. 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 2
February 2008
108. 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.
109. 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.
110. 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.
111. 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.
112. 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.
113. 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.
114. 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.
