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Meconium Aspiration Syndrome

ANATOMIC ALTERATION OF THE LUNGS
a. During normal intrauterine fetal development b. Physical presence of the meconium may result
➢ the fetus periodically demonstrates in an upper airway obstruction at birth because
normal rapid, shallow respiratory chest of the high viscosity of the meconium
movements, ➢ clumps of meconium can rapidly migrate
➢ pulmonary fetal fluid moves into and out of past,
the oropharynx, ➢ the glottis and penetrate the smaller
airways,
➢ glottis remains closed. ➢ meconium may already be present in the
b. During periods of fetal hypoxemia distal airways at birth,
➢ fetus may demonstrate very deep, ➢ when thick particulate meconium is
,

➢ gasping inspiratory movements that may aspirated into the small airways, the
force the contents of the nasopharynx to meconium can partially or totally obstruct
pass through the glottis into the airway, the airways,
➢ aspirate may contain meconium and ➢ Airways that are partially obstructed are
affected by a “ball-valve” effect.
amniotic fluid.
MECONIUM
➢ Excessive hyperinflation may lead to
➢ material that collects in the intestine of the alveolar rupture and air leak syndromes
fetus and forms the first stools of the such as pneumomediastinum or
newborn, pneumothorax.
➢ odorless, thick, sticky, blackish green
c. As a consequence of the hypoxemia
material,
associated with MAS, infants with the condition
➢ heterogeneous mixture of intestinal
often develop hypoxia-induced pulmonary
tract secretions, amniotic fluid, pulmonary
arterial vasoconstriction and vasospasm,
fetal fluid, and intrauterine debris.
which cause pulmonary hypertension.
ASPIRATION OF MECONIUM LEADS TO ONE OR
➢ blood shunting from right-to-left,
MORE OF THE FOLLOWING COMPLICATIONS:
➢ intrapulmonary shunts are also occasionally
a. MAS Meconium Aspiration Syndrome seen,
causes a chemical pneumonitis
➢ characterized by an acute ➢ pulmonary hypoperfusion,
inflammatory reaction and edema of the ➢ persistent pulmonary hypertension of
bronchial mucosa and alveolar epithelium
➢ leads to excessive bronchial secretions the neonate.
and alveolar consolidation
➢ Meconium also promotes the growth
of bacteria
➢ can also interfere with alveolar
pulmonary surfactant production
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MAJOR PATHOLOGIC OR STRUCTURAL

CHANGES ASSOCIATED WITH MAS ARE AS RADIOLOGIC FINDINGS (Chest Radiograph)

FOLLOWS:
a. Partially obstructed airways, air trapping, and
alveolar hyperinflation;
➢ Pulmonary air leak
syndromes (pneumomediastinum or
pneumothorax),
➢ Totally obstructed airways and
absorption atelectasis,
➢ Edema of the bronchial mucosa and
alveolar epithelium,
➢ Excessive bronchial secretions,
➢ Alveolar consolidation (or secondary
infection),
➢ Disrupted pulmonary surfactant production

ETIOLOGY AND EPIDEMIOLOGY

➢ 10,000 to 15,000 infants are diagnosed

with MAS annually
➢ 30% of them will require mechanical
ventilation
➢ 10% to 15% will develop pneumothorax
➢ fetal hypoxemia and stress
➢ rarely is seen in infants born at less than 36
weeks
➢ Post-term infants are especially at risk for
MAS
➢ Other infants who are at high risk for MAS
are those who are small for gestational age

CLINICAL DATA OBTAINED AT THE PATIENT’S

BEDSIDE

a. The Physical Examination

1. Vital Signs
➢ Increased Respiratory Rate (Tachypnea)
➢ Increased Heart Rate Pulse) and
Blood Pressure Apnea
2. Clinical Manifestations Associated with More
Negative Intrapleural Pressure during
Inspiration
3. Chest Assessment Findings
4. Expiratory Grunting
5. Cyanosis
6. Common General Appearance
7. Barrel chest (when airways are partially
obstructed)
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Congenital Heart Disease

CONGENITAL HEART DISEASES (CHDS)
➢ CHDs can involve the interior walls of the
heart, valves inside the heart, or arteries
and veins that carry blood to the heart or
body
➢ CHDs are the most common type of
birth defect, affecting 8 of every 1000
newborns.
➢ Nearly 40,000 infants are born with a
heart defect each year in the United
States, and more than 1 million adults are
living with CHD here
CHDS COMMONLY ENCOUNTERED BY THE
RESPIRATORY THERAPIST INCLUDE:
ETIOLOGY AND EPIDEMIOLOGY
➢ prematurity, low birth weight, high altitude
and low atmospheric oxygen tension,
hypoxia, and a variety of chromosomal
abnormalities
➢ more common in premature
➢ twice as common in girls as in boys
DIAGNOSIS
➢ based upon its characteristic clinical finding
➢ confirmed by echocardiography
➢ echocardiographic imaging
➢ Doppler color flow mapping

➢ patent ductus arteriosus (PDA),

CLINICAL MANIFESTATION
➢ atrial septal defect (ASD),
➢ ventricular septal defect (VSD),
➢ tetralogy of Fallot (TOF), and ➢ When PDA is complicated by persistent
➢ transposition of the great arteries (TGA) pulmonary hypertension of the newborn, the
clinical manifestations include:
HYPEROXIA TEST
✓ tachycardia, dyspnea, differential
➢ determine whether the infant’s cyanosis, low PaO2 and SpO2, increased
cyanosis is caused by lung disease or a
CHD (e.g., TOF or TGA) PaCO2, loud systolic/diastolic murmur
➢ the general procedure required for at the upper left sternal border,
the hyperoxia test is as follows:
➢ first, obtain an arterial blood gas (ABG) cardiomegaly, left subclavicular thrill,
➢ If hypoxemia is present, the infant is then prominent left ventricular impulse,
placed on an FIO2 of 1.0 (e.g., head hood)
for 10 minutes bounding pulse, , and widened pulse
➢ followed by a second ABG pressure.
➢ Complications of PDA in the newborn include
PATENT DUCTUS ARTERIOSUS pulmonary edema, congestive heart failure,
➢ Anatomic Alterations of the intraventricular hemorrhage, necrotizing
Heart Patent ductus enterocolitis, and bronchopulmonary dysplasia
arteriosus due to prolonged ventilator and/or oxygen

➢ congenital heart defect in which the ductus support

arteriosus
➢ normally open during fetal life, fails to close
shortly after birth
➢ a portion of the oxygenated blood from the
aorta flows through the open ductus back to the
pulmonary artery
➢ pathophysiologic effect of a PDA is a left-
to- right shun
➢ PDA results in excessive blood flow
through the pulmonary circulation and
hypoperfusion of the systemic circulation
✓ PDA patients who are 3 to 6
weeks old
commonly present with tachypnea,
diaphoresis, inability or difficulty with feeding,
and weight loss or no weight gain
✓ In the adult whose PDA has
undiagnosed, the signs and symptoms
include congestive heart failure, atrial
arrhythmia, and differential cyanosis
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CLINICAL MANIFESTATIONS
TREATMENT
➢ can present at any age
Medication ➢ small ASD, the baby may not have any
➢ catheter-based procedures
remarkable signs or symptoms
➢ surgery
➢ oxygen therapy protocol ➢ clinical manifestations are dependent on the
➢ bronchopulmonary hygiene therapy protocol, size of the defect and the degree of shunting
➢ lung expansion therapy protocol between the atria
➢ aerosolized medication therapy protocol ➢ some infants with a moderate to large ASD
➢ and ventilator support protocols ➢ older patient, common signs and symptoms
include
ATRIAL SEPTAL DEFECT
➢ In all ages, a moderate to large ASD
Anatomic Alterations of the Heart
TREATMENT
Atrial septal defect
➢ based on the seriousness of the signs and
➢ a hole in the septal wall between the right and symptoms and the size of the ASD
left atrium ➢ Catheter-based procedures/surgery
➢ oxygen therapy protocol, bronchopulmonary
2 most common types of ASD: ostium secundum ASD hygiene therapy protocol, lung expansion
and the primum ASD therapy protocol, aerosolized medication
a. Ostium secundum ASD therapy protocol, and ventilator support
protocols
➢ caused by arrested growth of the secundum
septum or excessive absorption of the primum VENTRICULAR SEPTAL DEFECT
septum
➢ resulting in an atrial septal wall defect Anatomic Alterations of the Heart
➢ presents as an isolated cardiac defect in the
fossa ovali Ventricular septal defect

b. Primum ASD ➢ an opening in the ventricular septum of

➢ caused by arrested growth of the apical portion the heart
of the atrial septum ➢ may be one or more openings in different
➢ associated with an anterior mitral valve clef locations of the ventricular septum

DEGREE OF PATHOPHYSIOLOGY ASSOCIATED common locations include:

WITH AN ASD DEPENDS ON: ✓ Conoventricular Ventricular Septal Defect
(1) the pulmonary and systemic vascular resistances ✓ Inlet Ventricular Septal Defect
✓ Perimembranous Ventricular Septal
(2) the compliance of the left and right ventricles, and Defect
✓ Muscular Ventricular Septal Defect
(3) the size of the ASD
At birth, the following physiologic events normally
occur: (1) an immediate fall in pulmonary vascular
ETIOLOGY AND EPIDEMIOLOGY
resistance, (2) the removal of the low resistance
➢ common and account for approximately 13% of placenta from circulation
all patients with CHD
(3) the closure of the ductus arteriosus
➢ over 1900 infants in the United States are born
each year with an ASD A VSD has the following two net effects:
➢ ASDs are not known, abnormal genes in
combination with certain maternal risk factors 1. the influx of blood into the right ventricle from
are believed to play a role the left ventricle increases the right ventricular
pressure and volume
DIAGNOSIS 2. the circuitous route of blood through the lungs
and back to the heart causes a volume
➢ based upon its characteristic clinical
overload
manifestations and confirmed by
echocardiography ETIOLOGY AND EPIDEMIOLOGY
➢ 2-dimensional echocardiographic imaging and
Doppler color flow mapping is both sensitive ➢ most common congenital heart disorder
and specific for the identification of ASD. ➢ 50% of all patients with CHD
➢ prevalence of VSD is about 42 of 10,000
babies each year
➢ causes of VSDs are not known
➢ abnormal genes in combination with certain
maternal risk factors

DIAGNOSIS
based upon its characteristic clinical findings and
confirmed by echocardiography
➢ 2-dimensional e
chocardiographic imaging and
Doppler color flow mapping
CLINICAL MANIFESTATIONS
➢ When the VSD is moderate or large, the
early clinical manifestations include
tachycardia, tachypnea, increased work of
breathing, poor weight gain, failure to
thrive, and diaphoresis
➢ Cardiac clinical manifestations include
systolic murmurs at the mid-to-lower left
sternal border, an increased second
heart sound (S2), diastolic murmurs at
the apex (indicates a Qp/Qs of 2 :1
or greater), and diastolic murmurs at the
midto-lower sternal border
➢ In patients with VSD and aortic
regurgitation, the left ventricle is especially
overloaded
➢ Clinical features include neck
pulsations, bounding pulse, wide pulse
pressure, early diastolic murmur,
diaphoresis, and vigorous precordial
movement
➢ volume and pressure loads on the left and
right ventricles. The chest radiograph
may show increased pulmonary vascular
markings, and enlargement of the left
atrium, left ventricle and pulmonary artery
TREATMENT
➢ medications to support the heart (e.g.,
digitalis and diuretics)
➢ oxygen therapy protocol,
bronchopulmonary hygiene therapy
protocol, lung expansion
therapy protocol, aerosolized medication
therapy protocol, and ventilator support
protocols—are all administered as needed
TETRALOGY OF FALLOT ANATOMIC
ALTERATIONS OF THE HEART
Tetralogy of Fallot (TOF) is a congenital heart defect
with the following four major anatomic alterations:
➢ Stenosis of the pulmonary artery
➢ Deviation of the aorta to the right
➢ Ventricular septal defect
➢ Right ventricular hypertrophy
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The pathophysiologic effects—and clinical
symptoms—of TOF are largely dependent upon the
degree of right ventricular outflow tract obstruction
One of the unique physiologic features of TOF is that
the right ventricular outflow tract obstruction often
fluctuates in response to transient increases and
decreases in the resistance caused by obstruction.
ETIOLOGY AND EPIDEMIOLOGY
➢ prevalence of TOF in the United States is
about 4 per 10,000 live births, and it
accounts for about 7% to 10% of the CHDs
➢ about 1600 infants are born each year
with TOF
➢ most common congenital heart disorder to
require intervention in the first year of life and
occurs equally in males and female
➢ causes of TOF are not known, abnormal genes
in combination with certain maternal risk
factors
DIAGNOSIS
➢ confirmed by echocardiography
➢ electrocardiogram and chest radiography
➢ Cardiac catheterization
CLINICAL MANIFESTATION
➢ depends on the degree of right
ventricular outflow tract obstruction
➢ cyanosis—i.e., “hypercyanotic “or “tet”
spells
➢ Oxygen saturation during hypercyanotic
spells is low
➢ prominent right ventricular impulse and
systolic thrill
➢ early systolic click (called an aortic
ejection click) along the left sternal
border may be heard
➢ Symptoms of heart failure may be
present
➢ heart murmur is commonly heard
TREATMENT
- medical care
- surgical palliative care and
- intracardiac repair, and
- long-term postoperative care
- need for medical intervention
- intravenous prostaglandin therapy (alprostadil)
- knee-chest positioning
- Intracardiac repair
- oxygen therapy protocol, bronchopulmonary
hygiene therapy protocol, lung expansion
therapy protocol, aerosolized medication
therapy protocol, and ventilator support
protocols—are all administered as needed

most common cyanotic congenital heart lesion that
presents in neonate
- a congenital heart defect in which the
pulmonary artery and the aorta are switched in
position, or transposed
- the most common form of TGA is the
dextrotransposition of the great arteries
- results in a pulmonary and systemic circulation
that functions in “parallel,” rather than “series.”
- This heart defect produces a right-to-left
shunt—a cyanotic disorder
The most common heart defects are the following:
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
When no other heart defects are present, it is
called Simple Transposition of the Great
Arteries (simple TGA)
When other defects are present, it is a Complex
Transposition of the Great Arteries (complex
TGA)
ETIOLOGY AND EPIDEMIOLOGY
- prevalence of TGA ranges from 2.3 to 4.7 per
10,000 live births
- approximately 1900 babies are born with TGA
each year
- associated with poor nutrition during
pregnancy, rubella, or other viral illness during
pregnancy, alcoholism, maternal age over 40
years, and Down’s syndrome
DIAGNOSIS
- based on clinical suspicion of an underlying
cyanotic CHD and is confirmed by
echocardiography
CLINICAL MANIFESTATIONS
Infants with TGA
- cyanosis, tachypnea (respiratory rates >60
breaths/min), poor feeding, and clubbing of
fingers and toes
- When there is a VSD, a pan systolic murmur is
usually present within a few days after birth at
the lower left sternal borders
In the patient with left ventricular outflow obstruction
- there may be a systolic ejection murmur3 along
the upper left sternal border
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TREATMENT
- directed at stabilizing the patient’s cardiac and
pulmonary function and ensuring adequate
systemic oxygenation
- prostaglandin E1 (alprostadil) therapy
- balloon atrial septostomy (BAS)
- surgical repair
➢ oxygen therapy protocol, bronchopulmonary
hygiene therapy protocol, lung expansion
therapy protocol, aerosolized medication
therapy protocol, and ventilator support
protocols—are all administered as needed
CROUP SYNDROME:
LARYNGOTRACHEALBRONCHITIS AND ACUTE
EPIGLOTTITIS
CROUP
- “barking or brassy sound” associated with a
partial upper airway obstruction
- Inspiratory barking sound heard in a patient
with a partial upper airway obstruction
- croup and laryngotracheobronchitis (LTB)
- Acute epiglottitis
- two types of partial upper airway
disorders—
LTB and acute epiglottis
ANATOMIC ALTERATIONS OF THE UPPER
AIRWAY
LARYNGOTRACHEOBRONCHITIS
- can affect the lower laryngeal area, trachea,
and occasionally the bronchi
- synonym for “classic” subglottic obstruction
- inflammatory process that causes edema and
swelling of the mucous membranes
- when edema develops in the upper airway,
fluid spreads and accumulates quickly
throughout the connective tissue
- The edema and swelling in the subglottic
region decrease the ability of the vocal cords to
abduct (move apart) during inspiration.
ACUTE EPIGLOTTIS
- a life-threatening emergency
- inflammation of the supraglottic region, which
includes the epiglottis, aryepiglottic folds, and
false vocal cords
- does not involve the pharynx, trachea, or other
subglottic structure
- As the edema in the epiglottis increases, the
lateral borders curl and the tip of the epiglottis
protrudes posteriorly and inferiorly

The major pathologic or structural changes associated
with inspiratory stridor are as follows:
LTB
EPIGLOTTITIS
ETIOLOGY AND EPIDEMIOLOGY
1. Laryngotracheobronchitis
- parainfluenza viruses cause most cases of
LTB
- also may be caused by influenza A and B,
respiratory syncytial virus (RSV), herpes
simplex virus, Mycoplasma pneumoniae,
rhinovirus, and adenoviruse
- seen in children 6 months to 5 years of age
- Boys are affected slightly more often than girls
- The onset of LTB is slow
- most common during the fall and winter
- child’s voice is hoarse, and the inspiratory
stridor is typically loud and high in pitch
- a bacterial infection that is almost always
caused by Haemophilus influenzae type B
- transmitted via aerosol droplets
- other causes of epiglottitis include aspiration of
hot liquid and trauma from repeated intubation
attempts
- may develop in all age groups
- most often occurs in children 2 to 6 years of
age
- Boys are affected more often than girls
- onset of epiglottitis is usually abrupt
- As the supraglottic area becomes swollen,
breathing becomes noisy, the tongue is often
thrust forward during inspiration, and the child
may drool
- typically seen in patients with neck trauma and
- those who have been intubated repeatedly,
and in drug abuse (crack cocaine) case
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CLINICAL DATA OBTAINED AT THE PATIENT’S
BEDSIDE The Physical Examination
1. Vital signs
- Increased Respiratory Rate (Tachypnea)
- Increased Heart Rate (Pulse) and Blood
Pressure
2. Chest Assessment Findings
3. Inspiratory Stridor
- slight narrowing of the upper (extrathoracic)
airway that naturally occurs during inspiration is
insignificant
- when the cross-section of the upper airway is
reduced because of the edema, the child will
generate stridor during inspiration
4. Cyanosis
5. Use of Accessory Muscles During Inspiration
6. Substernal and Intercostal Retractions
LATERAL NECK RADIOGRAPH
- Haziness in the subglottic area (LTB)
- Haziness in the supraglottic area (epiglottitis)
- Classic “thumb sign” (epiglottitis)
ANTERIO-POSTERIOR NECK RADIOGRAPH
- “Steeple point” or “pencil point” narrowing of
the upper airway (LTB)
- A lateral neck radiograph is usually done first to
rule out the diagnosis of epiglottitis
- “thumb sign”
- “pencil point” or “steeple point”
GENERAL MANAGEMENT OF
LARYNGOTRACHEOBRONCHITIS AND
EPIGLOTTITIS
- Early recognition of epiglottitis may save a
patient’s life; it is a true airway emergency
- Once the diagnosis is suspected or
confirmed by the lateral neck radiograph,
examination or
inspection of the pharynx and larynx is
only to be done in the operating room
under general
anesthesia with a fully trained team
- The patient with a confirmed
diagnosis of acute epiglottitis should
be intubated immediately
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AFTER THE DIAGNOSIS IS ESTABLISHED, THE
GENERAL MANAGEMENT OF LTB AND ACUTE
EPIGLOTTITIS IS AS FOLLOWS:
4. Antibiotic Therapy
- Because acute epiglottitis is almost always
caused by H. influenzae type B, appropriate
antibiotic therapy is part of the treatment plan
- Ceftriaxone (Rocephin) and Ampicillin/
sulbactam (Unasyn)

1. Supplemental Oxygen
- hypoxemia and significant work of breathing is 5. Endotracheal Intubation or Tracheostomy
associated with both LTB and - If the patient is anxious, restless, or
epiglottitis, uncooperative, restraints and sedation may be
supplemental oxygen may be required needed to prevent accidental extubation
- Oxygen therapy should be started when - After intubation, the patient should be
the patient’s SpO2 is under 92% transferred to the intensive care unit (ICU) and
placed on continuous positive airway pressure
(CPAP) or pressure support ventilation
- Mechanical ventilation.
2. Racemic Epinephrine
- Aerosolized racemic epinephrine is
administered to children with LTB
- Using the patient’s LTB score, the
administration of racemic epinephrine protocol
is as follows:
- • 3–5: Consider racemic epinephrine
- • >6: Administer racemic epinephrine 0.5 mL in
3 mL normal saline

3. Corticosteroids
- such as dexamethasone, have been shown to
reduce the severity and duration of LTB
- given when the patient presents with moderate
to severe symptoms
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