RESPIRATORY DISTRESS SYNDROME

DEFINITION

Respiratory distress syndrome (RDS), also called hyaline membrane disease

(HMD),is the result of a primary absence, deficiency, or alteration in the
production of pulmonary surfactant.

INCIDENCE

It is a complex disease that affects approximately 20,000 to 30,000 infants a

year in the United States, most of whom are preterm infants. RDS is a
complication in about 1% of pregnancies. The syndrome occurs more frequently
in premature Causasian infants than in infants of African descent and almost
twice as often in males as in females.

CAUSES

1. Prematurity: All preterm newborns—whether AGA, SGA, or LGA—and

especially infants of diabetic mothers are at risk for RDS. The incidence of RDS
increases with the degree of prematurity, and most deaths occur in newborns
weighing less than 1500 g. The maternal and fetal factors resulting in preterm
labor and birth, complications of pregnancy, caesarean birth (and its
indications), and familial tendency are all associated with RDS.

2. Surfactant deficiency disease: Normal pulmonary adaptation requires

adequate surfactant, a lipoprotein that coats the inner surfaces of the alveoli.
Surfactant provides alveolar stability by decreasing the alveoli’s surface tension
and tendency to collapse. Surfactant is produced by type II alveolar cells
starting at about 24 weeks’ gestation. In the normal or mature newborn lung, it
is continuously synthesized, oxidized during breathing, and replenished.
Adequate surfactant levels lead to better lung compliance and permit breathing
with less work. RDS is due to alterations in surfactant quantity, composition,
function, or production
PATHOPHYSIOLOGY
Development of RDS indicates a failure to synthesize surfactant, which is
required to maintain alveolar stability. On expiration this instability increases
atelectasis (lung collapse), which causes hypoxia and acidosis because of the
lack of gas exchange. These conditions further inhibit surfactant production and
cause pulmonary vasoconstriction. The resulting lung instability causes the
biochemical problems of hypoxemia (decreased Po2), hypercarbia (increased
Pco2), and acidemia (decreased pH), which further increases pulmonary
vasoconstriction and hypoperfusion. The cycle of events of RDS leading to
eventual respiratory failure. Because of these pathophysiologic conditions, the
newborn must expend increasing amounts of energy to reopen the collapsed
alveoli with every breath, so that each breath becomes as difficult as the first.
The progressive expiratory atelectasis upsets the physiologic homeostasis of the
pulmonary and cardiovascular systems and prevents adequate gas exchange.
Breathing becomes progressively harder as lung compliance decreases, which
makes it more difficult for the newborn to inflate the lungs and breathe.
CLINICAL ASSESSMENT

Clinical picture Significance

Skin Color
Pallor or mottling These represent poor peripheral
circulation due to systemic
hypotension and vasoconstriction and
pooling of independent areas (usually
in conjunction with severe hypoxia).
Cyanosis (bluish tint) Depending on hemoglobin
concentration, peripheral circulation,
intensity and quality of viewing light,
and acuity of observer’s color vision,
this is frankly visible in advanced
hypoxia. Central cyanosis is most
easily detected by examination of
mucous membranes and tongue.

Jaundice (yellow discoloration of skin Metabolic alterations (acidosis,

and mucous membranes due to hypercarbia, asphyxia) of respiratory
presence of unconjugated [indirect] distress mean the newborn is
bilirubin) predisposed to having bilirubin
dissociate from albumin binding sites
and be deposited in the skin and
central nervous system.

Edema (presents as slick, shiny skin)

This is characteristic of preterm infants
because their total protein
concentration is low, with a decrease
in colloidal osmotic pressure and
 transudation of fluid. Edema of hands
and feet is frequently seen within first
24 hours and resolved by fifth day in
infants with severe RDS

Respiratory System
Tachypnea (normal respiratory rate Increased respiratory rate is the most
30–60/minute, elevated respiratory frequent and easily detectable sign of
rate 60/minute) respiratory distress after birth. This
compensatory mechanism attempts to
increase respiratory dead space to
maintain alveolar ventilation and gas
exchange in the face of an increase in
mechanical resistance. As a
decompensatory mechanism, it
increases workload and energy output
by increasing respiratory rate, which
causes increased metabolic demand for
oxygen and thus increases alveolar
ventilation on an already overstressed
system. Shallow, rapid respirations
increase dead space ventilation, thus
decreasing alveolar ventilation.
Apnea (episode of nonbreathing for This poor prognostic sign indicates
more than 20 seconds; periodic cardiorespiratory disease, CNS
breathing, a common “normal” disease, metabolic alterations,
occurrence in preterm infants, is intracranial hemorrhage, sepsis, or
defined as apnea of 5–10 seconds immaturity. Physiologic alterations
alternating with 10–15 seconds of include decreased oxygen saturation,
ventilation) respiratory acidosis, and bradycardia

Inspection of the thoracic cage

Chest includes shape, size, and symmetry of
movement. Respiratory movements
should be symmetric and
diaphragmatic; asymmetry reflects
pathology (pneumothorax,
diaphragmatic hernia). Increased
anteroposterior diameter indicates air
trapping (meconium aspiration
syndrome).
Labored respirations Indicates marked increase in the work
of breathing.

These reflect the significant increase in

negative intrathoracic pressure
Retractions (inward pulling of soft necessary to inflate stiff, noncompliant
parts of the chest cage—suprasternal, lungs. Infants try to increase lung
substernal, intercostal, subcostal— at compliance by using accessory
inspiration) muscles. Lung expansion markedly
decreases. See saw respirations are
seen when the chest flattens with
inspiration and the abdomen bulges.
Retractions increase the work of
breathing and oxygen need so that
assisted ventilation may be necessary
due to exhaustion.
Flaring nares (inspiratory dilation of This compensatory mechanism
nostrils) attempts to lessen the resistance of the
narrow nasal passage.

Expiratory grunt (Valsalva maneuver This increases trans pulmonary

in which the infant exhales against a pressure, which decreases or prevents
closed glottis, thus producing an atelectasis, thus improving
audible moan) oxygenation and alveolar ventilation.
Rhythmic body movement with Intubation should not be tried unless
labored respirations (chin tug, head the infant’s condition is rapidly
bobbing, retractions of anal area) deteriorating, because it prevents this
maneuver and allows the alveoli to
collapse.
This is a result of using abdominal and
other respiratory accessory muscles
during prolonged forced respirations.
Decrease in breath sounds and distant
Auscultation of chest reveals quality may indicate interstitial or intra
decreased air exchange, with harsh pleural air or fluid.
breath sounds or fine inspiratory rales;
rhonchi may be present
Cardiovascular System
Continuous systolic murmur may be Patent ductus arteriosus is common
audible with hypoxia, pulmonary
vasoconstriction, right-to-left shunting,
and congestive heart failure.
Heart rate usually within normal limits A fixed heart rate indicates a decrease
(fixed heart rate may occur with a rate in vagal control.
of 110–120/minute)
Point of maximal impulse usually Displacement may reflect
located at fourth to fifth intercostal dextrocardia, pneumothorax, or
space, left sternal border diaphragmatic hernia.
Hypothermia This is inadequate functioning of
metabolic processes that require
oxygen to produce necessary body
heat.
Muscle Tone
These may indicate deterioration in the
Flaccid, hypotonic, unresponsive to newborn’s condition and possible CNS
stimuli Hypertonia and/or seizure damage due to hypoxia, acidemia, or
activity hemorrhage.
MANAGEMENT

Goal

The goals of postnatal therapy are to maintain adequate oxygenation and

ventilation, correct acid-base imbalance, and provide the supportive care
required to maintain homeostasis

Pharmacological management

Morphine or fentanyl: is used for its analgesic and sedative effects. Sedation
may be indicated for infants who have air leak respiratory problems.

pancuronium (Pavulon) :is used for muscle relaxation in infants with RDS is
controversial.

Supportive medical management

1. ventilation therapy: Ventilation therapy is directed toward preventing

hypoventilation and hypoxia. Mild cases of RDS may require only increased
humidified oxygen concentrations. Moderately afflicted infants may need
 continuous positive airway pressure (CPAP). Babies with severe RDS
require mechanical ventilatory assistance from a respirator
2. transcutaneous oxygen and carbon dioxide monitoring
3. blood gas monitoring
4. correction of acid-base imbalance
5. environmental temperature regulation
6. adequate nutrition
7. protection from infection.

Surgical management

High-frequency and extracorporeal membrane oxygenation (ECMO): a

form of heart-lung bypass, has been tried when conventional ventilator therapy
has not been successful. Both of these have specific protocols for eligibility for
use and require specially trained nurses and respiratory therapists.

Nitric oxide inhalation therapy: may also be a useful adjunctive therapy for
infants with RDS.

COMPLICATIONS

1.Hypoxia.

As a result of hypoxia, pulmonary blood vessels constrict and their resistance

increases, which reduces pulmonary blood flow. The increase in pulmonary
blood vessel resistance may cause a return to fetal circulation as the ductus
opens and blood flow is shunted around the lungs. This shunting increases the
hypoxia and further decreases pulmonary perfusion. Hypoxia also causes
impairment or absence of metabolic response to cold; reversion to anaerobic
metabolism, resulting in lactate accumulation (acidosis); and impaired cardiac
output, which decreases perfusion to vital organs.

2. Respiratory acidosis
 Persistently rising Pco2 and decreases in pH are poor prognostic signs of
pulmonary function and adequacy because increased Pco2 and decreased pH are
results of alveolar hypoventilation.

3. Metabolic acidosis

Because the cells lack oxygen, the newborn begins an anaerobic pathway of
metabolism, with an increase in lactate levels and a resulting base deficit (loss
of bicarbonate). As the lactate levels increase, the pH decreases in an attempt to
maintain acid-balance homeostasis

NURSING MANAGEMENT

ASSESSMENT

a) Look for characteristics of RDS such as increasing cyanosis, tachypnea (>

60 respirations/min), grunting respirations, nasal flaring, significant
retractions, and apnea.
b) Assess the signs of respiratory distress: The Silverman-Andersen index
may be helpful in evaluating the signs of respiratory distress in the birthing
area.

NURSING DIAGNOSIS

i) Risk for Ineffective Breathing Pattern related to immature lung development

ii) Ineffective Thermoregulation related to increased respiratory effort
iii) Risk for Ineffective Breathing Pattern related to immature lung development
iv) Ineffective Thermoregulation related to increased respiratory effort

PLANNING AND IMPLEMENTATION

1. Based on clinical parameters, the neonatal nurse implements therapeutic

approaches to maintain physiologic homeostasis and provides supportive
care to the newborn with RDS.
2. Nursing interventions and criteria for instituting mechanical ventilation
depend on institutional protocol.
3. These infants have severe respiratory distress and are cared for in NICUs by
nurses with advanced knowledge and training.
4. Ventilatory assistance with high-frequency ventilators has shown positive
results.
5. The parents of a baby with respiratory distress will need a very supportive
environment.

EVALUATION

Expected outcomes of nursing care include the following:

1) The newborn at risk of RDS is promptly identified and early intervention is

initiated The newborn is free of respiratory distress and metabolic
alterations.
2) The parents verbalize their concerns about their baby’s health problem and
survival and understand the rationale behind the management of their
newborn
ASPHYXIA NEONATORUM

DEFINITION

Asphyxia neonatorum is a condition that occurs when a baby doesn’t get

enough oxygen during the birth process. It can be fatal. Another more common
name for it is perinatal asphyxia, or birth asphyxia. Hypoxic-ischemic
encephalopathy may be a result of severe asphyxia neonatorum.

INCIDENCE

The frequency of perinatal asphyxia is approximately 1% to 5 %of live birth in

the western countries.

ETIOLOGY

a. Factors that increase the risk of perinatal asphyxia include the

following

i) Impairment of maternal oxygenation

ii) Decreased blood flow from mother to placenta

iii) Decreased blood flow from placenta to fetus

iv) Impaired gas exchange across the placenta or at the fetal tissue level
 v) Increased fetal O2 requirement

b.etiologies of perinatal hypoxia- ischemia include the following

i) Maternal factors:hypertension, infection,diabetes,hypotension

ii) Placenta; factors:infarction, fibrosis, abruption, hydrops

iii) Uterine rupture

iv) Umbilical cord accidents:prolapsed,compression

v) Abnormalities of umbilical vessels

vi) Fetal factors: anemia, infection, cardiomyopathy

PATHOPHYSIOLOGY

SYMPTOMS

1. Skin that appears pale or blue

2. Difficulty breathing, which may cause symptoms such as nasal flaring or

abdominal breathing

3. A slow heart rate

4. Weak muscle tone

DIAGNOSTIC EVALUATION

a) Perinatal assessment of risk:includes awareness of pre-existing maternal or

fetal problems that may predispose to perinatal asphyxia and of changing
 placental and fetal conditions ascertained by usg , biophysical profile, non
stress test

b) Clinical presentations: can be variable. Common clinical scenarios include a

postdates infant with asphyxia, meconium aspiration, pulmonary
hypertension, pneumothorax or birth trauma

c) Low apgar score:apgar score <3>5 minutes

d) Umbilical cord or first blood gas determination

MANAGEMENT

A. PERINATAL MANAGEMENT OF HIGH RISK PREGNANCIES

 Fetal HR rhythm abnormalities may provide supporting evidence of

asphyxia,especially if accompanied by bpresence of thick meconium

 Measurement of fetal scalp pH is a better determinents of fetal oxygenation

than Po2.

 Close monitoring of progress of labor with awareness of other sign of in

utero stress.

B. DELIVERY ROOM MANAGEMENT

i) A= Establish open airway: Suctioning, if necessary endotracheal

intubation

ii) B= Breathing: Through tactile stimulation, PPV, bag and mask, or

through endo tracheal tube
 iii) C= Circulation: Through chest compressions and medications if needed

iv) D= Drugs: Adrenaline .01 of .1 solution

v) Hypothermia treatment to reduce the extent of brain injury

vi) Epinephrine 1:1000 (0.1-0.3ml/kg) IV

vii) Saline solution for hypovolemia

C. POSTNATAL MANAGEMENT OF NEUROLOGIC EFFECTS OF

ASPHYXIA

 Ventilation:CO2 should be maintained in the normal range. Hypercapnia can

cause cerebral acidosis and cerebral vasodilation

 Oxygenation: Oxygen levels should be maintained in the normal range,

although poor peripheral perfusion may limit the accuracy of continuous non
invasive monitoring

 Temperature: should be maintained in the normal range and hyperthermia

should be avoided

 Maintain physiologic metabolic state:

i) Hypocalcemia is a common metabolic alteration after neonatal asphyxia. It is
important to maintain calcium in the normal range

ii) Hypoglycaemia is often seen in asphyxiated infants:blood glucose level

should be maintained in the normal range for term infants

 Judicious fluid management:is needed and fluid over load should be avoided

 Control of seizures: use anticonvulsants

D. MANAGEMENT OF OTHER TARGET ORGAN INJURY

 Cardiac dysfunction should be managed with correction of hypoxemia,

acidosis and hypoglycaemia and avoidance of fluid over load

 Arterial BP should be maintained

 CVP should be monitored

 Renal function should be monitored

 Feeding should be with held until good boel sounds are heard and stools are
negative for blood

NURSING ASSESSMENT AND DIAGNOSIS

i) Communication between the obstetric office or clinic and the birthing area
helps the birthing area nurse identify new-borns who may need resuscitation.

ii) When the woman arrives in the birthing area, have the antepartal record
ready.
iii) Note any contributory perinatal history factors and assess present fetal status.

iv) As labor progresses, continue ongoing monitoring of fetal heartbeat and its
response to contractions, assist with fetal scalp blood sampling, and observe
for the presence of meconium in the amniotic fluid to assess for fetal
asphyxia.

v) Alert the resuscitation team and the pracitioner responsible for the newborn’s
care of any potential high-risk laboring women.

PLANNING AND IMPLEMENTATION

Hospital-Based Nursing Care

i) In the high-risk nursery, resuscitation may be needed at any time. Check and
maintain equipment to ensure its reliability at all times. Inspect all
equipment, bag and mask, oxygen and flow meter, laryngoscope, and suction
machine for damaged or non functioning parts before a birth or when setting
up an admission bed. Sterilize resuscitative equipment in the birthing room
after each use.

ii) Asystematic check of the emergency cart and equipment is a routine

responsibility of each shift. It is a good idea to be prepared by assembling
equipment for pH and blood gas determination.

iii) During resuscitation it is essential to keep the newborn warm. Dry the
newborn quickly with warmed towels or blankets to prevent evaporative heat
loss, remove the wet blankets, and place him or her under the radiant
warmer.
iv) This device provides an overhead radiant heat source (a thermostatic
mechanism taped to the infant’s abdomen triggers the radiant warmer to turn
on or off to maintain consistent temperature). Set the servo control at 36.5 ̊C
(97.7 ̊F). Cover the newborn’s head with a hat as the head is a major source
of heat loss

v) An open bed is necessary for easy access to the newborn. Training and
knowledge about resuscitation are vital to personnel in the birth setting for
both normal and at-risk births. Since resuscitation must be a two-person
effort for high-risk newborns, call for additional support as needed.

vi) One member must have the skill to perform airway management and
ventilation. Record resuscitative efforts on the newborn’s chart so that all
members of the healthcare team have access to the information.

Parent Teaching

i) The new CPR guidelines favor family members being present during
resuscitation in the birthing room and in the neonatal intensive care unit
(NICU), but the procedure is particularly distressing for parents.

ii) Advise parents that a support person will be available for them if
resuscitation is necessary.

iii) As soon as the infant’s condition has stabilized, a member of the

interdisciplinary team needs to discuss the newborn’s condition with the
parents.

iv) The parents may have many fears about the reasons for resuscitation and the
condition of their baby after resuscitation.
EVALUATION

Expected outcomes of nursing care include the following:

i) The newborn requiring resuscitation is promptly identified, and intervention

is started early.

ii) The newborn’s metabolic and physiologic processes are stabilized, and
recovery is proceeding without complications.

iii) The parents can verbalize the reason for resuscitation and what was done to
resuscitate their newborn.

iv) The parents can verbalize their fears about the resuscitation process and
potential implications for their baby’s future.

Nursing diagnoses that may apply to the newborn withasphyxia and the
newborn’s parents include the following:

1. Ineffective Breathing Pattern related to lack of spontaneous respirations

at birth secondary to in utero asphyxia

2. Decreased Cardiac Output related to impaired oxygenation

3. Ineffective Family Coping: Compromised related to baby’s lack of

spontaneous respirations at birth and fear of losing their newborn
MECONIUM ASPIRATION

INCIDENCE

a. Meconium stained amniotic fluid (MSAF) complicates delivery in

approximately 8% to 15% of live birth.
b. The incidence of MSAF in preterm infant is very low .
c. Most babies with MSAF are 37 weeks or older and most meconium-stained
infants are post mature and small for gestational age.
d. Approximately 5% of neonates born through MSAF develop meconium
aspiration syndrome (MAS).
e. MSAF is associated with an increased risk of respiratory disorder and
approximately 50% of these infants require mechanical ventilation

CAUSES

i) Acute or chronic hypoxia

ii) Infection : can result in the passage of meconium in utero.
iii) In this setting gasping by the fetus or newly born infant can cause aspiration
of amniotic fluid contaminated by meconium.
iv) Meconium aspiration before or during birth can obstruct airways interfere
with gas exchange and cause severe respiratory distress

PATHOPHYSIOLOGY

1. Meconium is a sterile thick black-green odorless material that results from

the accumulation of debris in the fetal intestine during the third month of
gestation.Thecompontents of meconium include water (72%-80%)
desquamated cells from the intestine and skin gastrointestinal mucin lanugo
hair fatty material from the vernix cascosa amniotic fluid and intestinal
secretion blood-group specific glycoproteins and bile.
2. Passage of meconium in utero. MSAF may result from a post – term fetus
with rising motilin levels and normal gastrointestinal function,vagal
stimulation produced by cord or head compression or in utero fetal stress.
Amniotic fluid that is thinly stained is described as watery. Moderately
stained fluid is opaque without particles and fluid with thick meconium with
particles is sometimes called pea soup.
3. Aspiration of meconium. In the presence of fetal stress gasping by the
fetus can result in aspiration of meconium before during or immediately
following delivery Severe MAS appears to be caused by pathologic
intrauterine processes primarily chronic hypoxia acidosis and infection.
Meconium has been found in the lungs of stillborn infants who died soon
after birth without a history of aspiration at delivery.
4. Effects of meconium aspiration. When aspirated into the lung, meconium
may stimulate the release of cytokines and vaso active substances that result
in cardiovascular and inflammatory responses in the fetus and newborn.
Meconium itself or the resultant chemical pneumonitis, mechanically
obstructs the small airways, causes atelectasis and a ball-valve effects with
resultant air trapping and possible air leak. Aspirated meconium leads to
vasospasm hypertrophy of the pulmonary arterial musculature and
pulmonary hypertension that lead to extrapulmonary right-to-left shunting
through the ductus arteriosus or the foramen ovale and results in worsened
ventilation-perfusion (V/Q) mismatch, leading to severe arterial hypoxemia.
Approximately one third of infant with MAS develop persistent pulmonary
hypertension of the new born (PPHN) which contributes to the mortality
associated with this syndrome (see Chapter 24f) Aspirated meconium also
inhibits surfactant function.
 Meconium in the lungs

a ball-valve action (air is allowed in but not exhaled)

alveoli over distend and rupture

pulmonary air leaks (pneumomediastinum or pneumothorax)

meconium triggers a chemical pneumonitis

oxygen and carbon dioxide trapping

lungs to hyper inflate.

CLASSIFICATION OF RESPIRATORY DISEASE

1. Mild MAS is a disease requiring <40% oxygen for <48 hours.

2. Moderate MAS is a disease requiring >40% oxygen for >48 hours without
air leak.
3. Severe MAS is a disease requiring assisted ventilation for >48 hours,often
associated with PPHN.

CLINICAL MANIFESTATION

(1) Fetal hypoxia : in utero a few days or a few minutes before birth, indicated
by a sudden increase in fetal activity followed by diminished activity, slowing
of FHR or weak and irregular heartbeat, loss of beat-to-beat variability, and
meconium staining of amniotic fluid

(2) Signs of distress at birth: such as pallor, cyanosis, apnea, slow heartbeat,
and low Apgar scores (below 6) at 1 and 5 minutes. Newborns with intrauterine
asphyxia, meconium-stained newborns, or newborns that have aspirated
meconium are depressed at birth and require resuscitation to establish adequate
respiratory effort

PREVENTION OF MAS

1) Prevention of passage of meconium in utero : Mothers at risk for

uteroplacental insufficiency include those with preeclampsia or increased
blood pressure,chronic respiratory or cardiovascular disease,poor uterine
growth post-term pregnancy and heavy smokers. These women should be
carefully monitored during pregnancy. During labor the fetal heart rate
should be monitored,with fetal scalp blood samples obtained for PH
dtermination when indicated.
2) Amnioinfusion: The use of amnioinfusion in women whose labor is
complicated by MSAF does not reduce neonatal morbidity related to
meconium aspiration although the technique effectively treats repetitive
variable fetal heart rate decelerations by relieving umbilical cord
compression in labor. A large randomized trial of amnioinfusion for women
with thick meconium-stained fluid with or without variable fetal heart rate
decleration showed no reduction of the risk of moderate or severe MAS
perinatal death,or caesarean delivery. However the study did not have
adequate power to determine definitively if amnioinfusion may benefit the
group with variable decelerations.
3) Timing and mode of delivery: In pregnancies that continue past the due
date, induction as early as 41 weeks may help prevent MAS by avoiding
 passage of meconium. Delivery mode does not appear to significantly impact
the risk of aspiration.

MANAGEMENT OF INFANTS DELIVERED THROUGH MECONIUM-

STAINED FLUID.

Oropharyngeal and nasopharyngeal suctioning on the perineum and routine

tracheal intubation and aspiration of meconium in vigorous infants are not
effective in preventing MAS. Infants should be assessed and intervention
reserved for infants who are depressed or have respiratory distress.

A. Initial assessment: At a delivery complicated by MSAF the clinician should

determine whether the infant is vigorous, demonstrated by heart rate >100
beats per minute spontaneous and good tone (spontaneous movement or
some degree of flexion) The infant will be depressed approximately 20% to
30% of the time.
1. If the infant appears vigorous routine care should be provided regardless of
the consistency of the meconium.
2. If respiratory distress develops or the infant becomes depressed the trachea
should be incubated under direct laryngoscopy and intra tracheal suctioning
performed. Visualization of the cords without suctioning is not adequate
because significant meconium may be present below the cords.
3. In questionable cases it is safer to incubate and suction as MAS can occur in
infants delivered through thinily stained amniotic fluid.
B. Suctioning technique
1. The infant should be placed on a radiant warmer and given free-flow
oxygen.
2. Delay drying and stimulation and postpone emptying of any gastric
contents until the infant has stabilized.
3. A clinician (eg,Pediatrician, Anesthesiologist, advanced practice nurse)
should incubate the trachea under direct laryngoscopy preferably before
inspiratory efforts have been initated. A 3.0 mm or 3.5 mm internal –
diameter endotracheal tube is used in term infants.
 4. After incubation the tube is attached to wall suction at a pressure of 80 to
100 mm Hg by means of a plastic adapter (Neotech Meconium Aspirator ,
Neotech product Chatsworth CA) Continuous suction is applied as the tube
is being withdrawn: the procedure is repeated until the trachea is cleared or
resuscitation needs to be initiated.
5. Avoid positive pressure ventilation,if possible until tracheal suctioning is
accomplished.
C. Complications of intubation Include bleeding, laryngospasm stridor apnea
and cyanosis. This procedure should be accomplished rapidly and ventilation
with oxygen should be initiated before significant bradycardia occurs. The
infants general condition must not be ignored in persistent attempts to clear
the trachea. Because a few inspiratory efforts by the infant will move the
meconium from the trachea to the smaller airways .exhaustive attempts to
remove it are unwise.

MANAGEMENT OF MAS

A. Observation: Infants who are depressed at birth and have had meconium
suctioned from the trachea are at risk for meconium aspiration pneumonia
and should be observed closely for respiratory distress.
1. A chest radiograph may help determine those infant who are most likely to
develop respiratory distress although a significant number of asymptomatic
infant will have an abnormal appearing chest film. The classic
roentgenographic finding are diffuse asymmetric patcy infiltrates areas of
consolidation and hyperinflation.
2. Monitoring of oxygen saturation during this period aids assessment of the
severity of the infants condition and avoids hypoxemia.
B. Routine care
1. The infant should be maintained in a neutral thermal environment and
tractile stimulation should be minimized.
2. Blood glucose and calcium levels should be assessed and corrected if
necessary. Severely depressed infants may have severe metabolic acidosis
that may need to be corrected.
3. Fluids should be restricted as much as possible to prevent cerebral and
pulmonary edema.
4. Infants may also require specific therapy for hypotension and poor cardiac
output including including cardiotonic medications such as dopamine.
5. Circulatory support with normal saline or packed red blood cells should be
provided in patients with marginal oxygenation. In infants with substantial
oxygen and ventilator requirments . We usually maintain a hemoglobin
concentration above 15 g (hematocrit above 40%)
6. Renal function should be continuously monitored
C. Oxygen therapy.: Management of hypoxemia should be accomplished by
increasing the inspired oxygen concentration and by monitoring blood gases
and PH. An indwelling arterial catheter is usually required for blood
sampling. It is crucial to provide sufficient oxygen because repeated hypoxic
insults may result in ongoing pulmonary vasoconstriction and contribute to
the development of PPHN.
D. Assisted in ventilation:
 Continuous positive airway pressure
 Mechanical ventilation
E. Medications
1. Antibiotics
2. Surfactant
3. Corticosteroids

COMPLICATIONS

a. Pulmonary air leaks

b. anoxic cerebral injury manifested by convulsions
c. myocardial injury evidenced by congestive heart failure or cardiomegaly
d. disseminated intravascular coagulation (dic) resulting from hypoxic hepatic
damage
e. Anoxic renal damage demonstrated by hematuria, oliguria, or anuria;
f. Fluid overload
g. Sepsis secondary to bacterial pneumonia
h. intestinal necrosis from ischemia
i. gastrointestinal obstruction
j. hemorrhage.

NURSING MANAGEMENT

Assessment

1. During the intrapartum period, observe for signs of fetal hypoxia and
meconium staining of amniotic fluid.
2. At birth assess the newborn for signs of distress.
3. Carefully observe for complications

Nursing diagnoses

1. Impaired Gas Exchange related to aspiration of meconium and amniotic fluid

during birth
2. Altered Nutrition: Less than Body Requirements related to respiratory
distress and increased energy requirements
3. Ineffective Family Coping: Compromised related to life threatening illness
in term newborn

Planning and implementation

Hospital-Based Nursing Care

i) Initial interventions are aimed at preventing aspiration by helping remove the

meconium from the infant’s oropharynx and nasopharynx before the first
extra uterine breath.
ii) When significant aspiration occurs, the primary goals of therapy are to
maintain appropriate gas exchange and minimize complications.
iii) Nursing interventions after resuscitation should include maintaining
adequate oxygenation and ventilation, regulating temperature, performing
glucose testing by glucometer at 2 hours of age to check for hypoglycemia,
observing intravenous fluids administration, calculating necessary fluids
(which may be restricted in the first 48 to 72 hours due to cerebral edema),
 providing caloric requirements, and monitoring intravenous antibiotic
therapy

Evaluation

Expected outcomes of nursing care include the following:

1) The newborn at risk of MAS is promptly identified, and early intervention is

initiated.
2) The newborn is free of respiratory distress and metabolic alterations.
3) The parents verbalize their concerns about their baby’s health problem and
survival and understand the rationale behind the management of their
newborn.