Author

Gina M Geis, MD Attending Neonatologist, Associate Director, Neonatal-Perinatal

Medicine Fellowship Program, Albany Medical Center; Assistant Professor, Department of
Pediatrics, Albany Medical College

Gina M Geis, MD is a member of the following medical societies: American Academy of

Pediatrics, American Society for Bioethics and Humanities, Capital District Pediatric Society

Disclosure: Nothing to disclose.

Coauthor(s)

David A Clark, MD Chairman, Professor, Department of Pediatrics, Albany Medical College

David A Clark, MD is a member of the following medical societies: Alpha Omega Alpha,
American Academy of Pediatrics, American Pediatric Society, Christian Medical and Dental
Associations, Medical Society of the State of New York, New York Academy of Sciences,
Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical

Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP Professor of Pediatrics, University of Missouri-Kansas City

School of Medicine; Attending Physician, Division of Neonatology, Children's Mercy
Hospital and Clinics; Faculty, Children's Mercy Bioethics Center

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega
Alpha, American Academy of Hospice and Palliative Medicine, American Academy of
Pediatrics, American Pediatric Society, American Society for Bioethics and Humanities,
American Society of Law, Medicine & Ethics, Society for Pediatric Research, National
Hospice and Palliative Care Organization

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology,

Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of

Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American
Medical Association, Connecticut State Medical Society, Society for Pediatric Research
Disclosure: Nothing to disclose.

Additional Contributors

Melinda B Clark, MD Associate Professor of Pediatrics, Department of Pediatrics, Albany

Medical College

Melinda B Clark, MD is a member of the following medical societies: Alpha Omega Alpha,
Academic Pediatric Association, American Academy of Pediatrics, Medical Society of the
State of New York

Disclosure: Nothing to disclose

Background

Meconium aspiration syndrome (MAS) is the aspiration of stained amniotic fluid, which can
occur before, during, or immediately after birth. Meconium is the first intestinal discharge
from newborns, a viscous, dark-green substance composed of intestinal epithelial cells,
lanugo, mucus, and intestinal secretions (eg, bile. Water is the major liquid constituent,
comprising 85-95% of meconium; the remaining 5-15% of ingredients consists of solid
constituents, primarily intestinal secretions, mucosal cells, and solid elements of swallowed
amniotic fluid, such as proteins and lipids.

Meconium is sterile and does not contain bacteria, which is the primary factor that
differentiates it from stool. Intrauterine distress can cause passage of meconium into the
amniotic fluid. Factors that promote the passage in utero include placental insufficiency,
maternal hypertension, preeclampsia, oligohydramnios, infection, acidosis, and maternal drug
abuse, especially use of tobacco and cocaine.

As noted above, meconium-stained amniotic fluid may be aspirated before or during labor
and delivery. Because meconium is rarely found in the amniotic fluid prior to 34 weeks'
gestation, meconium aspiration primarily affects infants born at term and postterm.

Pathophysiology

In utero meconium passage results from neural stimulation of a maturing gastrointestinal (GI)
tract, usually due to fetal hypoxic stress. As the fetus approaches term, the GI tract matures,
and vagal stimulation from head or spinal cord compression may cause peristalsis and
relaxation of the rectal sphincter, leading to meconium passage.

The effects of meconium in amniotic fluid are well documented. [1] Meconium directly alters
the amniotic fluid, reducing antibacterial activity and subsequently increasing the risk of
perinatal bacterial infection. In addition, meconium is irritating to fetal skin, thus increasing
the incidence of erythema toxicum. However, the most severe complication of meconium
passage in utero is perinatal aspiration of stained amniotic fluid (before, during, or
immediately after birth)ie, meconium aspiration syndrome (MAS). Aspiration of
meconium-stained amniotic fluid may occur if the fetus is in distress, leading to a gasping
breathing pattern. This aspiration induces hypoxia via four major pulmonary effects: airway
obstruction, surfactant dysfunction, chemical pneumonitis, and pulmonary hypertension. [1]

Airway obstruction

Complete obstruction of the airways by meconium results in atelectasis. Partial obstruction

causes air trapping and hyperdistention of the alveoli, commonly termed the ball-valve effect.
Hyperdistention of the alveoli occurs from airway expansion during inhalation and airway
collapse around inspissated meconium in the airway, causing increased resistance during
exhalation. The gas that is trapped (hyperinflating the lung) may rupture into the pleura
(pneumothorax), mediastinum (pneumomediastinum), or pericardium (pneumopericardium).

Surfactant dysfunction
Meconium deactivates surfactant and may also inhibit surfactant synthesis. [2, 3] Several
constituents of meconium, especially the free fatty acids (eg, palmitic, stearic, oleic), have a
higher minimal surface tension than surfactant and strip it from the alveolar surface, resulting
in diffuse atelectasis. [4]

Chemical pneumonitis

Enzymes, bile salts, and free fatty acids in meconium irritate the airways and parenchyma,
causing a release of cytokines (including tumor necrosis factor (TNF-, interleukin (IL)-1,
IL-6, IL-8, IL-13), which initiate a diffuse pneumonitis that may begin within a few hours of
aspiration.

All of these pulmonary effects can produce a gross ventilation-perfusion (V/Q) mismatch.

Persistent pulmonary hypertension of the newborn

To complicate matters further, many infants with meconium aspiration syndrome (MAS) have
primary or secondary persistent pulmonary hypertension of the newborn (PPHN) as a result
of chronic in utero stress and thickening of the pulmonary vessels. PPHN further contributes
to the hypoxemia caused by meconium aspiration syndrome. [5]

Finally, although meconium is sterile, its presence in the air passages can predispose the
infant to pulmonary infection

Etiology

Factors that promote the passage of meconium in utero include the following:

Placental insufficiency
Maternal hypertension

Preeclampsia

Oligohydramnios

Maternal drug abuse, especially of tobacco and cocaine

Maternal infection/ chorioamnionitis

Fetal hypoxia

Epidemiology

United States data

In the industrialized world, meconium in the amniotic fluid can be detected in 8-25% of all
births after 34 weeks' gestation. Historically, approximately 10% of newborns born through
meconium-stained amniotic fluid developed meconium aspiration syndrome (MAS).
However, changes in obstetric and neonatal practices appear to be decreasing its incidence. [6]
 MAS was the admission diagnosis for 1.8% of term neonates in one large retrospective study
from 1997-2007. [1]

International data

In developing countries with less availability of prenatal care and where home births are
common, the incidence of MAS is thought to be higher and is associated with a greater
mortality rate.

Age-, sex-, and race-related demographics

MAS is exclusively a disease of newborns, especially those delivered at or beyond the

mother's estimated due date. [1] MAS affects both sexes equally.

A study of 499,096 singleton live births in London, England, reported the rates of meconium-
stained amniotic fluid varied by ethnicity: It was 22.6% in the black population, 16.8% in
south Asian groups, and 15.7% in the white population. [7] The study also demonstrated that
meconium-stained amniotic fluid occurred more often in later-gestational-age pregnancies
and in babies in the breech presentation.

Prognosis

Most infants with meconium aspiration syndrome (MAS) have complete recovery of
pulmonary function; however, MAS infants have a slightly increased incidence of respiratory
infections in the first year of life because the lungs are still in recovery. Severely affected
infants have an increased risk of developing reactive airway disease (RAD) in the first 6
months of life. [8]

Children with MAS may develop chronic lung disease from intense pulmonary intervention.

Prenatal and intrapartum events that initiate the meconium passage may cause the infant to
have long-term neurologic deficits, including central nervous system (CNS) damage,
seizures, mental retardation, and cerebral palsy.

Morbidity/mortality

A large retrospective analysis demonstrated the overall mortality rate for MAS to be 1.2% in
the United States.The mortality rate for MAS resulting from severe parenchymal pulmonary
disease and pulmonary hypertension is as high as 20%. Other complications include air leak
syndromes (eg, pneumothorax, pneumomediastinum, pneumopericardium), which occur in
10-30% of infants with MAS. The neurologic disabilities of survivors are not due primarily to
the aspiration of meconium, but rather by in-utero pathophysiology, including chronic
hypoxia and acidosis.

A large retrospective analysis demonstrated the overall mortality rate for MAS to be 1.2% in
the United States. [1] The mortality for MAS resulting from severe parenchymal pulmonary
disease and pulmonary hypertension is as high as 20%. Other complications include air-leak
syndromes (eg, pneumothorax, pneumomediastinum, pneumopericardium) and pulmonary
interstitial emphysema, which occur in 10-30% of infants who have MAS. The neurologic
disabilities of survivors are not due primarily to the aspiration of meconium, but rather owing
to in utero pathophysiology, including chronic hypoxia and acidosis. [9]

History

The presence of meconium in amniotic fluid is required to cause meconium aspiration

syndrome (MAS), but not all neonates with meconium-stained fluid develop this condition.
The diagnosis of MAS requires the presence of meconium-stained amniotic fluid or neonatal
respiratory distress, as well as characteristic radiographic abnormalities.

Historically, efforts to reduce the development of MAS included oropharyngeal suctioning at

the perineum, followed by intubation and tracheal suction of meconium immediately
following delivery. This universal practice was abandoned over a decade ago when studies
showed that infants who were vigorous at birth did not benefit from this intervention.
Following this practice change, the Neonatal Resuscitation Program (NRP) recommended
intubation and tracheal suctioning only for nonvigorous infants born through meconium-
stained fluid.

However, in 2015, these recommendations changed again: It is no longer recommended to

intubate and suction nonvigorous infants born through meconium-stained fluid due to a lack
of evidence to support this practice. [10, 11] Instead, in this setting, the NRP now recommends
having a practitioner skilled at endotracheal intubation be present at the time of birth, and
they should begin with the initial steps of resuscitation (ie, provide warmth, position the head
and neck to open the airway, clear secretions with a bulb syringe, dry, and stimulate the
infant). [10, 11] The 2017 American College of Obstetricians and Gynecologists
(ACOG) opinion number 689 indicates that, regardless of whether infants with meconium-
stained amniotic fluid are vigorous or nonvigorous, do not routinely administer intrapartum
suctioning. [11]

In a 2015 developing nation retrospective study (2008-2009) that evaluated the effect of
intrapartum oropharyngeal suction on MAS in 509 meconium-stained, term singleton
neonates without major congenital malformations, investigators found that outcomes in those
who received suctioning were similar to those in the control group (who did not undergo
suctioning). [12] The incidence and severity of MAS, as well as oxygen requirements longer
than 48 hours, were comparable between the groups.

Diagnostic ConsiderationsImportant considerations

Many infants who have experienced meconium aspiration syndrome (MAS) have had
prenatal and postnatal periods of hypoxia and acidosis; therefore, these individuals are at
increased risk of significant central nervous system (CNS) damage.

Typically, medicolegal action is initiated by parents whose newborn develops long-term

sequelae from significant perinatal hypoxia. Although the delivering physician is the primary
focus of such a lawsuit, additional liability to other healthcare professionals may ensue from
a poorly planned and executed resuscitation.

Providers of the tertiary intensive care may also be included in these lawsuits, usually due to
complications of necessary complex and aggressive care.
Differential Diagnoses

Aspiration Syndromes
Congenital Heart Disease with Pulmonary Hypertension

Pediatric Congenital Diaphragmatic Hernia

Pediatric Idiopathic Pulmonary Artery Hypertension

Pediatric Pneumonia

Pediatric Sepsis

Persistent Newborn Pulmonary Hypertension

Surfactant Deficiency

Transient Tachypnea of the Newborn

Transposition of the Great Arteries

Laboratory Studies

Acid-base status

Ventilation-perfusion (V/Q) mismatch and perinatal stress are prevalent in meconium

aspiration syndrome (MAS); therefore, assessment of the infant's acid-base status is crucial.

Metabolic acidosis from perinatal stress is complicated by respiratory acidosis from

parenchymal disease and persistent pulmonary hypertension of the newborn (PPHN).

Measurement of arterial blood gas (ABG) pH, partial pressure of carbon dioxide (pCO2), and
partial pressure of oxygen (pO2), as well as continuous monitoring of oxygenation by pulse
oximetry are necessary for appropriate management. The calculation of an oxygenation index
(OI) can be helpful when considering advanced treatment modalities, such as extracorporeal
membrane oxygenation (ECMO).

Serum electrolytes

Obtain sodium, potassium, and calcium concentrations at 24 hours of life in infants with
MAS, because syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and
acute renal failure are frequent complications of perinatal stress.

Complete blood cell (CBC) count

Note the following:

In utero or perinatal blood loss, as well as infection, contributes to postnatal stress.

 Hemoglobin and hematocrit levels must be sufficient to ensure adequate oxygen-carrying
capacity.

Thrombocytopenia increases the risk for neonatal hemorrhage.

Neutropenia or neutrophilia with left shift of the differential may indicate perinatal bacterial
infection.

Polycythemia may be present secondary to chronic fetal hypoxia; polycythemia is associated

with decreased pulmonary blood flow and may exacerbate the hypoxia associated with MAS
and PPHN.

There is little evidence that empiric antibiotic therapy after obtaining a blood culture is
beneficial, except in the case of prolonged rupture of the membranes and maternal fever.

Fetal scalp blood lactate sampling has not been shown to reduce the risk of respiratory
distress syndrome in infants with meconium-stained amniotic fluid. [13]

Imaging Studies

Chest radiography

Chest radiography is essential in order to achieve the following:

Confirm the diagnosis of meconium aspiration syndrome (MAS) and determine the extent of
the intrathoracic pathology
Identify areas of atelectasis and air leak syndromes

Ensure appropriate positioning of the endotracheal tube and umbilical catheters

See the images below.

 Air trapping and hyperexpansion from airway
obstruction.

View Media Gallery

Acute atelectasis.

View Media Gallery

 Pneumomediastinum from gas trapping
and air leak.

View Media Gallery

Left pneumothorax with depressed diaphragm and

minimal mediastinal shift because of noncompliant lungs.

View Media Gallery

 Diffuse chemical pneumonitis from
constituents of meconium.

View Media Gallery

Ultrasonography

Echocardiography is necessary to ensure normal cardiac structure and for assessment of

cardiac function, as well as to determine the severity of pulmonary hypertension and right-to-
left shunting.

A prospective observational study of 117 newborns with MAS (and 100 controls)
demonstrated that pulmonary ultrasonography may be a convenient, noninvasive, and
accurate imaging modality for the diagnosis of MAS. [14] The primary features of MAS noted
on sonograms included the following [14] :

Pulmonary consolidation with air bronchograms (all patients)

Pleural line anomalies and absence of the A-line (all patients)

Alveolar-interstitial syndrome or B-lines in nonconsolidated regions (all patients)

Atelectasis in severe MAS (16.2% of severe cases)

Pleural effusion (13.7% of patients)

Brain imaging studings

Later in the course of MAS, when the infant is stable and if the infant's neurologic
examination is abnormal, imaging studies of the brain (eg, magnetic resonance imaging
[MRI], computed tomography [CT] scanning, cranial ultrasonography) are indicated.

Medical Care

The American College of Obstetricians and Gynecologists (ACOG) continues to provide

guidance regarding the appropriate indications for delivery to prevent neonatal complications
of a prolonged pregnancy, as well as for avoiding the unnecessary delivery of a preterm baby.
[15, 16]

In patients with meconium aspiration syndrome (MAS), a thorough cardiac examination and
echocardiography are necessary to evaluate for congenital heart disease and persistent
pulmonary hypertension of the newborn (PPHN).

Quantifying the degree of pulmonary hypertension, prior to instituting therapy, is essential.

Prevention of MAS

Prevention of MAS is paramount. Obstetricians should closely monitor fetal status in an

attempt to identify fetal distress.

When meconium is detected, amnioinfusion with warm, sterile saline is theoretically

beneficial to dilute the meconium in the amniotic fluid, thereby minimizing the severity of
the aspiration. However, current evidence does not support routine amnioinfusion to prevent
MAS. [17, 18, 19] One large, multicenter study determined that amnioinfusion did not reduce the
risk of moderate or severe MAS or MAS-related death. [20]

As noted earlier under Presentation, current recommendations no longer advise routine

intrapartum suctioning for infants born to mothers with meconium staining of the amniotic
fluid. [10, 11, 21, 22, 23]

No clinical trials justify suctioning on the basis of the meconium consistency. Do NOT
perform the following harmful techniques in an attempt to prevent aspiration of
meconium-stained amniotic fluid:

Squeezing the chest of the baby

Inserting a finger into the mouth of the baby

The American Academy of Pediatrics (AAP) Neonatal Resuscitation Program Steering

Committee and the American Heart Association (AHA) have promulgated guidelines for
management of babies exposed to meconium. [10] The guidelines are under continuous review
and are revised as new evidence-based research becomes available. The seventh edition of the
Neonatal Resuscitation Program modified its previous recommendations regarding
endotracheal suctioning for the nonvigorous infant. The most recent guidelines are as follows
[10, 11]
:

If the baby is vigorous (defined as havin a normal respiratory effort and normal muscle tone),
the baby may stay with the mother to receive the initial steps of newborn care. A bulb
syringe can be used to gently clear secretions from the nose and mouth.
 If the baby is not vigorous (defined as having a depressed respiratory effort or poor muscle
tone), place the baby on a radiant warmer, clear the secretions with a bulb syringe, and
proceed with the normal steps of newborn resuscitation (ie, warming, repositioning the
head, drying, and stimulating). If, after these initial steps are taken, the baby is still not
breathing or the heart rate is below 100 beats per minute (bpm), administer positive
pressure ventilation.

Resuscitation should follow the same principles for infants with meconium-stained fluid as
for those with clear fluid.

Continued care in the neonatal intensive care unit (NICU)

Maintain an optimal thermal environment to minimize oxygen consumption.

Minimal handling is essential because these infants are easily agitated. Agitation can increase
pulmonary hypertension and right-to-left shunting, leading to additional hypoxia and
acidosis. Sedation may be necessary to reduce agitation.

An umbilical artery catheter should be inserted to monitor blood pH and blood gases without
agitating the infant.

Continue respiratory care includes oxygen therapy via hood or positive pressure, and it is
crucial in maintaining adequate arterial oxygenation. Mechanical ventilation is required by
approximately 30% of infants with MAS. [5] Make concerted efforts to minimize the mean
airway pressure and to use as short an inspiratory time as possible. Oxygen saturations should
be maintained at 90-95%.

Surfactant therapy is commonly used to replace displaced or inactivated surfactant and as a

detergent to remove meconium. [24, 25, 26] Although surfactant use does not appear to affect
mortality rates, it may reduce the severity of disease, progression to extracorporeal membrane
oxygenation (ECMO) utilization, [27] and decrease the length of hospital stay.

Although conventional ventilation is commonly used as initial management, high-frequency

oscillation and jet ventilation are alternative effective therapies. Hyperventilation to induce
hypocapnia and compensate for metabolic acidosis is no longer a primary therapy for
pulmonary hypertension, because hypocarbia often results in decreased cerebral perfusion
(partial pressure of carbon dioxide [PaCO2] <30 mm Hg). Prolonged alkalosis has been
shown to cause neuronal injury in animals and humans, providing another reason to avoid
alkalosis in these patients. [28]

Jet ventilator therapy aimed at minimizing mean airway pressure and tidal volume should be
used if pulmonary interstitial emphysema or a pneumothorax is present.

For treatment of persistent pulmonary hypertension of the newborn (PPHN), inhaled nitric
oxide is the pulmonary vasodilator of choice. [29] Oxygen is also a potent pulmonary
vasculature vasodilator. Phosphodiesterase inhibitors, including sildenafil and milrinone, are
being increasingly used as adjunctive therapies for PPHN.

Pay careful attention to systemic blood volume and blood pressure. Volume expansion,
transfusion therapy, and systemic vasopressors are critical in maintaining systemic blood
pressure greater than pulmonary blood pressure, thereby decreasing the right-to-left shunt
through the patent ductus arteriosus. Dopamine is often the first-line vasopressor for neonates
with MAS requiring vasopressor support.

Ensure adequate oxygen carrying capacity by maintaining the hemoglobin concentration at a

minimum of 13 g/dL.

Corticosteroids are not recommended. Evidence supporting the use of steroids in the
management of MAS is insufficient. [30]

Neonates with MAS have historically been routinely treated with empiric broad-spectrum
antibiotics, but this practice is being increasingly called into question. No studies have shown
prophylactic antibiotics to reduce the incidence of sepsis in neonates born through
meconium-stained amniotic fluid; thus, antibiotic use may be reserved for suspected or
documented infections.

ECMO is used if all other therapeutic options have been exhausted. Although it is effective in
treating MAS, note that ECMO is associated with a high incidence of poor neurologic
outcomes.

Consultations

Evaluation by a pediatric cardiologist is necessary for echocardiographic assessment of the

cardiac structures and to assess the severity of pulmonary hypertension and right-to-left
shunting.

Evaluation by a pediatric neurologist is helpful in the presence of neonatal encephalopathy or

seizure activity.

Transfer

Although initial stabilization is necessary at community hospitals, infants with MAS

frequently require high-frequency ventilation, inhaled nitric oxide (NO), or ECMO.
Therefore, infants with a significant aspiration should be transferred to a regional NICU as
soon as possible.

Diet

Perinatal distress and severe respiratory distress preclude feeding at the early stages of the
disease.

Intravenous fluid therapy begins with adequate dextrose infusion to prevent hypoglycemia.
Intravenous fluids should be provided at mildly restricted rates (60-70 mL/kg/day).

Progressively add electrolytes, protein, lipids, and vitamins to ensure adequate nutrition and
to prevent deficiencies of essential amino acids and essential fatty acids.

Outpatient care
Infants with MAS are at increased risk for adverse developmental outcomes and should be
referred for developmental assessment as an outpatient.

Surgical Care

Although primary management of air leak syndromes (pneumothorax or pneumopericardium)

is achieved by thoracic drainage tubes inserted by a neonatologist, a pediatric surgical
consultation may be necessary in severe cases. Therapy with fibrin glue has been shown to be
effective in patients with a persistent air leak. [31]

Medication Summary

In addition to the treatments discussed earlier and the medications listed below, surfactant
replacement therapy is frequently used in infants with meconium aspiration syndrome
(MAS). Natural lung extract is administered to replace the surfactant that has been stripped.
Surfactant also acts as a detergent to break up residual meconium, thereby decreasing the
severity of lung disease. Surfactant is used in patients with MAS; however, its efficacy,
dosage regimen, and most effective product are not yet established.

Class Summary

Inhaled nitric oxide (NO) has the direct effect of pulmonary vasodilatation without the
adverse effect of systemic hypotension. It is approved for use, if concomitant hypoxemic
respiratory failure occurs.

Nitric oxide, inhaled

View full drug information

Endogenously produced from the action of the enzyme NO synthetase on arginine.

Exogenously inhaled NO is used in an attempt to decrease pulmonary vascular resistance and
improve lung blood flow. It relaxes vascular smooth muscle by binding to the heme moiety of
cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of
cGMP, which then leads to vasodilation.

Systemic vasoconstrictors

Class Summary

These agents are used to prevent right-to-left shunting by raising systemic pressure above
pulmonary pressure. Systemic vasoconstrictors include dopamine, dobutamine, and
epinephrine. Dopamine is the most commonly used.

Dopamine

View full drug information

At lower doses, dopamine stimulates beta1-adrenergic and dopaminergic receptors (renal
vasodilation, positive inotropism); at higher doses, it stimulates alpha-adrenergic receptors
(renal vasoconstriction).

Dobutamine

View full drug information

Increases blood pressure primarily via stimulation of beta1-adrenergic receptors. This drug
appears to have a more prominent effect on cardiac output than on blood pressure.

Epinephrine

View full drug information

Used for severe bronchoconstriction, especially in patients with underlying reactive airway
disease. Alpha-agonist effects include increased peripheral vascular resistance, reversed
peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist
effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Sedatives

Class Summary

These agents maximize efficiency of mechanical ventilation, minimize oxygen consumption,

and treat the discomfort of invasive therapies. However, some controversy exists around the
unknown long-term effect(s) of analgesics and sedatives on the developing brain.

Morphine

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Used for analgesia and sedation.

Fentanyl

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Potent opioid used for analgesia, sedation, and anesthesia. Has a shorter duration of action
than morphine.

Phenobarbital

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An anticonvulsant that may be used as a sedative. Suppresses the CNS from the reticular
activating system (ie, presynaptic, postsynaptic).
Phenobarbital remains a first-line therapy for neonatal seizures, which may occur in the
setting of perinatal depression.

Neuromuscular blocking agents

Class Summary

These agents are used for skeletal muscle paralysis to maximize ventilation by improving
oxygenation and ventilation. They are also used to reduce barotrauma and minimize oxygen
consumption.

The use of paralytics remains controversial and should be considered in newborns whose
management with sedatives alone is failing.

Pancuronium or vecuronium

View full drug information

Neuromuscular blocker whose effects are reversed by neostigmine and atropine.