Neonatal Resuscitation

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Neonatal Resuscitation

Neonatal Resuscitation
Author: Robin L Bissinger, PhD, APRN, NNP-BC; Chief Editor: Ted Rosenkrantz, MD more...
Updated: Sep 17, 2012

Neonatal resuscitation skills are essential for all health care providers who are involved in the delivery of newborns.
The transition from fetus to newborn requires intervention by a skilled individual or team in approximately 10% of all
This figure is concerning because 81% of all babies in the United States are born in nonteaching, nonaffiliated level I
or II hospitals. In such hospitals, the volume of delivery service may not be perceived as sufficient economic
justification for the continuous in-hospital presence of personnel with high-risk delivery room experience, as
recommended by the American Academy of Pediatrics (AAP) and the American College of Obstetricians and
Gynecologists (ACOG).[1]
Perinatal asphyxia and extreme prematurity are the 2 complications of pregnancy that most frequently necessitate
complex resuscitation by skilled personnel. However, only 60% of asphyxiated newborns can be predicted ante
partum. The remaining newborns are not identified until the time of birth. Additionally, approximately 80% of
low-birth-weight infants require resuscitation and stabilization at delivery.
Nearly one half of newborn deaths (many of which involve extremely premature infants) occur during the first 24
hours after birth. Many of these early deaths also have a component of asphyxia or respiratory depression as an
etiology. For the surviving infants, effective management of asphyxia in the first few minutes of life may influence
long-term outcome.
Even though prenatal care can identify many potential fetal difficulties ante partum, allowing maternal transfer to the
referral center for care, many women who experience preterm labor are not identified prospectively and therefore are
not appropriately transferred to a tertiary perinatal center. Consequently, many deliveries of extremely premature
infants occur in smaller hospitals.
For this reason, all personnel involved in delivery room care of the newborn should be trained adequately in all
aspects of neonatal resuscitation. Additionally, equipment that is appropriately sized to resuscitate infants of all
gestational ages should be available in all delivering institutions, even if the institution does not care for preterm or
intensive care infants.
Along with the necessary skills, the practitioner should approach any resuscitation with a good comprehension of
transitional physiology and adaptation, as well as an understanding of the infant's response to resuscitation.
Resuscitation involves much more than possessing an ordered list of technical skills and having a resuscitation
team; it requires excellent assessment skills and a grounded understanding of physiology.
This article reviews the adaptation process at delivery, outlines the steps necessary to resuscitate neonates, serves
as a review for practitioners who already resuscitate infants, and highlights special problems and controversies. New
practitioners must complete the Neonatal Resuscitation Program (NRP) or some other program that introduces
resuscitation material and allows skill assessment. After reading the material and practicing the skills, they should
work with experienced personnel before providing resuscitation at deliveries.
For patient education resources, see the Public Health Center, as well as Cardiopulmonary Resuscitation (CPR).

Transition to Extrauterine Physiology
To decrease neonatal morbidity and mortality, the practitioner must be able to rapidly identify infants whose transition
from an intrauterine to extrauterine physiology is delayed. Neonatal transition requires spontaneous breathing and
successful cardiopulmonary changes, as well as other changes to independent organ system functions. A thorough
understanding of normal transitional physiology leads to a better understanding of the needs of the infant who is
experiencing difficulties and thus should result in a more effective resuscitative effort.

Respiratory adaptation
After birth, the airways and the alveoli must be cleared of fetal lung fluid so that the lungs can operate as a functional
respiratory unit providing adequate gas exchange. Pulmonary blood flow must increase, and spontaneous
respirations must be established. In utero, most of the blood flow is shunted away from the lungs and directed to the
placenta where fetoplacental gas exchange occurs.
Fetal pulmonary vascular resistance is high, and the fetal systemic vascular resistance is low. Within minutes of
delivery, the newborn's pulmonary vascular resistance may decrease 8- to 10-fold, causing a corresponding increase
in neonatal pulmonary blood flow. At birth, the lungs must transition rapidly to become the site for gas exchange, or
else cyanosis and hypoxia will rapidly develop.
Accordingly, an understanding of the structure and function of the fetal pulmonary vasculature and the subsequent
transition to neonatal physiology is important for facilitating the necessary adaptations during resuscitation. In utero,
the lungs develop steadily from early in gestation (see Table 1 below). Knowledge of the stages of development
clarifies why neonates born before about 23-24 weeks' gestational age often lack sufficient lung development for

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survival because of the absence of a capillary network adjacent to the immature ventilatory units.
Table 1. Embryologic Stages of Lung Development (Open Table in a new window)

5 wk

Structure Development
Bronchi develop, and airway branching occurs; pulmonary veins return to left


5-17 wk

Lungs take on glandular appearance, and there is continual branching of tracheal
bronchial tree (ending at 18-19 wk gestation); blood vessels and lymphatics begin
to form, and diaphragm develops


13-25 wk

Rich vascular supply develops, and capillaries are brought closer to airways;
primitive respiratory bronchioles begin to form

Terminal air sac

24-40 wk

Alveoli appear and begin increasing in number, and blood-gas interface develops;
type II alveolar cells appear between 20 and 25 wk and start producing surfactant
between 24 and 25 wk, though normal intra-airway concentrations are not reached
until ~34 wk


40 wk to 8 y Thinning of alveolar sac linings and continued alveolar proliferation occur

Fetal pulmonary physiology
At term, the fetal lung is filled with approximately 20 mL of fluid. Fetal airways, alveoli, and terminal saccules are
open and stable at normal fetal lung volumes, distended by lung fluid secreted by the pulmonary epithelium. This
lung fluid maintains lung volume at about the functional residual capacity (FRC) and is a determinant of normal lung
growth. A constant flow of this fluid is secreted into the alveolar spaces throughout development, which contributes
to the fetal amniotic fluid.
Pulmonary and bronchial circulation also develops as the alveoli appear. Because of the compressive effect of the
fetal lung fluid and the low alveolar partial pressure of oxygen (PA O2) in utero, the pulmonary capillary bed and
pulmonary blood vessels remain constricted. High vascular resistance and low pulmonary blood flow result.
The placenta provides the respiratory function for the fetus. The placental circulation has 2 major characteristics that
enable the placenta to maintain adequate oxygenation of the fetus. First, the placenta has a multivillous circulation
that provides the maximum surface area for the exchange of oxygen and carbon dioxide between the mother and
fetus. Second, several factors result in the lowering of maternal pH and increasing of fetal pH, which results in
increased transfer of oxygen from maternal to fetal hemoglobin or red blood cells (RBCs).
Maternal blood, carrying oxygen on adult hemoglobin, releases oxygen to the fetal circulation and accepts both
carbon dioxide and various byproducts of metabolism from the fetal circulation. These transfers decrease maternal
placental blood pH and shift the maternal oxygen-dissociation curve to the right, which results in lower affinity of the
hemoglobin for oxygen and the release of additional oxygen to the fetal hemoglobin. The corresponding shift in the
fetal oxygen-dissociation curve to the left allows the fetal hemoglobin to bind more oxygen.
Fetal "breathing" (ie, chest wall and diaphragmatic movement) begins at approximately 11 weeks' gestation and
increases in strength and frequency throughout gestation. Fetal breathing is controlled by chemoreceptors located in
the aorta and at the bifurcation of the common carotid artery. These areas sense both pH and partial pressure of
carbon dioxide (PCO2).
A reflex response to altered pH and PCO2 is present at approximately 18 weeks' gestation; however, the fetus is not
able to regulate this response until approximately 24 weeks' gestation. Some studies have indicated that this
response cannot be elicited in utero even when the pH and PCO2 are altered, leading researchers to believe that the
response is suppressed in utero and is not activated until birth.
Studies also suggest that the low PA O2 in utero may be the mechanism that inhibits continuous breathing, finding
that when PA O2 is increased, continuous breathing is stimulated.[2]

Neonatal pulmonary physiology
As noted (see above), the fetal airways and alveoli are filled with lung fluid that needs to be removed before
respiration. Only a small portion of this fetal lung fluid is removed physically during delivery. During the thoracic
squeeze, 25-33% of the fluid (sometimes markedly less) may be expressed from the oropharynx and upper airways.
Thoracic recoil allows passive inspiration of air into the larger bronchioles. Effective transition requires that any
remaining liquid be quickly absorbed to allow effective gas exchange.
The decrease in lung fluid begins during labor. Studies using a fetal lamb model showed that the production of lung
fluid decreases with the onset of labor. The subsequent reduction in lung fluid was associated with improved gas
exchange and acid-base balance. Labor is also associated with increased catecholamine levels, which stimulate
lymphatic drainage of the lung fluid.
In addition, with the onset of labor, the fetus produces adrenaline and the mother produces thyrotropin-releasing
hormone, which stimulates the pulmonary epithelial cells to begin readsorption of fluid. These findings could account
for the increased incidence of transient tachypnea of the newborn after birth by cesarean delivery without labor.
After birth, lung fluid is removed by several mechanisms, including evaporation, active ion transport, passive
movement from Starling forces, and lymphatic drainage. Active sodium transport by energy-requiring sodium
transporters, located at the basilar layer of the pulmonary epithelial cells, drives liquid from the lung lumen into the
pulmonary interstitium, where it is absorbed by the pulmonary circulation and lymphatics.
Exposure to an air interface, along with high concentrations of glucocorticoids and cyclic nucleotides, reverses the
direction of ion and water movement in the alveoli and leads to highly selective sodium channels. These changes
shift the fetal lung epithelial cells from a pattern of chloride secretion to one of sodium reabsorption, which
accelerates reabsorption of fetal lung fluid.

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The first breath must overcome the viscosity of the lung fluid and the intra-alveolar surface tension. This first breath
must also generate high transpulmonary pressure, which helps drive the alveolar fluid across the alveolar epithelium.
With subsequent lung aeration, the intraparenchymal structures stretch, and gases enter the alveoli, resulting in
increased PA O2 and pH. The increased PA O2 and pH result in pulmonary vasodilation and constriction of the ductus
Lung expansion and aeration is also a stimulus for surfactant release, which results in the establishment of an
air-fluid interface and the development of FRC. Normally, 80-90% of FRC is established within the first hour of birth
in term neonates with spontaneous respirations. Premature and critically ill infants with surfactant deficiency or
dysfunction may have limited ability to clear lung fluid and establish FRC.
The pulmonary vasculature is stimulated to dilate by chemical mediators, nitric oxide (NO), and prostaglandins. NO
is released when pulmonary blood flow and oxygenation increases. The formation of certain prostaglandins, such as
prostacyclin, is induced by the presence of increased oxygen tension. Prostacyclin acts on the pulmonary vascular
smooth muscle bed to induce pulmonary vasodilation. It has a short half-life in the bloodstream and therefore does
not affect the systemic circulation.
Soon after birth, fetal respiratory activity must transition to normal spontaneous breathing. To overcome the viscosity
of the lung fluid and the resistance generated by the fluid-filled lungs and the recoil and resistance of the chest wall,
lungs, and airways, the infant must generate a negative pressure so that air moves from an area of higher pressure
to one of lower pressure. There are 2 major physiologic responses that govern the initial lung inflation in the neonate.
The first response is the so-called rejection response, in which the neonate responds to positive-pressure lung
inflation by generating a positive intraesophageal pressure to resist the inflation. That is, the infant actively resists
attempts to inflate the lungs by performing an active exhalation. This response not only acts to reduce lung inflation
but also may cause high transient inflation pressures.
The second response is Head's paradoxical response, in which the neonate responds to positive-pressure lung
inflation with an inspiratory effort, which generates a negative intraesophageal pressure. This inspiratory effort and
the resultant negative pressure produce a fall in inflation pressures but result in a transient increase in tidal volume.
Of course, the neonate may demonstrate no response to the inflation attempt and may not generate any change in
intraesophageal pressure during positive-pressure inflation, in which case passive inflation results. These physiologic
responses to positive-pressure inflation in the delivery room may cause large variability in tidal volume and
intrapulmonary pressures, despite constant delivery of inflation pressure.
Stimuli for the first breath may be multifactorial. The environmental changes that occur with birth (eg, tactile and
thermal changes and increased noise and light) activate a number of sensory receptors that may help initiate and
maintain breathing. Clamping of the cord removes the low resistance placenta, causing an increase in systemic
vascular resistance and consequently causing an increase in both systemic blood pressure and pulmonary blood
Certain evidence also suggests that the increased arterial partial pressure of oxygen (Pa O2) after the initial breaths
may be responsible for the development of continuous breathing via hormonal or chemical mediators that are still
When the newborn lungs fill with air, the Pa O2 should rise gradually. In term infants with a persistent hypoxia, an
initial increase in ventilation occurs, followed by a decrease in ventilation occurs. This effect is even more profound in
premature infants whose central nervous system (CNS) is not as mature.
The carotid bodies and peripheral chemoreceptors located at the bifurcation of the common carotid artery are
stimulated during hypoxia to increase minute ventilation. In asphyxiated infants who cannot increase minute
ventilation (eg, because of extreme prematurity or sedation), profound bradycardia may result.

Cardiovascular adaptation
Fetal circulation
To understand the cardiovascular changes that occur in the neonate at birth, an understanding of normal fetal
circulation is necessary. The umbilical vein carries the oxygenated blood from the placenta to the fetus. Blood flow in
this vein divides at the porta hepatis, with 50-60% of the blood passing directly to the inferior vena cava (IVC) via the
ductus venosus and the remainder passing into the portal circulation. This portal blood flow perfuses the liver and
then passes into the IVC.
Flow studies have revealed that relatively little mixing of the blood from these 2 sites occurs in the IVC. The more
highly oxygenated blood, which has bypassed the liver, streams into the IVC to pass preferentially through the patent
foramen ovale into the left atrium. The desaturated blood returning from the liver and lower body streams into the
IVC to the right atrium.
In the right atrium, the desaturated blood mixes with blood returning from the coronary sinus and superior vena cava
(SVC) and flows into the right ventricle. The more highly oxygenated blood that crosses the foramen ovale mixes
with the small amount of pulmonary venous return and then crosses the mitral valve into the left ventricle. The output
from the left ventricle passes into the ascending aorta to the heart, brain, head, and upper torso. The less saturated
blood from the right ventricle passes into the pulmonary arteries.
Because the pulmonary vessels are constricted and highly resistant to flow, only about 12% of this blood from the
right ventricle enters the lungs; the remainder takes the path of least resistance through the patent ductus arteriosus
into the descending aorta. Approximately one third of this blood is carried to the trunk, abdomen, and lower
extremities, with the remainder entering the umbilical artery, where it is returned to the placenta for reoxygenation.
Neonatal circulation
The aeration of the lung results in an increase in arterial oxygenation and pH, with a resulting dilation of the
pulmonary vessels. Decompression of the capillary lung bed further decreases the pulmonary vascular resistance. A
corresponding decrease in right ventricular and pulmonary artery pressures is also noted. The decrease in

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pulmonary vascular resistance leads to an increase in blood flow to the lungs and in pulmonary venous return.
Clamping of the umbilical cord removes the low-resistance placental vascular circuit and thereby raises total
systemic vascular resistance, with a resultant increase in left ventricular and aortic pressures. The increased
systemic vascular resistance, combined with the decreased pulmonary vascular resistance, reverses the shunt
through the ductus arteriosus (from right-to-left shunting to left-to-right shunting) until the ductus closes completely.
All of these events result in closure of the other fetal shunts. With the decrease in right atrial pressure and the
increase in left atrial pressure, the 1-way "flap-valve" foramen ovale is pushed closed against the atrial septum. This
functional closure at birth is followed by anatomic closure, which usually occurs at several months of age.
The ductus venosus closes because of the clamping of the umbilical cord, which terminates umbilical venous return.
Functional mechanical closure of the ductus venosus is accomplished by the collapse of the thin-walled vessels.
Anatomic closure subsequently occurs at approximately 1-2 weeks.
Permanent closure of the ductus venosus may be delayed in preterm infants or infants with persistent pulmonary
hypertension. The constriction and closure of the ductus arteriosus is accomplished by contractile tissue within the
walls of this blood vessel. The contraction of this tissue is dependent both on the increase in arterial oxygen related
to the onset of spontaneous respirations and on a fall in circulating prostaglandin E2 (PGE2).
Because the placenta is a major site of fetal PGE2 production, removal of the placenta from the circulation causes
circulating PGE2 concentration to decrease markedly. Further reductions in PGE2 concentration occur because of
increased blood flow to the lungs (the site of PGE2 metabolism). Functional closure of the ductus generally occurs
within 72 hours of life, with anatomic closure by age 1-2 weeks.
In summary, functional postnatal circulation generally is established within 60 seconds; however, completion of the
transformation can take up to 6 weeks.

Response to asphyxia
A fetus or newborn that is subjected to asphyxia (see the image below) initiates a "diving" reflex (so termed because
of certain similarities to the physiology of diving seals) in an attempt to maintain perfusion and oxygen delivery to
vital organs. Hypoxia and acidosis lead to pulmonary arteriolar vasoconstriction. Pulmonary vascular resistance
increases, leading to decreased pulmonary blood flow and increased blood flow directly to the left atrium.

Fetal response to asphyxia illustrating initial redistribution of blood flow to vital organs. With prolonged asphyxial insult and failure
of compensatory mechanisms, cerebral blood flow falls, leading to ischemic brain injury.

Systemic cardiac output is redistributed, with increased flow to the heart, brain, and adrenal glands and decreased
flow to the rest of the body. Early in the course of asphyxia, systemic blood pressure increases. With ongoing
hypoxia and acidosis, however, the myocardium fails and bradycardia occurs; this causes a decrease in blood
pressure and tissue perfusion, leading to eventual tissue ischemia and hypoxia.
Infants who are undergoing asphyxia exhibit an altered respiratory pattern. Initially, they have rapid respirations.
These respiratory efforts eventually cease with continued asphyxia (primary apnea). During primary apnea, the infant
responds to stimulation with reinstitution of breathing. However, if the asphyxia continues, the infant then begins
irregular gasping efforts, which slowly decrease in frequency and eventually cease (secondary apnea).
Infants who experience secondary apnea do not respond to tactile or noxious stimulation and require positivepressure ventilation (PPV) to restore ventilation. Primary and secondary apnea cannot be clinically distinguished.
Therefore, if an infant does not readily respond to stimulation, PPV should be instituted as outlined in the Neonatal
Resuscitation Program (NRP) guidelines.
If an infant is experiencing primary apnea, the stimulation of the ventilatory efforts causes the infant to resume
breathing. If the infant is in secondary apnea, PPV is required for a longer period. The longer the infant undergoes
asphyxia, the longer the onset of spontaneous respirations is delayed after the initiation of effective ventilation
through the use of PPV.

Preparation for Resuscitation
Numerous sources of information are available on the training, skills, and procedures needed for delivery room
resuscitation of the newborn. Among the most highly respected of these sources is the Neonatal Resuscitation
Program (NRP), jointly developed by the American Academy of Pediatrics (AAP) and the American Heart
Association (AHA). The following sections contain a review of resuscitation procedures in a format that is similar to
the format used by the NRP.
Completion of the NRP should be considered by all hospital personnel who may be involved in the stabilization and
resuscitation of neonates in the delivery room. To develop true expertise, additional supervised experience with
skilled personnel is essential.
Although the NRP is considered highly authoritative, it is important that more research continue to evaluate the
effectiveness of the techniques of neonatal resuscitation. The NRP has already evolved considerably and will
continue to evolve as new data from clinical studies and basic physiologic research become available.

Rapid assessment

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Newborn infants who need extensive resuscitation should be rapidly identified. Term infants with clear amniotic fluid,
adequate respiratory effort, and good muscle tone should receive routine care, which includes provision of warmth,
clearing of the airway (if needed), drying of the infant, and assessment of the infant's color. These infants should
remain with their mothers during and after routine care.
Infants who do not meet the criteria for routine care need additional steps in their resuscitation. For such infants,
resuscitation may include not only initial stabilization (providing warmth, positioning, clearing the airway, drying,
stimulating, and repositioning) but also ventilation, chest compressions, and medications.

Anticipation of potential problems
The goals of resuscitation are to assist with the initiation and maintenance of adequate ventilation and oxygenation,
adequate cardiac output and tissue perfusion, and normal core temperature and serum glucose. These goals may
be attained more readily when risk factors are identified early, neonatal problems are anticipated, equipment is
available, personnel are qualified and available, and a care plan is formulated.
A large number of antepartum and intrapartum maternal conditions carry an increased risk for intrapartum asphyxia.
Many excellent texts describe the extensive medical and surgical problems of the obstetrical patient; a detailed
review of these problems is beyond the scope of this article to review.

Resuscitation equipment
The delivery room should be equipped with all the tools necessary for successful resuscitation of a newborn of any
size or gestational age. The equipment should include a radiant warmer, warmed blankets, a source of oxygen,
instruments for visualizing and establishing an airway, a source of regulated suction, instruments and supplies for
establishing intravenous (IV) access, trays equipped for emergency procedures, and drugs that may be useful in
Respiration equipment includes the following:
Oxygen supply
Assorted masks
Neonatal bag and tubing to connect to an oxygen source
Endotracheal tubes (size 2.5-4)
Tape and scissors
Laryngoscope (with size 0 and 1 blades)
Extra bulbs and batteries
Carbon dioxide detectors
Stylettes for endotracheal tubes (optional)
Laryngeal mask airway (optional)
Suction equipment includes the following:
Bulb syringe
Regulated mechanical suction
Suction catheters (6, 8, and 10 French)
Suction tubing
Suction canister
Replogle or Salem pump (10 French catheter)
Feeding tube (8 French catheter)
Syringe, catheter-tipped (20 mL)
Meconium aspirator
Fluid equipment includes the following:
IV catheters (22 g)
Tape and sterile dressing material
Dextrose 10% in water (D10W)
Isotonic saline solution
Syringes, assorted (1-20 mL)
Drugs used include epinephrine (1:10,000).
Procedural equipment includes the following:
Umbilical catheters (2.5 and 5 French)
Chest tube (10 French catheter)
Sterile procedure trays (eg, scalpels, hemostats, forceps)

Trained personnel
For all deliveries, at least 1 person should be present who is skilled in neonatal resuscitation and is responsible only
for the infant. This person must be skilled in the initiation of resuscitation, the use of bag-mask ventilation, and the
performance of chest compressions.
Additional personnel should be immediately available to assist in tasks that may be required as part of resuscitation,
including intubation, medication administration, and emergency procedures, if needed. If the delivery is identified as
high-risk, 2 or more skilled individuals should be assigned to the infant at delivery.
Remember that staff trained in neonatal resuscitation must apprentice with experienced personnel for some time
before they can be independently responsible for an infant at a delivery. Simulation is likely to become an
increasingly important component of training in neonatal resuscitation.[3]

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Resuscitation of Neonates
Preventing heat loss during resuscitation is essential. Intrauterine thermoregulation is passive, with no use of
calories or oxygen by the fetus. This passive thermoregulation process allows the fetus to achieve maximal
intrauterine growth without having to expend energy on thermal homeostasis. Brown fat storage begins during the
third trimester. Brown fat may be used for heat production in the newborn period.
Several factors lead to increased heat losses in the newborn. Neonates have a high ratio of skin surface area to
body weight, which increases heat loss and evaporative fluid loss. The fluid loss from the skin (due not to sweating
but to direct transdermal water loss) results in massive heat loss. The thin fetal skin, with blood vessels that are near
the surface, provides poor insulation, which leads to further heat loss.
Additionally, the newborn infant (especially if premature) has a limited capacity to change body position for heat
conservation. Animals ordinarily attempt to decrease heat loss by decreasing their exposed surface area (eg, by
curling up). This reduction in exposed surface area is accomplished by assuming a flexed position; however,
premature, critically ill, and depressed infants are unable to accomplish flexed positioning.
Neonates have a very limited capacity for metabolic heat production. The newborn infant has limited energy stores,
largely because of decreased subcutaneous fat and brown fat stores, and this paucity of fat stores is more
pronounced in premature and growth-retarded infants. Moreover, infants are not capable of effective shivering, which
is a major source of heat production in the adult. The main source of heat production in the newborn is nonshivering
Thermoreceptors in the face are markedly sensitive to heat and cold. Cold stimulation leads to norepinephrine
production and thyroid hormone release, causing brown fat to be metabolized. Brown fat is highly vascularized and
stored in pockets around the neonate's body. When it is metabolized, triglycerides are hydrolyzed to fatty acids and
glycerol. Additionally, glycolysis is initiated and glycogen stores are used, both of which result in glucose production.
Heat is produced as a byproduct of the increased metabolic rate and oxygen consumption.
Infants who experience heat loss have an increased metabolic rate and use more oxygen. Increased oxygen
consumption can be dangerous in infants who are experiencing respiratory compromise. The addition of cold stress
in infants who are poorly oxygenated can potentially trigger a change from aerobic to anaerobic metabolism. This
change in metabolism may lead to tissue hypoxia and acidosis because of the buildup of metabolic byproducts such
as lactate.
Because of the inefficiency of anaerobic metabolism, the infant uses up glucose and glycogen reserves rapidly while
still generating only a limited amount of energy for heat production. Therefore, cold stress can lead to both metabolic
acidosis and hypoglycemia. Infants with asphyxia have thermoregulatory instability, and hypothermia delays recovery
from acidosis.
Hypothermia on admission to the neonatal unit has been shown to be associated with an increased mortality.[4] In
view of this finding, it is clearly essential to prevent excessive heat loss in the delivery room and throughout
stabilization and transport to the neonatal unit. Normothermia and hypothermia in infants have been defined by the
World Health Organization (WHO) as outlined in Table 2 below.
Table 2. Axillary Temperatures in Infants Weighing Less Than 1500 g (Open Table in a new window)
Potential cold stress


Action Needed

C Continue

36-36.5o C Cause for concern

Moderate hypothermia

32-36o C

Danger; immediate warming of baby needed

Severe hypothermia

< 32o C

Outlook grave; skilled care urgently needed

The American Heart Association (AHA) and the American Academy of Pediatrics (AAP) have stated that the goal (of
the first temperature) should be an axillary temperature of 36.5o C. The aim is to achieve normothermia and avoid
hyperthermia, which is associated with progressive cerebral injury.
The environmental temperature is also important in controlling heat loss in the newborn. For a fetus, the thermal
environment is precisely regulated by the mother's core temperature, and heat losses are nonexistent. After delivery,
even with drying and the use of a radiant heat source are used, infants continue to lose large amounts of heat
through convective and evaporative mechanisms. When the environmental air is cooler than the neutral thermal
environment for the infant being resuscitated, further thermal losses ensue.
Heat losses are related both to the difference in water concentration between the skin and the air and to the absolute
temperature gradient. The primary goal in neonatal thermoregulation is prevention of heat loss, as opposed to later
correction of heat loss through rewarming. Ideally, a specific area (eg, a stabilization room) should be maintained
separate from the operating room (OR) or labor room so that special attention can be paid to the unusual thermal
and environmental needs of the newborn high-risk infant.
This stabilization area should be kept as warm as possible, with the requirements of the high-risk infant balanced
against the comfort of the adult staff in that area. Low delivery room temperatures can predispose to hypothermia,
and Neonatal Resuscitation program (NRP) guidelines recommend that if a preterm delivery is anticipated, the
delivery room temperature should be increased. Ideally, a dedicated room would be available in which ambient
temperature can be well controlled.
Suggested delivery room temperatures by age and weight (determined on the basis of consensus groups—still
considered an evolving clinical practice) are as follows[5] :
Estimated gestational age (EGA) less than 26 weeks, estimated birth weight (EBW) less than 750 g, or both 76o F or higher, target 78-80o F

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EGA 27-28 weeks, EBW less than 1000 g, or both - 74o F or higher, target 78-80o F
EGA 29-32 weeks, EBW 1001-1500 g, or both - 72o F, target 75o F
EGA 33-36 weeks, EBW 1501-2500 g, or both - 72o F, target 75o F
EGA 27-42 weeks, EBW greater than 2500 g, or both - 70o F, target 75o F
Newborns should be dried with prewarmed blankets or towels and placed on a prewarmed heat source. Open bed
warmers, which use radiant heat, are used in most delivery rooms. They provide warmth during resuscitation and for
any subsequent invasive procedures. It is important for the practitioner to keep in mind that this source of heat does
not protect the infant from evaporative heat loss but, instead, encourages evaporative heat losses.
Continuous monitoring of temperature should occur as soon as possible after the delivery. Premature infants (< 1500
g) should be covered in plastic wrap (polyethylene) to prevent excessive heat loss. A full resuscitation, including line
placement, can and should be performed with the plastic wrap in place. A woolen head cap should be used.
Weights should be obtained on radiant warmer bed scales. Adequately warming the transport incubator is essential.
The infant's temperature should be documented as soon as possible after birth and every 10-15 minutes thereafter
until continuous temperature monitoring has been established.
Another common source of heat loss in the neonate undergoing resuscitation is the use of unheated nonhumidified
oxygen sources for the bag-valve-mask device. The inspired gases sent to the lungs are subsequently heated and
humidified by the infant; this results in massive heat exchange from evaporative heat loss and insensible water loss.
Whenever possible, warmed and humidified gases should be provided in the resuscitation area. Alternatively, the
intubated and ventilated infant should be placed on a heated ventilator circuit as soon as is feasible.

Airway management
Once in a heated environment, the infant should be positioned so as to open the airway, and the mouth and nose
should be suctioned. A bulb syringe should be used for the initial suctioning.
Infants have a vagal reflex response to sensory stimulation of the larynx, which may induce apnea, bradycardia,
hypotension, and laryngospasm. Thus, suctioning the posterior oral airway or the trachea with a catheter because of
extremely thick or meconium-stained fluids may cause profound central apnea, potentially profound bradycardia, and
laryngospasm. Accordingly, it should be limited to infants with thick mucus that cannot be removed by bulb syringe or
used for the aspiration of stomach contents (when necessary).
Instillation of saline into the trachea also has been shown to stimulate the afferent sensory neurons leading to these
sequelae and consequently has no place in the immediate resuscitation period. Lung inflation has been shown to
reverse the effects of vagal stimulation. Vigorous suctioning of the nares with a catheter can lead to edema of the
nasal tissues with resulting respiratory distress after the infant leaves the delivery room. Wall suction should be set
so that pressures do not exceed 100 mm Hg.

Drying and suctioning often provide enough stimulation to initiate breathing; however, if more vigorous stimulation is
necessary, slapping the soles of the feet or rubbing the back may be effective. The back should be visualized briefly
for any obvious defect in the spine before beginning these maneuvers.
If there is no response to stimulation, it may be assumed that the infant is in secondary apnea, and positive-pressure
ventilation (PPV) should be initiated. At this point, the infant's respiratory rate, heart rate, and color should be
evaluated. Most infants do not require further intervention. This is considered routine care for most term infants with
clear amniotic fluid who are actively breathing and crying and have good muscle tone.

Supplemental oxygen
Infants who do not meet the criteria for routine care or who have difficulties with respiratory effort, tone, or color need
further intervention. Further resuscitative efforts should be guided by simultaneous assessment of respirations, heart
rate, and color.
Most infants need observational care. Neonatal transition occurs over time. Infants who have a sustained heart rate
higher than 100 beats/min and adequate respiratory effort but who remain cyanotic should receive blow-by oxygen
via oxygen tubing or a mask. Heated humidified oxygen is arguably advantageous, but it is rarely available in the
delivery room environment.
Supplemental oxygen should be initially provided with a fraction of inspired oxygen (FI O2) of 1 at a flow rate of 8-10
L/min. If supplemental oxygen is to be provided for a prolonged period, heated humidified oxygen should be supplied
via an oxygen hood, with the FI O2 adjusted to result in pulse-oximetry saturations of 92-96% in the term infant and
88-92% in the preterm infant.
Term infants may also be resuscitated with a FI O2 of less than 1, but this value should be increased if the infant
does not improve within 90 seconds. In premature infants, oxygen should be on a blender and blended up or down
to keep the saturation around 90%. If a blender is not available, an FI O2 of 1 should be used; this has not been
shown to be detrimental to premature infants for a brief duration.

Positive-pressure ventilation
For a number of reasons (see Transition to Extrauterine Physiology), it can be difficult for the infant to clear fluid from
the airways and establish air-filled lungs. Initial respiratory efforts may have to be augmented by the addition of either
continuous positive airway pressure (CPAP) or PPV.
Postresuscitative care is the term used for the management of infants who require more extensive resuscitation. The
addition of positive pressure aids in the development of functional residual capacity (FRC) and is needed more
commonly in premature infants. Mechanical lung inflation is also important to reverse persistent bradycardia in an
apneic asphyxiated infant. Call for assistance when beginning PPV if other team members are not already in

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Infants with adequate respirations who are experiencing respiratory distress (manifested by tachypnea, grunting,
flaring, retracting, or persistent central cyanosis) may benefit from positive end-expiratory pressure (PEEP), CPAP, or
both. If the infant is apneic, is making inadequate respiratory efforts (gasping), or has a heart rate lower than 100
beats/min, PPV should be initiated immediately. Infants who have continued central cyanosis despite supplemental
oxygen should also receive PPV.
The ideal bag is equipped to deliver PEEP, and the appropriately sized mask should be applied firmly to the face. A
T-piece resuscitator device gives a measured pressure through a mask with thumb occlusion and provides PEEP. It
has been shown to be just as effective as flow-inflating and self-inflating bags. It allows more precise delivery of
inflation pressure and inspiratory times.[6]
In term infants, an FI O2 of 1 should be used when PPV is started. If an FI O2 of less than 1 is used, this value should
be increased to 1 if the infant does not respond within 90 seconds. If supplemental oxygen is not available, room air
should be used to deliver PPV.
Premature infants (< 32 wk) who require PPV should begin with oxygen concentrations between room air and 100%
to maintain an oxyhemoglobin concentration of around 90% as determined by pulse oximetry. If the oxyhemoglobin
concentration rises to about 95%, oxygen should be weaned. Any infant who does not respond to PPV with a heart
rate of about 100 beats/min should be placed on an FI O2 of 1 and have the mask repositioned.
Some infants respond to brief mechanical ventilation and subsequently begin independent ventilation; others need
continued ventilatory support. Sufficient, but not excessive, initial pressure must be used to adequately inflate the
lungs, or else bradycardia and apnea will persist.
A pressure manometer should always be used with a pressure release valve, limiting the positive pressure to 30-40
cm H2 O during the first breaths. This may have to be reduced to 20-24 cm H2 O in preterm infants with an increase
in pressures if the chest does not rise or the heart rate does not rapidly increase.[7] To provide adequate distending
pressure, the infant must be properly positioned and the upper airway must be cleared of secretions; the mask must
be the correct size and form a tight seal on the face.
When assisted breaths are being provided, the primary measure of adequate initial ventilation is a rapid increase in
heart rate. A rise and fall in the chest wall movement is not always adequately assessed.[7] If no chest rise occurs,
either the airway is blocked or insufficient pressure is being generated by the squeezing of the bag.
Ventilatory rates of 40-60 breaths/min should be provided initially, with proportionally fewer assisted breaths provided
if the infant's spontaneous respiratory efforts increase. Although this practice has not been extensively studied, initial
inflation of the newborn's lungs with either slow-rise or square-wave inflation to a pressure of 30-40 cm H2 O for
approximately 5 seconds has been reported to result in more rapid formation of FRC.
At the moment of delivery and first breath, the neonatal lung is converting from a fetal nonaerated status to a
neonatal status. The neonatal lung has a requirement for gas exchange, and this requires the development of FRC
with the resorption of lung fluid and the resolution of most of the atelectasis. Therefore, initial slow ventilation with
more prolonged inspiratory times may be useful to assist in this task, balanced against the need to avoid
inappropriate inspiratory pressures.
Flow-controlled, pressure-limited mechanical devices are acceptable for delivering PPV. These mechanical devices
control flow and limit pressure and have been shown to be more consistent than bags. Self-inflating and flow-inflating
bags remain a standard of care. Laryngeal mask airways are effective for assisted ventilation when bag-mask
ventilation and intubation are unsuccessful.
Premature infants are at high risk for lung injury from large-volume inflation. Monitoring the pressure used in these
patients and providing consistent inflations without high pressures is essential. Initial inflation pressures of 20-25 cm
H2 O are usually adequate. Higher pressures may be needed if no improvement in heart rate or chest movement is
noted. CPAP may be beneficial in premature infants once they are breathing spontaneously.
The effectiveness of assisted ventilation should be evaluated by observing an increase in heart rate. Other signs that
should be monitored include improvement in color, spontaneous breathing, and improvement in muscle tone. All of
these signs should be assessed within 30 seconds of PPV administration.

Infants may require tracheal intubation if direct tracheal suctioning is required, effective bag-mask ventilation cannot
be provided, chest compressions are performed, endotracheal (ET) administration of medications is desired,
congenital diaphragmatic hernia is suspected, or a prolonged need for assisted ventilation exists.
See the video on assisted ventilation in the newborn, below.
Assisted ventilation newborn –Intubation and meconium aspiration. Video courtesy of Therese Canares, MD, and Jonathan
Valente, MD, Rhode Island Hospital, Brown University.

An appropriate blade (Miller size 0 or 1) should be chosen in accordance with the size of the infant. Premature
infants may be more easily intubated with a size 0 blade, and term infants require a size 1 blade. An appropriately
sized endotracheal tube should be chosen in accordance with the weight of the infant (see Table 3 below).
Table 3. Endotracheal Tube Size and Measurement at Lip According to Infant Weight (Open Table in a new window)
Infant Weight Endotracheal Tube Size Endotracheal Tube Measurement at Lip
< 1000 g


7 cm

1000-2000 g


8 cm

2000-3000 g


9 cm

> 3000 g


10 cm

Once inserted, the ET tube should be advanced until the vocal cord guide mark near its distal tip is observed to be
slightly past the vocal cords. This guide mark is positioned a variable distance from the distal tip (depending on the

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tube size) and is designed to result in the placement of the tube tip between the vocal cords and the carina at the
bifurcation of the right and left mainstem bronchi. Once correctly positioned, the ET tube should be secured and cut
to an appropriate length to minimize dead space and flow resistance.
Another way of estimating correct placement of the ET tube is to take the weight of the infant in kilograms and add 6
to yield at the number of centimeters at which the tube should be secured at the lip. Before the tube is secured, the
infant should be assessed for equal bilateral breath sounds with maintenance of oxygenation. An increase in the
heart rate within 5-15 seconds is an excellent indicator of adequate ventilation and appropriate ET tube placement.
Measurement of exhaled carbon dioxide provides secondary confirmation. Carbon dioxide detectors use a
colorimetric change to indicate exhalation of the gas. The use of such detectors is the only technique that has been
evaluated for confirmation of ET tube placement in infants and is therefore recommended.[8, 6] When carbon dioxide
detectors are used in infants with poor pulmonary blood flow that cannot deliver sufficient carbon dioxide to the
lungs, a false negative result may occur, leading to unnecessary extubation.
Ultimately, ET tube position is confirmed with chest radiography. Free-flow oxygen should be provided throughout the
procedure, and effective ventilation should be provided via the bag or ventilator after the infant is intubated.

Cardiovascular support and chest compressions
Most infants who present at delivery with a heart rate lower than 100 beats/min respond to effective ventilatory
assistance by rapidly increasing their heart rate to normal levels. In contrast, if an effective airway and effective
ventilation are not established, further support is not effective. Chest compressions should be initiated after only 30
seconds of effective PPV if the heart rate remains below 60 beats/min.
An assessment of the heart rate can be obtained through palpation of the umbilical stump at the level of insertion of
the infant's abdomen or through direct auscultation of the precordium. Chest compressions should be discontinued
as soon as the heart rate is higher than 60 beats/min.
Chest compressions may be performed either by circling the chest with both hands and using a thumb to compress
the sternum or by supporting the infant's back with one hand and using the tips of the middle and index finger to
compress the sternum. The thumb technique is preferred because it allows better depth control during
compressions. This technique may also generate higher peak systolic and coronary perfusion. The 2-finger
technique may be used when access to the umbilicus is required.
Pressure should be applied to the lower portion of the sternum, depressing it to a depth of about one third of the
anterior-posterior diameter. The chest should fully reexpand during relaxation, but the rescuer's thumbs should not
remain in place. One ventilation should be interposed after every 3 chest compressions. An overall rate of 120
compression/ventilation events per minute is recommended; with the 3:1 compression-to-ventilation ratio, this
equates to 90 compressions and 30 breaths each minute.
Evaluate heart rate and color every 30 seconds. Infants who fail to respond may not be receiving effective ventilatory
support; thus, constantly evaluating ventilation is imperative. Chest compressions should be discontinued when the
heart rate is 60 beats/min or higher.

Neonatal resuscitation drugs should be stocked in any area where neonates are resuscitated, including each
delivery and stabilization area, as well as the emergency department (ED). Personnel should be familiar with
neonatal medications, concentrations, dosages, and routes of administration. Drugs currently recommended include
epinephrine (1:10,000) and isotonic sodium chloride solution (0.9%) as an intravascular volume expansion agent.
Epinephrine should be considered only when the heart rate is below 60 beats/min and ventilation has been
established and provided for at least 30 seconds. The only exception to this rule may be in infants born without a
detectable pulse or heart rate. The recommended dose is 0.01-0.03 mg/kg (0.1-0.3 mL of the 1:10,000 solution),
preferably administered intravenously (IV). Higher IV doses are not recommended, and the postresuscitation
hypertension could put premature infants at risk for intraventricular hemorrhage.
If vascular access cannot be obtained, epinephrine may be given via the ET tube, but in such cases, the dose should
be increased to 3 times the IV dose. Ensure that the small volume is not deposited on the ET tube connector or in
the lumen of the tube. Administration of epinephrine may be followed with infusion of 0.5-1 mL of saline to ensure
that the drug is delivered to the lung, where it is absorbed and delivered to the heart.
If an umbilical venous catheter is used for medication administration, the catheter should be inserted only as far as
the point where blood flow is obtained (usually 3-5 cm). Because the dosing recommendations for epinephrine
include ET administration, the need for emergent placement of umbilical venous catheters has been reduced
markedly in the delivery room.
In an editor's note commenting on an article addressing cardiopulmonary resuscitation in the delivery room,[9]
Catherine DeAngelis wrote, "[C]heck the airway (optimize respiratory support) one more time before compressing
the chest. More often than not, you and the infant can then take deep breaths, and you can beat your own chest
instead of the infant's."
In the study described in this article, approximately one third of the infants with neonatal depression at birth had
associated fetal acidemia.[9] However, in the remaining infants without fetal acidemia, chest compressions were
initiated as a consequence of improper or inadequate ventilatory support at birth.
In the population of infants without initial acidemia, chest compression or epinephrine therapy was ineffective.[9] The
heart rate only improved after effective tracheal intubation established a patent airway or after incremental increases
in PPV exceeded the opening pressure of the lungs, establishing ventilation.
This study and others continue to reinforce the primary importance of the establishment of effective ventilation.
Without ventilation, other therapies, including medications, will not be effective in establishing adequate heart rate
and perfusion.

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Sodium bicarbonate had previously been recommended in the delivery room to reverse the effects of metabolic
acidosis related to hypoxia and asphyxia. However, studies show that 0.9% saline provides better cardiac and blood
pressure support to correct both the metabolic acidosis itself and the underlying cause of the acidosis. Use of sodium
bicarbonate in the delivery room has been associated with an increased incidence of intraventricular hemorrhage in
very low birth weight infants.
The data are insufficient to support recommending routine use of bicarbonate in neonatal resuscitation. However,
sodium bicarbonate may be useful in cases of prolonged arrest after adequate ventilation is established. A dose of 2
mEq/kg may be administered IV. If sodium bicarbonate is used in the face of a persistent respiratory acidosis and
elevated partial pressure of carbon dioxide (PCO2), the acidosis is not corrected.
Volume expansion may be used in neonates with evidence of acute blood loss or with evidence of shock of any
etiology. In general, the neonatal heart responds well to the increase in preload at the atrial level caused by the
volume expansion. Hypovolemia may be masked in a newborn infant because of the significant peripheral
vasoconstriction caused by the elevation in catecholamine levels after delivery. Systolic blood pressure also may be
elevated falsely with pain.
The current recommendations for volume expansion during resuscitation include isotonic sodium chloride solution or
lactated Ringer solution, 5% albumin, plasma protein fraction (eg, Plasmanate), or O-negative blood that has been
cross-matched with the mother. However, because of the advantages of long shelf life, low cost, and ready
availability, coupled with the lack of evidence for the superiority of any other agents, isotonic sodium chloride solution
is the most frequently used agent for volume expansion.
The currently recommended dosage of isotonic sodium chloride solution for volume expansion is 10 mL/kg IV over
5-10 minutes; the solution may be infused more cautiously in extremely preterm infants. When blood loss is known,
consider use of O-negative packed red blood cells (RBCs). Restoring the critical oxygen-carrying capacity is

Immediate Postresuscitation Period
Maintenance of airway and ventilation
The goal of delivery room management is to stabilize the airway and ensure effective oxygenation and ventilation.
Once initial lung recruitment is obtained, avoiding overdistention is essential. Breaths delivered by bag-mask
ventilation may be difficult to control and may result in overdistention and consequent pneumothorax or
pneumomediastinum. Additionally, the unheated nonhumidified oxygen can quickly cool the infant via the large
surface area of the lungs, resulting in hypothermia. Therefore, mechanical ventilation should be initiated as soon as
possible once the infant is stabilized.
Although the ideal mode of assisted ventilation is controversial, providing adequate positive end-expiratory pressure
(PEEP) to prevent atelectasis, while at the same time preventing overinflation, is indicated. Once the appropriate
functional residual capacity (FRC) is obtained, it is essential to use the lowest possible level of support that still
allows adequate oxygenation and ventilation.
Oxygen saturation should be monitored continually and arterial blood gas analysis performed as needed during the
initial stabilization period. Saturations should be maintained in the 90-96% range for the term infant and in the
88-92% range for the preterm infant after the initial stabilization.

Fluid and electrolyte management
In utero, nutrients are provided in their basic form. Glucose is the major energy substrate of the fetus. Fetal glucose
uptake parallels maternal blood glucose concentration. The liver, heart, and brain receive the greatest cardiac output
and consequently the largest amount of glucose. The fetus uses glucose, lactate, and amino acids to store fuels that
are used during transition.
Neonates must develop a homeostatic balance between energy requirements and the supply of substrate as they
move from the constant glucose supply of fetal life to the normal intermittent supply of glucose and other fuels that is
characteristic of extrauterine life. With the clamping of the cord, the maternal glucose supply is cut off. A fall in blood
glucose during the first 2-6 hours of life occurs in healthy newborns. The blood glucose usually reaches a nadir and
stabilizes at 50-60 mg/dL.
The immediate goals of fluid and electrolyte support after resuscitation are to maintain an appropriate intravascular
volume and to achieve glucose homeostasis and electrolyte balance. The neonatal cardiovascular system is very
sensitive to preload, requiring adequate intravascular volume to maintain adequate cardiac output. Therefore,
expansion of intravascular volume with appropriate solutions (eg, isotonic sodium chloride solution) often is
considered in the neonate with inadequate blood pressure or perfusion.
Additionally, hypoglycemia may occur rapidly in critically ill or premature infants. Blood glucose determinations
should be performed as soon as possible, and a continuous infusion of glucose should be started at 4-6 mg/kg/min
for infants who are unable to tolerate enteral feedings.
Dextrose boluses should be limited to symptomatic infants because they may result in transient hyperosmolarity and
rebound hypoglycemia. Electrolytes (eg, sodium, potassium, and chloride) should not be added initially, because the
fluid shifts from other body compartments allow adequate electrolyte supply until adequate renal function is
The practitioner should monitor the weight, clinical hydration status, urine output, and serum sodium concentrations
closely because inappropriate fluid overload or restriction can lead to increased mortality and morbidity. The infant's
environment must be taken into account in the calculation of fluid requirements. Fluid may be started at a rate of
60-80 mL/kg/day for the infant in a humidified incubator, whereas it may have to be given at a much higher rate for
the infant in a dry radiant-warmer environment.

Preparation for transport

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Preparation of the infant for transfer to a remote nursery for care after resuscitation involves the following key
considerations (see Transport of the Critically Ill Newborn):
Complete all the routine care that is required of newborn infants; these basics of care may be neglected in the
rush to prepare the infant for transport, with potentially disastrous results
Secure all lines, tubes, catheters, and leads for transport; monitoring in the transport environment is possible
only with functioning leads in place, which is frequently difficult to accomplish
Provide rapid and complete documentation of the resuscitation and subsequent therapies for the use of future

Special Problems During Resuscitation
A number of congenital and other neonatal conditions may present in the delivery room and may have an effect on
the course of resuscitation. The most important of these are briefly reviewed below.

Extreme prematurity
Premature infants have special needs that must be considered during the critical period immediately after delivery if
mortality and morbidity are to be decreased in this group. This population is at increased risk for respiratory failure,
insensible water losses, hypoglycemia, and intraventricular hemorrhage. A full discussion of the many difficulties of
extreme prematurity is beyond the scope of this article, but additional information may be found elsewhere (see
Insensible water loss in the premature infant is increased secondary to the infant's poorly cornified epidermis and
immature stratum corneum, which presents only an insignificant barrier to evaporative heat loss. The stratum
corneum is not functionally mature until 32-34 weeks' gestation. Differences in skin maturity, prenatal nutritional
status, ventilation requirements, and environmental conditions all may influence the magnitude of insensible water
loss that occurs after birth.
The skin is the most important route for water depletion after delivery of the extremely immature infant.
Transepidermal water loss (TEWL) is highest at birth in infants who are born before 28 weeks' gestation and
decreases slowly with advancing gestational age. Despite declines in TEWL with advancing age, infants born before
28 weeks' gestation continue to have increased TEWL for 4-5 weeks after birth, compared with infants born at term.
Because of high evaporative loss with the accompanying heat loss, the ability to achieve and maintain
thermoregulation is compromised further. The skin barrier dysfunction increases the risk of infection, especially with
organisms that colonize the skin surface (eg, staphylococcal species). This thin skin barrier also places the
extremely immature infant at risk for toxic reactions to topically applied substances. Additionally, skin integrity is
easily disrupted by the use of adhesives, which should be limited in premature infants.
Premature infants need increased fluid administration rates initially if they are on radiant warmers for a prolonged
period. With increased parenteral fluid administration using dextrose-containing fluids, the dextrose must be
monitored closely to ensure euglycemia. Placing infants in a humidified environment decreases TEWL, improves
maintenance of body temperature, and does not delay skin maturation.
Measures to decrease insensible water loss should be initiated at delivery. Because radiant warmers are used
routinely at deliveries out of a need for maximal patient access, infants weighing less than 1000 g should be
wrapped in a plastic blanket or other barrier to decrease evaporative water loss until they can be placed in a
humidified environment. However, care should be taken to ensure that the barrier does not block the transmission of
heat from the radiant source.
Premature infants are at risk for intraventricular hemorrhage and periventricular leukomalacia (PVL) secondary to
their immature cerebral vascular regulation and the persistence of the germinal matrix. These disorders often lead to
serious permanent neurodevelopmental disabilities.
Prevention of these conditions or reduction of their severity may begin in the delivery room. Mechanical ventilation
and fluid administration must be managed cautiously in this group of infants. Volume expansion should be
administered only in the face of true hypotension. Knowledge of normal blood pressure values for infants of various
gestational ages is essential. Volume expansion in the face of normal blood pressure increases the risk of
intraventricular hemorrhage.
Additionally, it is important to administer any hyperosmolar medications (eg, sodium bicarbonate) slowly. Mechanical
ventilation may lead to harmful fluctuations in cerebral blood flow, especially when the partial pressure of carbon
dioxide (PCO2) and pH are rapidly altered. Rapid alterations in PCO2 and pH result in acute fluctuations in the
cerebral blood flow of the premature infant with immature cerebral vascular autoregulation.
Premature infants are also at high risk for volutrauma caused by poor lung compliance and overventilation after the
administration of exogenous surfactants if changes in lung compliance are not monitored carefully. Overventilation
with excessive tidal volumes and hypocarbia is associated with chronic lung disease.
Stabilization of the infant using the lowest peak inspiratory pressure (PIP) that will still yield adequate oxygenation
and ventilation is essential. Hand ventilation of an intubated infant, especially when done by inexperienced
personnel, often leads to inconsistent tidal volumes and pressures. Use of a mechanical ventilator designed for
infants offers the advantages of more consistent tidal volumes and a reduction of the heat losses associated with the
use of unheated nonhumidified air in hand ventilation.
Although artificial surfactant administration is associated with a reduction of adverse sequelae in infants, it may lead
to hyperventilation and overdistention if not carried out by experienced and attentive personnel. After the instillation
of artificial surfactant, personnel must remain alert so that they can react rapidly to changes in pulmonary compliance
to prevent the onset of hypocarbia and alkalosis.
After the institution of mechanical ventilation, care should be taken with airway suctioning because vigorous or
frequent airway suctioning is associated with hypoxia, intraventricular hemorrhage, and periventricular leukomalacia.
Prematurity with respiratory distress syndrome (RDS) is not associated with mucus production in the first 24 hours of

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life; thus, suctioning protocols should be altered to provide minimal suctioning during this time.

Airway problems
Choanal atresia
Choanal atresia is caused by a failure of embryologic regression of nasal airway tissue, which results in partial or
complete occlusion of the nasal airway. These choanal defects may be bony or membranous, with most having a
bony component. Complete bilateral stenosis usually results in a neonatal respiratory emergency at birth because
infants generally are obligate nasal breathers during the first 6-8 weeks of life. At rest, these infants usually manifest
severe apnea, retractions, and respiratory distress that may be relieved with crying.
Wheezing or stridor may be audible with inspiration, and collapse of the small airways with vigorous inspiratory effort
can occur. The infant in respiratory distress should be stimulated to cry, and an artificial oral airway may be used to
avoid intubation. The clinical diagnosis is based on the inability to pass a small-caliber catheter through the nasal
passages. However, the act of passing catheters, especially if repeated, may cause nasal passage swelling in any
infant, and the subsequent iatrogenic occlusion can mimic the congenital condition.
An alternative noninvasive method of excluding the diagnosis of complete atresia is to place a glass slide under the
nasal orifices and look for fogging with expiration. Supplemental oxygen should be administered to infants with
choanal atresia, and an oral airway may be of assistance. If the infant remains in significant respiratory distress,
intubation is necessary. Intubation relieves the obstruction so that little if any ventilation will be required.
Pierre Robin syndrome
Pierre Robin syndrome presents with micrognathia and resultant displacement of the tongue into the posterior
pharynx, which may occlude the upper airway. A central cleft of the soft palate is usually present. Respiratory
distress and cyanosis are caused by the obstruction of the upper airway.
In the delivery room, the infant should be given supplemental oxygen and placed in a prone position in an attempt to
induce the tongue to move forward in a dependent fashion from the posterior pharynx and thereby relieve the airway
obstruction. If the infant continues to have persistent respiratory distress, an oral airway may be placed.
Alternatively, an appropriately sized endotracheal (ET) tube may be passed through the nose into the hypopharynx.
Tracheotomies are generally not necessary and should be avoided. Intubation of these infants often is not easy,
because visualization of the larynx is difficult.
Tracheal webbing
The pathogenesis of tracheal webbing originates in the 10th week of gestation, when an arrest in the development of
the larynx near the vocal cords results in a residual web of tissue persisting in the airway. Approximately 75% of
tracheal webs occur at the level of the vocal cords. These lesions are critical if more than 50% of the airway diameter
is occluded, but this degree of occlusion is rare. Tracheal webs may be relatively asymptomatic at birth, with the
development of distress later when activity increases and the need for airway flow increases.
During attempted intubation, an obstructive covering may be observed over the larynx and may occlude the airway
completely. If this membrane is thin, the ET tube may be pushed beyond the obstruction. If the membrane is thick,
the infant requires an emergency tracheotomy. If the infant is in severe distress, a large-bore needle or catheter may
be placed in the trachea to allow gas exchange while emergency treatment is being arranged for. Inexperienced
personnel may confuse this rare disorder with simple inability to visualize the vocal cords.
Esophageal atresia with or without tracheoesophageal fistula
Esophageal atresia is rarely considered a life-threatening emergency; however, early diagnosis is essential to
prevent further complication. It may be divided into 5 types as follows:
Type I (esophageal atresia with a distal fistula) - This is the most common type (85%); air is present in the
stomach; a blind upper esophageal segment is present, with the distal segment of the esophagus connected
to the trachea via a fistula
Type II (esophageal atresia only) - A blind upper and lower esophageal segment is present; air is absent from
the lower gastrointestinal (GI) tract, but an air-filled blind upper pouch may be observed
Type III (H-type esophageal atresia) - An isolated fistula connects the esophagus and trachea, usually
occurring at the upper portion of the trachea and esophagus
Type IV (esophageal atresia with a proximal fistula) - This type is rare; an upper esophageal segment is
present with a fistula to the trachea and a blind lower esophageal segment; air is absent from the lower GI
Type V (esophageal atresia with a double fistula) - This type is rare; an upper esophageal segment is present
with a fistula to the trachea, and a second fistula connects the distal esophagus and trachea; air is present in
the stomach
The most common clinical symptoms of esophageal atresia with or without a tracheoesophageal fistula include
coughing, choking, and cyanosis. Infants with isolated esophageal atresia usually do not demonstrate respiratory
distress immediately in the delivery room but may have excess secretions. The atretic air-filled esophageal pouch
occasionally may be observed on a chest radiograph, manifested by a midthoracic rounded lucency. This pouch is
visualized more readily by the passage of a radiopaque catheter into the esophagus before the chest radiograph.
Because secretions or oral feedings cannot pass into the stomach, the contents of the esophageal pouch readily
reflux, placing these infants at high risk for aspiration. A Replogle suction catheter should be inserted to reach the
esophageal pouch and placed on low continuous suction as soon as possible. Infants with an associated distal
fistula to the trachea are also at high risk for aspiration of gastric contents into the lungs via the gastrobronchial
fistula, which most often empties into the airway near the carina.
If at all possible, positive-pressure ventilation (PPV) should be avoided in these infants. Any positive pressure
applied to the airway results in inflation of the fistula, stomach, and bowel, which then results in abdominal distention.
This distending pressure cannot be relieved by esophageal reflux through the atretic esophagus. Relief of the
distending pressure occurs with reflux of gastric contents into the lungs via the fistula. The continued application of

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PPV also may lead to massive gastric distention and possible rupture.
In rare emergency situations, percutaneous gastrotomy may be required to decompress the stomach; however,
controlled surgical placement of a gastrostomy tube is preferable.
Cystic adenomatoid malformation
Cystic adenomatoid malformations of the lung are masses that may cause a spectrum of symptoms, from massive
mediastinal shifts in the fetus (resulting in pulmonary hypoplasia) to isolated subsegmental lobar masses in the
newborn (or adult) with minimal associated symptoms. Severe lesions also may cause fetal cardiac compromise and
result in hydrops.
If the infant requires PPV, extreme caution must be used, because the distending pressure may inflate the cystic
malformation. An inflated cystic malformation is capable of massive expansion, causing respiratory embarrassment
because of the prevention of ventilation of other normal lung tissue.
Cystic hygromas
Cystic hygroma is the result of a congenital deformity of the lymphatic channels. Lymph accumulates and may
compress the airway, depending on the size and location of the lymph accumulation. Approximately 80% of these
lymphatic cystic accumulations occur in the neck and may compress the trachea.
These infants may present with significant respiratory distress and may require immediate intubation with deep
positioning of the ET tube to relieve the obstruction by stenting open the airway. However, most of these lesions
expand outward from the neck and do not cause significant airway compromise in the delivery room.

Pulmonary compression
Congenital diaphragmatic hernia
The pathogenesis of congenital diaphragmatic hernia involves the incomplete formation of the diaphragm in the
fetus, resulting in a migration of the abdominal viscera into the chest during development. If the defect is large and
the abdominal viscera have caused long-standing compression of the developing lungs, pulmonary hypoplasia may
The diagnosis of diaphragmatic hernia is frequently established by means of prenatal ultrasonography, which allows
management to be transferred to a perinatal referral center where pediatric surgery and appropriate medical support,
including extracorporeal bypass, are available. In the delivery room, the infant often presents with respiratory
distress. Physical signs may include a scaphoid abdomen and a shift in heart sounds to the right hemithorax.
Respiratory distress in the delivery room may be caused by pulmonary hypoplasia or may be secondary to
expansion of the bowel caused by swallowed air. The expansion of the bowel results in compression of the lung.
Delivery room management includes immediate intubation and passage of a large catheter for gastric
decompression. Intubation prevents distention of the stomach and bowel contents because of crying or
bag-valve-mask ventilation. The gastric decompression should be achieved with a Replogle or Salem pump suction
catheter connected to a low continuous drain. Constant maintenance of gastric suction during the preoperative and
immediate postoperative periods is essential.
New modes of ventilation, such as high-frequency oscillatory ventilation (HFOV), have decreased the use of
extracorporeal membrane oxygenation (ECMO) in this population. However, the survival rate for infants with this
anomaly has not changed over the past decade.
Pneumothorax and pneumomediastinum
Air leak syndromes are disorders produced when a rupture of pulmonary tissue occurs, leading to the escape of air
into spaces where air would not normally be present. The incidence of pneumothorax varies with gestational age,
severity of pulmonary disease, need for assisted ventilation, mode of ventilation, and expertise of delivery room
After the initial rupture of a small airway or an alveolus, air may enter the perivascular and peribronchial spaces and
track along the lymphatic channels. Air that dissects into the hilum results in a pneumomediastinum; air that tracks
into the pleural space manifests as a pneumothorax. Spontaneous rupture of the lung directly into the pleural space
is thought to occur rarely but may be caused iatrogenically by the percutaneous insertion of a chest tube. Caution is
Pneumomediastinum frequently is an isolated disorder that occurs spontaneously in infants with minimal pulmonary
disease. These infants usually are asymptomatic or minimally symptomatic because the air in the mediastinum can
escape to the tissues of the neck. Intrathoracic tension is relieved, and circulation is not compromised. Infants with a
pneumomediastinum should be observed. Intervention usually is unnecessary.
Pneumothorax may occur immediately in the delivery room or later, when significant pulmonary disease has
developed. Pneumothorax often is associated with PPV, but it also may occur in infants who are not receiving
assisted ventilation. After the initial air leak, the subsequent expansion of intrathoracic spaces often results in a rapid
increase of intrathoracic pressure to the point where the lungs cannot be ventilated and venous blood cannot be
returned to the heart. This condition is termed a tension pneumothorax.
The rapid clinical deterioration of infants with this condition is caused by circulatory collapse and inability to ventilate.
Any infant who has a sudden precipitous change in ventilatory status associated with an abrupt fall in blood pressure
should immediately be evaluated for a pneumothorax. Transillumination of the chest may be used for the rapid
diagnosis of severe tension pneumothorax. When the clinical situation allows it, radiography should be performed to
establish or confirm the diagnosis.
Infants in acute distress should undergo needle aspiration to evacuate the extrapulmonary air while preparations are
made to place a chest tube. Symptomatic pneumothorax is managed with the insertion of a chest tube until the
pulmonary leak is resolved. A chest tube may not be required if the pneumothorax is small and the infant is not

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receiving PPV. Supplemental oxygen (fraction of inspired oxygen (FI O2) of 1) often is administered for 6-12 hours to
hasten reabsorption of the trapped intrapleural air.

Miscellaneous conditions
Multiple gestation
The delivery and subsequent resuscitation of multiple infants presents a considerable challenge to the labor and
delivery team. The first consideration to be addressed with the initial prenatal diagnosis of multiple births is to ensure
that care is being provided at an institution capable of adequately supporting both the mother and multiple infants at
A minimum of 2 experienced staff members should be available for each infant. Multiple-gestation infants are often
born prematurely (especially with higher-order gestation), and more personnel may be required for each infant.
Therefore, for higher-order gestation involving triplets or more, preparation to ensure the presence of appropriate
personnel and equipment must be planned well in advance of the delivery.
The team should be led and organized by a designated experienced leader, and the planning phase should involve
healthcare providers from a number of disciplines, including neonatologists, perinatologists, nurse practitioners,
pediatricians, nursery and obstetrics nurses, respiratory therapists, and pharmacists. The delivery team should
consist of individuals who are prepared to make complex decisions, perform technical skills, and respond quickly to
changing circumstances.
Organization and teamwork are essential, with adequate personnel prospectively identified as designated
responders to each infant. Such preparations are becoming more commonplace, now that assisted conception is
giving rise to an increasing number of multiple-birth pregnancies.
When preparing for the resuscitation of an infant with hydrops fetalis, sufficient skilled personnel must be in the
delivery room to ensure that the multiple needs of this significantly compromised neonate can be met. Equipment
should be prepared before the delivery, and all personnel in the room should be assigned specific procedures, such
as paracentesis or thoracentesis (if required). These procedures may have to be performed immediately if the fluid
accumulation is causing difficulties in ventilation.
If the hydrops is caused by anemia, blood for transfusion should be available in the delivery room. Because of the
excess fluid in the lungs, it is often necessary to use high pressures and oxygen initially. Artificial surfactant
administration also has been employed in the delivery room to treat any surfactant deficiency in an attempt to
improve pulmonary function. Umbilical venous and arterial lines should be placed and central venous pressures
Omphalocele and gastroschisis
Gastroschisis is an abdominal wall defect lateral to the umbilicus that does not have a sac or membrane covering the
bowel. In contrast, an omphalocele involves herniation of the bowel through the umbilical opening, with the bowel
covered by a thin membrane, unless the membrane has been ruptured during birth.
For both omphalocele and gastroschisis, maintain adequate intravascular fluid volume, maintain thermoregulation,
and prevent bowel ischemia. Preoperatively, infants with these conditions have increased fluid requirements unless
the bowel is appropriately wrapped with an airtight material.
The bowel may be first wrapped with warmed saline-soaked gauze. Care should be taken to support the bowel and
not compromise blood flow. Observe the bowel closely to ensure that no areas are compromised as a result of the
bowel twisting. A 10 French Replogle or Salem pump suction catheter should be placed on low continuous suction to
decompress the bowel and prevent further ischemic injury.
If the infant is diagnosed with an omphalocele, the blood glucose level should be assessed because this defect may
be associated with Beckwith-Wiedemann syndrome. Trisomy 18 is associated with this anomaly. Therefore, if the
condition is recognized prenatally, amniocentesis for chromosomal analysis should be offered to the family. If
chromosomal information is not available at the time of delivery and there are other anomalies consistent with
trisomy 18, surgery should be delayed until a complete genetic evaluation is complete.
Congenital anomalies
Severe malformations observed in the delivery room should not alter resuscitative management unless skilled and
experienced care providers are able to determine that the condition is incompatible with life. The family should be
involved in any decision involving the withholding of resuscitation. Infants with severe malformations should be
resuscitated and stabilized until an accurate diagnosis can be made.

Controversies in Resuscitation
The development of a certification program has led to the standardization of neonatal resuscitation. Evaluation of the
current standards is an ongoing process. As new research is published, it is essential to assess the quality of the
studies and to determine whether the evidence is sufficient to mandate changes in practice. Even with the current
standardization, there remain some important controversies and concerns in resuscitation.

Room air versus 100% oxygen
Oxygen is a drug with potentially serious adverse effects that must be considered. Oxygen free radicals are capable
of tissue injury and have been implicated in several disease states in the neonate. The use of lower oxygen
concentrations in neonatal resuscitation may decrease the number of oxygen free radicals and their damaging
adverse effects.
In one study, resuscitation with room air was shown to be as effective as 100% oxygen at lowering pulmonary
vascular resistance. Other investigations have shown that there is no benefit to raising the partial pressure of oxygen

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(PO2) above 50 mm Hg. A 2011 meta-analysis concluded that the literature was insufficient to support any statement
regarding the superiority of oxygen or room air as the initial gas mixture for neonatal resuscitation.[10]
Although large controlled multicenter trials indicate that room air (fraction of inspired oxygen [FI O2) = 0.21) is just as
effective as 100% oxygen in resuscitating term infants, long-term outcomes are pending. The only follow-up study
looking at these infants at 18-24 months showed no significant difference in somatic growth or neurologic handicaps
between infants resuscitated in room air and infants receiving 100% oxygen.
The current consensus is that supplemental oxygen should be provided whenever positive-pressure ventilation
(PPV) is required during resuscitation. Free-flowing oxygen should also be used in infants with central cyanosis.
Clinicians may begin resuscitation with an oxygen concentration of less than 100% and may even consider starting
with room air as new research data become available.
Research studies indicate that the immediate outcomes of these 2 approaches are similar in term infants without
underlying lung disease. In general, the data suggest that in situations where 100% oxygen is not available,
resuscitation should proceed with the use of room air and a self-inflating bag.

Timing of artificial surfactant administration
Surfactant deficiency, the primary factor in the development of respiratory distress syndrome (RDS), is the most
common cause of persistent and progressive respiratory distress in premature infants.
Controlled, randomized clinical studies have shown that prophylactic administration of exogenous surfactant to
premature infants effectively reduces death secondary to RDS. Studies have also shown that treatment of only
infants who develop RDS symptoms yields a significant reduction in death secondary to RDS. Prophylactic dosing of
artificial surfactant is performed in the delivery room before the first breath or within 15 minutes after birth.
Controversies related to prophylactic artificial surfactant use are related to the interruption of the standard
resuscitation paradigm for the administration, treatment, and attendant risk management of a population of infants
who would not develop RDS, as well as the additional costs related to this dosing scheme.
The argument for prophylactic surfactant dosing is that treated infants who require surfactant replacement have more
uniform and effective drug distribution when the lungs are fluid-filled and do not have air-fluid interfaces. Obviously,
treatment of only infants with a confirmed diagnosis of RDS results in a smaller number of infants being treated. The
proportion of infants given prophylactic artificial surfactant therapy who would not develop RDS depends on the entry
criteria for prophylactic treatment and on population characteristics.
Studies have demonstrated that early prophylactic dosing of surfactant is efficacious and is associated with better
outcomes in extremely premature infants. Researchers have recommended that whenever possible, infants with
surfactant deficiency should be identified before delivery by using the lecithin-sphingomyelin ratio or testing for the
presence of phosphatidylglycerol.
Researchers also suggest that all infants delivered earlier than 30 weeks' gestation should receive their first dose of
surfactant in the delivery room within the first few minutes of life, after cardiopulmonary stabilization. Infants born
later than 30 weeks' gestation should receive rescue therapy as soon as they show clinical signs of RDS. Infants
born at 30-36 weeks' gestation may benefit from surfactant with rapid extubation to continuous positive airway
pressure (CPAP).[11, 12, 13, 14]

Intubation and suctioning for meconium aspiration
Meconium-stained amniotic fluid (MSAF) is present in 10-15% of all deliveries but is rarely seen before 34 weeks'
gestation. Of newborns born through MSAF, 60% require stabilization or resuscitation. Of these 60%, 3-4% are
diagnosed with meconium aspiration syndrome (MAS). Meconium aspiration in a newborn can lead to atelectasis,
overdistention of the alveoli, pneumothorax, pneumonitis, surfactant deficiency, and persistent pulmonary
hypertension. Mortality is as high as 5-10% in these infants.[15]
Trained personnel should be in attendance at all meconium-stained deliveries. Suctioning of the oropharynx and
nasal pharynx once the head is delivered is no longer recommended. A large, multicenter, randomized trial with 2514
infants showed that intrapartum suctioning did not decrease the risk of MAS. The current Neonatal Resuscitation
program (NRP) guidelines and recommendations no longer advise routine intrapartum oropharyngeal and
nasopharyngeal suctioning for infants born to mothers with MSAF.[16]
A multicenter, prospective, randomized, controlled trial concluded that regardless of the type of meconium, vigorous
infants (defined as those with a strong respiratory effort, good muscle tone, and a heart rate higher than 100
beats/min) are not at increased risk for MAS if they are not intubated and suctioned.[17] The study also indicated that
depressed infants, regardless of the type of meconium, do benefit from intubation and suctioning before the initiation
of PPV.
Depressed infants should be placed on a radiant heat source, and no drying or stimulation should be provided until
they are intubated and direct tracheal suctioning is performed. A meconium aspirator should be applied directly to
the endotracheal (ET) tube, and a continuous pressure of 120-150 mm Hg should be applied as the tube is removed.
If meconium is obtained, the heart rate must be evaluated before a second intubation is performed. With the second
intubation, provision of PPV through the ET tube may be considered after suctioning.
Once an infant has been stabilized, intubation and suctioning can be performed again. Researchers have stated that
meconium can be suctioned from the trachea up to an hour or even longer after birth. Note that infants who are
vigorous at delivery and then manifest respiratory distress or become depressed should also undergo intubation and
suctioning before initiation of PPV, if meconium was present.
Preliminary studies show potential benefits from using dilute surfactant lavage in infants with MAS. Surfactant is
inactivated by meconium, and surfactant lavage may wash out the residual meconium, improve mucociliary removal,
and mitigate the residual effects on exogenous surfactant.[18]
Research has shown that infants who receive surfactant replacement therapy within 6 hours of delivery have

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improved oxygenation and a reduced incidence of air leaks, pulmonary morbidity, and length of stay; however,
further studies are still necessary before this approach can be recommended as standard care.

Current data are insufficient to support recommendation of systemic or head cooling for infants with suspected
asphyxia. Study results are conflicting. One multicenter trial did not show a difference in the number of survivors with
severe disabilities when head cooling was used. Another large multicenter trial that evaluated systemic hypothermia
found a significant decrease in death or moderate disability at age 12 months and 18 months, as did a smaller trial.
Hypothermia carries risks of arrhythmias, bleeding, thrombosis, and sepsis; however, current studies of modest
hypothermia have not reported these complications. Future clinical trials are needed to determine the benefits of
hypothermia and to compare methods of cooling. Avoiding hyperthermia in infants who have suffered a hypoxicischemic event at birth is essential. Studies have shown that hyperthermia of 2-3° can worsen outcome.

Withholding and discontinuing resuscitation
Neonatal morbidity and mortality vary throughout the United States. The obstetric and neonatal team, in conjunction
with the parents, should decide whether and when to withhold or discontinue resuscitative efforts. Infants whose
gestational age, birth weight, and congenital anomalies are associated with certain death should not be resuscitated.
These may include infants with extreme prematurity (< 23 weeks' gestation), extremely low birth weight (< 400 g) or
chromosomal anomalies inconsistent with life (eg, trisomy 13).
In other situations where the prognosis is uncertain but the associated morbidity is high, parental desires should be
considered. Discontinuing resuscitation may be justified in infants who have not responded to continuous and
appropriate resuscitation for a full 10 minutes and who have no heart rate or respiratory effort (ie, no signs of life).

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Contributor Information and Disclosures
Robin L Bissinger, PhD, APRN, NNP-BC Graduate Program Director, Neonatal Nurse Practitioner Coordinator,
Associate Professor, Medical University of South Carolina College of Nursing
Disclosure: Nothing to disclose.
Bryan L Ohning, MD, PhD Medical Director of NICU, Medical Director of Neonatal Transport, Division of
Neonatology, Children's Hospital, Greenville Hospital System, University Medical Center; GHS Professor of
Clinical Pediatrics, University of South Carolina School of Medicine; Clinical Associate Professor of Pediatrics,
Medical University of South Carolina
Bryan L Ohning, MD, PhD is a member of the following medical societies: American Academy of Pediatrics,
American Thoracic Society, and South Carolina Medical Association
Disclosure: Pediatrix Medical Group of SC Salary Employment; Draeger Medical, Inc. Consulting fee Consulting
Chief Editor
Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of NeonatalPerinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American
Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric
Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.
Additional Contributors
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 & Dental Society, Medical Society of the State of New
York, New York Academy of Sciences, and Society for Pediatric Research
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of
Pharmacy; Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

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