The American Academy of Pediatrics (AAP) guidelines mandate that at least 1 skilled person capable of carrying out resuscitation of a newborn be present at every delivery. When a delivery is identified as high risk, 2 or more skilled people may be required to provide adequate care. Often it is useful to assign roles to the resuscitation staff to ensure that the resuscitation flows as smoothly as possible. The equipment required for resuscitation, such as the bag and mask used for ventilation, the blender for oxygen and air delivery, the suction equipment, the radiant warmer, and the monitors, should be checked prior to the delivery. Communication between the obstetric and neonatal staff about the maternal medical and obstetric history as well as the prenatal history of the fetus is essential to ensure that the neonatal team can anticipate and interpret the problems the newborn may have in the delivery room.
Although the expectations may be different and the need for resuscitation more common, the same principles apply to a high-risk delivery as to a routine delivery: The newborn should be kept warm and rapidly assessed to determine the need for intervention.
The initial evaluation and resuscitation may take place in the delivery room or, in centers with a high-risk delivery service, preferentially in an adjacent room specifically designed for high-risk resuscitations. Typically the newborn is brought immediately to a radiant warmer, although some institutions weigh extremely premature infants prior to transfer to the warmer bed in order to determine the birth weight if viability is in question. The infant is dried with prewarmed towels to prevent heat loss. At some centers, LBW newborns are put into polyurethane bags or wrapped with polyethylene occlusive wrap after delivery; these measures have been shown to significantly improve temperature stability during stabilization and transport to the neonatal intensive care unit (NICU). In addition, a knit hat is used to prevent heat loss from the head. Preterm infants are at increased risk for thermal instability given their greater body surface area to weight ratio, thinner skin, and relative paucity of subcutaneous fat compared to term infants. Hypothermia (body temperature <36°C) can occur rapidly in the preterm infant and may cause complications such as hypoglycemia and acidosis.
After rapidly drying the infant and removing the wet towels, the resuscitation team should position and clear the airway. The team then assesses the newborn's respiratory effort, heart rate, color, and activity to determine the need for intervention. Drying the patient and suctioning the airway usually provide adequate stimulation for the newborn to breathe. Rubbing the back or flicking the soles of the feet may be done to provide additional stimulus if initial respirations are irregular.
Positive-pressure ventilation (PPV) should be started if the newborn is apneic or has a heart rate less than 100 bpm. Figure 22–1 shows the correct positioning of the neck and placement of the mask. PPV will not be effective if the airway is not extended slightly and the mask is not applied to the face in the correct manner, with a tight seal around the nose and mouth. In addition, sufficient pressure must be given to produce adequate chest wall movement. A pressure manometer should be attached to the bag to monitor the amount of pressure that is being delivered. Overdistention of the lung causes significant trauma to the lung parenchyma and may cause complications such as a pneumothorax or lead to development of pulmonary interstitial emphysema (PIE), especially in the very-low-birth-weight (VLBW) neonate (birth weight <1500 g). Inability to move the chest wall with high pressures may indicate the lack of a good seal between the mask and the face, an airway obstruction, or significant pulmonary or extrapulmonary pathology compromising ventilation, such as pleural effusions, a congenital chest or abdominal mass, or a congenital diaphragmatic hernia (CDH). If the infant's respiration is markedly depressed, endotracheal intubation should be considered.
Technique of bag and mask ventilation of the newborn. The neck should be slightly extended. An anesthesia bag should have a manometer attached; a self-inflating bag should have an oxygen reservoir attached.
Chest compressions should be initiated if the heart rate is less than 60 bpm after 30 seconds of effective PPV. Figure 22–2 shows the acceptable methods for administering compressions to a neonate. Pressure should be applied to the sternum to depress it one-third of the anteroposterior diameter of the chest. Compressions should be coordinated with breaths: A single cycle should consist of 3 compressions followed by a single breath, and each cycle should last for 2 seconds. Compressions should be continued until the heart rate rises above 60 bpm. PPV should be continued until the heart rate is >100 bpm and the patient is showing adequate respiratory effort. If the heart rate remains <60 bpm after 30 seconds of compressions, administration of epinephrine is indicated. Failure to respond to PPV and chest compressions is a clear indication for endotracheal intubation; intubation should be attempted at this time if it has not already been performed. Figure 22–3 shows the landmarks used to guide placement of the endotracheal tube (ETT) between the vocal cords.
A: Thumb technique for performing chest compressions on an infant. The two thumbs, placed either side by side or overlapping one another, are used to depress the lower third of the sternum, with the hands encircling the torso and the fingers supporting the back. B: Two-finger method for performing chest compressions on an infant. The tips of the middle finger and either the index finger or ring finger of one hand are used to compress the lower third of the sternum.
Landmarks for placement of the laryngoscope.
Epinephrine can be given via an ETT or an umbilical venous catheter. The standard dose of epinephrine in neonates is 0.01–0.03 mg/kg. The 2010 AAP guideline recommends giving epinephrine via the intravenous (IV) route and only giving endotracheal epinephrine if IV access cannot be obtained. If using the ETT, a dose of 0.05–0.1 mg/kg of the 1:10,000 concentration solution is recommended. The dose can be repeated every 3–5 minutes until the heart rate rises above 60 bpm.
When the infant's response to resuscitation is poor, other factors that may be complicating successful resuscitation of a newborn should be considered. Previous recommendations from the AAP have stated that the use of naloxone (Narcan) may be considered in cases of recent (<4 hours prior to delivery) administration of narcotics to the nonsubstance-using mother. However, the 2010 AAP recommendations do not recommend the use of naloxone under any circumstances and recommend only appropriate support of respiratory depression and oxygenation. Hypovolemia should be suspected if there is a perinatal history consistent with blood loss (eg, placental abruption, placenta previa) or sepsis and the baby is hypotensive and pale, with weak pulses and cool extremities. A 10 cc/kg IV infusion of normal saline, lactated Ringer's solution, or O-negative blood, if available and anemia is suspected, can be given to treat the suspected hypovolemia. The dose can be repeated if there is minimal improvement with the initial bolus. Metabolic acidosis may be present at birth if the baby was significantly distressed in utero or may develop after birth if oxygenation and/or perfusion are compromised. Although use of bicarbonate in resuscitation is not included in the AAP recommendations, significant acidosis will cause pulmonary vasoconstriction and poor myocardial contractility and should be treated. The umbilical artery can be catheterized to provide ongoing access to blood samples for determination of the extent of acidosis and the response to treatment during resuscitation. If bicarbonate is used, the dose is 2 mEq/kg IV of a 0.5 mEq/mL (4.2%) solution. Bicarbonate should be given slowly via an IV line and should be used only after ventilation is established so that the carbon dioxide (CO2) produced with bicarbonate administration can be removed. Otherwise, bicarbonate administration may result in a significant increase in intracellular acidosis.
Apgar scores are assigned at 1 and 5 minutes of life and continued at 5-minute intervals for up to 20 minutes as long as the score remains below 7. The Apgar score is a means of communicating the newborn's status during resuscitation; it should not be used to determine the need for resuscitation. The initial assessment of the newborn and assignment of the Apgar score are discussed in further detail in Chapter 9.
In the past, 100% oxygen has been the standard for neonatal resuscitation; however, 2 recent meta-analyses have demonstrated increased survival when resuscitation is initiated with air as compared to 100% oxygen. Therefore, the 2010 AAP recommendations now recommend beginning resuscitation with room air. There have been few studies looking at the use of blended oxygen and target oxygen saturations in either preterm or term infants. However, given the known toxicities of oxygen, the recent recommendations are to use blended oxygen when available and to target arterial saturations in the interquartile range for each gestational age (Fig. 22–4). If blended oxygen is not available and the baby remains bradycardic after 90 seconds of resuscitation, it is recommended to increase the oxygen to 100% until recovery of a normal heart rate.
Heart rate and blood pressure changes during apnea.
Specific Considerations in the Delivery Room
Meconium-stained fluid is present in 10–20% of deliveries. It is extremely rare if delivery takes place prior to 34 weeks' gestation. Passage of meconium in utero usually indicates fetal distress, and those personnel present at the delivery should be alerted by the presence of meconium to the possibility that the newborn may be depressed at birth.
It is no longer recommended by the AAP that all meconium-stained babies receive intrapartum suctioning. An active, crying, well-appearing infant does not require endotracheal intubation regardless of the presence of meconium staining or the thickness of the meconium. If the newborn is in distress or has depressed respiratory effort, the appropriate intervention is to intubate and suction the trachea before stimulating the baby in any way. If no meconium is suctioned from the airway, resuscitation should proceed according to the standard algorithm. If meconium is suctioned from the trachea, another attempt should be made to intubate the patient and suction the trachea again. However, if the patient has significant bradycardia, it may be appropriate to defer repeated suctioning and provide PPV.
The majority (94–97%) of infants born through meconium-stained fluid will not develop meconium aspiration syndrome, but when it does occur, infants are often critically ill. Meconium can block the airway and prevent the newborn's lungs from filling with air, a vital step in normal transitioning. Meconium aspiration into the lungs can cause obstruction of the small airways and consequently areas of atelectasis, gas trapping, and overdistention in addition to a chemical pneumonitis. The infant born through meconium may have pulmonary hypertension and inadequate oxygenation and requires close observation and early initiation of treatment when appropriate.
Despite optimal prenatal care, some infants sustain injury prior to or during delivery that results in asphyxia. Perinatal asphyxia is characterized by the presence of hypoxemia, hypercapnia, and metabolic acidemia. It is the result of compromised oxygen delivery and blood flow to the fetus, either chronically or acutely, that stems from processes such as placental insufficiency, cord compression, trauma, and placental abruption.
If significant prepartum or peripartum hypoxic–ischemic injury has occurred, the infant likely will be depressed at birth and may not respond to initial interventions to establish respiration. The initial response in the newborn to hypoxemia is rapid breathing, followed shortly thereafter by a period of apnea, termed primary apnea. Drying the infant and rubbing the back or flicking the soles of the feet is sufficient to stimulate respiration during primary apnea. However, without intervention at this point, continued oxygen deprivation will lead to a series of gasps followed by a period of secondary apnea. It is important to recognize that an infant who does not respond to stimulation is likely exhibiting secondary apnea and requires further intervention. Respiration will not resume with stimulation if secondary apnea has begun, and positive pressure is necessary to reverse the process. Heart rate changes typically begin toward the end of primary apnea, whereas blood pressure typically is maintained until the period of secondary apnea.
Effective resuscitation of an asphyxiated newborn usually requires treatment of acidosis. Perinatal asphyxia may also be complicated by hypoglycemia and hypocalcemia. Myocardial dysfunction may be present, and fluid boluses and continuous infusion of inotrope may be required for adequate blood pressure support. However, in the presence of significant myocardial dysfunction, repeated volume boluses will worsen the cardiovascular status. In these cases, early administration of an inotrope (eg, dobutamine) with or without low to moderate doses of a vasopressor (eg, dopamine) is appropriate. In addition, seizures may occur in the newborn with perinatal asphyxia. Seizures usually are the result of hypoxic–ischemic injury to the cerebral cortex, but hypoglycemia and hypocalcemia also may cause seizure activity in the depressed neonate. In the newborn, phenobarbital (15–20 mg/kg IV) typically is given as the first-line treatment of seizures not caused by hypoglycemia or hypocalcemia. An additional 5–10 mg/kg bolus can be given to control status epilepticus. Asphyxiated infants are at increased risk for persistent pulmonary hypertension (discussed in detail later in the section Pathology & Care of the High-Risk Term Neonate).
The severity of the insult sustained by the newborn can be difficult to assess in the neonatal period. The presence of abnormal findings on the neurologic examination and the severity and persistence of those abnormalities are the most useful measures for assessing the degree of brain injury. Laboratory (umbilical cord and baby blood gases, serum creatinine level, liver function tests, blood lactate level, and cardiac enzyme levels) studies, radiographic (brain magnetic resonance imaging [MRI]) studies, and electroencephalographic (EEG) findings provide additional information to help predict the likelihood and anticipated extent of an adverse neurodevelopmental outcome. Early onset of seizure activity has been shown to increase the likelihood of a poor outcome. Infants with severe hypoxic–ischemic encephalopathy, which is characterized by absent reflexes, flaccid muscle tone, seizures, and a markedly altered level of consciousness, either die within several days of birth or have significant neurologic sequelae. It is a misconception that perinatal asphyxia is the cause of cerebral palsy. A minority of cases of cerebral palsy are actually attributable to intrapartum complications.
Several randomized, controlled studies have shown that induced hypothermia is protective in babies with mild-moderate asphyxia. Both selective hypothermia (ie, head cooling) and total body cooling have been shown to be effective. Devices are now available to regulate and safely cool neonates to a core temperature of 33.5–34.5°C. Therefore, it is now recommended that infants with moderate asphyxia should be cooled. Ideally the therapy should be initiated within 6 hours of the event (ie, birth). Timely transfer to a center that provides therapeutic hypothermia is of the utmost importance.
The newborn who fails to respond to initial attempts at resuscitation may be in circulatory shock. A number of different pathophysiologic processes can result in shock in the delivery room. Circulatory collapse can result from absolute (hemorrhage, capillary leak) or relative (vasodilatation) hypovolemia, cardiac dysfunction (asphyxia, congenital heart disease [CHD]), abnormal peripheral vasoregulation (prematurity, asphyxia, sepsis), or a combination of these factors. The peripartum history often helps elucidate the etiology. The presence of risk factors for sepsis (prolonged rupture of membranes, maternal fever, chorioamnionitis), hemorrhage (placenta previa, placental abruption, trauma), or perinatal asphyxia may be informative. Pallor or peripheral hyperemia, weak pulses with tachycardia, and cool or warm extremities are present on examination. Hypotension in the newborn immediately following delivery is commonly defined as a mean arterial pressure that is equal to or less than the gestational age. It is worth noting that blood pressure is normal in the early (compensated) phase of shock; hypotension may only develop as the process progresses.
As mentioned earlier in Delivery Room Management, a 10 cc/kg normal saline bolus typically is given to the newborn with hypotension. An additional 10–20 cc/kg is often given if the improvement in circulation is inadequate. Unmatched O-negative blood can be transfused in 10–15 cc/kg aliquots if severe anemia from blood loss is suspected. Volume should be administered slowly and judiciously to preterm infants who lack the mechanisms to autoregulate cerebral blood flow and protect the brain against reperfusion injury. Excessive volume may worsen the patient's status if cardiac dysfunction is the cause of hypotension. As discussed earlier, administration of sodium bicarbonate or THAM (tromethamine) may be indicated to treat metabolic acidosis in the newborn in shock. Vasopressor/inotrope infusions should be initiated in neonates who do not respond to volume resuscitation.
Although acrocyanosis (cyanosis of the hands and feet) is often normal in the newborn, central cyanosis is not. Cyanosis is due to inadequate oxygen delivery to the tissue, either as a result of poor blood flow (peripheral vasoconstriction in acrocyanosis or low cardiac output in cardiogenic shock) or insufficiently oxygenated blood (pulmonary hypertension or severe parenchymal lung disease). Free-flow oxygen can be administered if a newborn has central cyanosis despite regular respirations. Free-flow oxygen can be delivered by holding a mask or oxygen tubing that is connected to a flowing source of 100% oxygen close to the baby's nose and mouth. Oxygen can be gradually withdrawn when the newborn turns pink. PPV is often indicated if the baby remains cyanotic despite free-flow oxygen. Lack of improvement of central cyanosis with administration of free-flow oxygen necessitates an evaluation of the cause of cyanosis. As discussed earlier, provision of 100% oxygen may have significant side effects if it is used for newborn resuscitation.
The delivery of a preterm infant requires a skilled multidisciplinary resuscitation team that has an understanding of the myriad problems associated with preterm delivery and has experience handling VLBW newborns. The presence at delivery of physicians, nurses, and a respiratory therapist trained in newborn resuscitation will optimize the early care of the newborn. Details of the delivery room care of the preterm infant are discussed in the section Delivery Room Management earlier in this chapter.
The neonatal team should meet with the family prior to delivery whenever possible. The parents should be informed about the prognosis for the fetus and need for intensive care admission if appropriate. It is critical that the family understand the plan for resuscitation in the delivery room and the anticipated short- and long-term problems the newborn may face. Often it is helpful to families to discuss the emotional impact of the admission and the possibility of a prolonged stay of their newborn in the intensive care unit. If the fetus is at the limits of viability, currently considered 23–24 weeks' gestation and/or weight <500 g, it is essential that the parents understand the considerable risk of death and the serious cognitive, motor, and pulmonary complications that may occur if the newborn does survive. The neonatal team must have a clear conversation with the parents about the possible options for postnatal management. Unfortunately, it often is difficult to make definitive plans given that the margin of error for prenatal determination of birth weight and gestational age is wide enough to have a significant impact on the viability of the fetus. Although many physicians have strong feelings of their own, it is vital that the course of resuscitation of a newborn at the limits of viability incorporates the family's wishes. Nevertheless, parents should understand that the fetus's viability will be reassessed after delivery, and that the maturity of the newborn, the newborn's condition at delivery, and the response to the resuscitative efforts made, in combination with available outcomes data, ultimately will determine the management in the delivery room.
Gastroschisis is the herniation of abdominal contents through an abdominal wall defect. The defect in gastroschisis usually is small and to the right of the umbilicus, and the intestines are unprotected by the peritoneal sac. Omphalocele also involves the herniation of abdominal contents through the abdominal wall, but the defect is in the umbilical portion of the abdominal wall, and the herniated viscera are covered by the peritoneal sac. Both defects require emergent care in the delivery room. Current delivery room recommendations suggest positioning the baby right side down to avoid kinking the mesenteric blood vessels and compromising blood flow to the intestines. The baby's lower body, including the defect and externalized organs, should be placed in a "bowel bag," which is then secured at the mid-thorax. This allows for direct visualization of the intestines while also limiting fluid losses. A nasogastric tube (at least 10 French) should be placed to allow for adequate decompression of the stomach and intestines.
Despite these measures, patients will still have increased heat and insensible fluid losses, and IV fluid should be started promptly at 1.5 times normal maintenance requirements to prevent dehydration and hypernatremia. Electrolytes and fluid status must be monitored closely. A surgical consultation should occur prenatally if the defect is diagnosed in utero. An urgent surgical evaluation should be obtained upon admission of the newborn to the NICU.
Kattwinkel J, Perlman JM, Aziz K, et al. Neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics
Paneth N. The evidence mounts against use of pure oxygen
in newborn resuscitation. J Pediatr
Spector LG, Klebanoff MA, Feusner JH, et al. Childhood cancer following neonatal oxygen
supplementation. J Pediatr
Tan A, Schulze A, O'Donnell CP, Davis PG. Air versus oxygen
for resuscitation of infants at birth. Cochrane Database Syst Rev