Critically ill neonates depend on extrinsic factors to maintain homeostasis. This is particularly true when birth occurs before term; the complexity of care is often inversely related to birth weight and gestational age. Aspects of clinical care that deserve special consideration when preparing neonates for transport can be remembered using the STABLE mnemonic described earlier.13 Common neonatal emergencies are discussed in chapter 114, Neonatal Emergencies and Common Neonatal Problems, and specific considerations for transport are summarized in the following.
The most common metabolic abnormality in newborns is hypoglycemia, which is discussed in detail in chapter 144, Metabolic Emergencies in Infants and Children. At birth, blood glucose in the neonate is approximately 60% to 70% of the maternal level and falls to approximately 40 milligrams/dL (2.22 mmol/L) within 1 to 2 hours. This decline may be accentuated in premature or small-for-gestational-age infants, acutely ill infants with increased glucose utilization, and certain other high-risk infants (e.g., infants of diabetic mothers, large-for-gestational-age infants). Because of the risk of hypoglycemia, all neonates should receive glucose-containing fluids in preparation for and during transport. An initial glucose infusion rate of 4 to 6 milligrams/kg/min should be targeted, and this can be achieved with 10% dextrose in water infused at a rate of 80 mL/kg/d. Sometimes a bolus of dextrose may be necessary, which can be achieved with 4 to 5 mL/kg of 10% dextrose solution. Repeat measurement of blood sugar at 15- to 30-minute intervals, with a goal to maintain serum glucose at 50 milligrams/dL (2.7 mmol/L).
The normal core temperature range for a neonate is 36.5°C to 37.5°C (97.7°F to 99.5°F). A neutral thermal environment is provided when the infant's body temperature is normal and there is a minimal gradient between the core and the skin temperature.
Newborns attempt to conserve heat by several mechanisms: (1) peripheral vasoconstriction, (2) increasing voluntary muscle activity, (3) flexion to conserve exposed surface area, and (4) nonshivering thermogenesis. All of these mechanisms, except nonshivering thermogenesis, are less effective in the neonate than in older infants and children. Unintentional hypothermia in the neonate and young infant can lead to apnea, multisystem organ failure, inability to resuscitate, or intracranial hemorrhages in those most susceptible. The transport vehicle should be equipped with a closed heated incubator with an automatic temperature regulator. If the transport vehicle does not have a closed incubator, an overhead radiant heat source and increasing the heat inside the transport vehicle are other options. During transport, it is necessary to monitor the patient's body temperature frequently to avoid hyper- or hypothermia.
Therapeutic hypothermia is now a standard of care for neonates with perinatal asphyxia. Guidelines from the International Liaison Committee on Resuscitation recommend therapeutic hypothermia for term or near-term infants with evolving moderate to severe hypoxic-ischemic encephalopathy. Hypothermia lowers mortality rates and improves neurodevelopmental outcomes (number needed to treat = 9).23 Initiate cooling to a temperature of 33.5°C within the first 6 hours of life using the whole-body method or selective head cooling, and continue cooling throughout transport.
Recommendations from the 2010 international consensus on neonatal resuscitation23 state that resuscitation of term babies should begin with room air rather than 100% oxygen and that administration of supplemental oxygen should be regulated by blending oxygen and room air, to a concentration guided by pulse oximetry. A normal newborn would not be expected to achieve normal oxygen saturation during the first 10 minutes. Begin resuscitation of neonates <32 weeks of gestation with 30% to 90% oxygen and titrate according to pulse oximetry (Table 107-2); if blended oxygen and air is not available, use room air (see chapter 108, Resuscitation of Neonates).
TABLE 107-2Target Ranges for Oxygenation and Ventilation of Neonates ||Download (.pdf) TABLE 107-2 Target Ranges for Oxygenation and Ventilation of Neonates
|Oxygenation ||Arterial Blood Gas ||Pulse Oximetry |
|Premature infant with RDS* ||Pao2 50–70 mm Hg ||Sao2 85%–94% |
|Term infant (no lung disease) ||Pao2 60–90 mm Hg ||Sao2 >95% |
|Infant with persistent pulmonary hypertension of the newborn ||Pao2 60–90 mm Hg ||Sao2 >95% |
|Infant with CHD ||Pao2 35–50 mm Hg ||Sao2 75%–85% |
|Premature infant with respiratory distress syndrome ||Paco2 50–55 mm Hg |
|Term infant (no lung disease) ||Paco2 35–50 mm Hg |
|Infant with persistent pulmonary hypertension ||Paco2 30–40 mm Hg |
|Infant with CHD ||Paco2 35–50 mm Hg |
For mechanically ventilated patients, arterial blood gas is the gold standard for assessing the efficacy of ventilation and oxygenation and modifying ventilator settings; however, capillary or venous blood is acceptable for measurement of the partial pressure of carbon dioxide and pH in the absence of access to arterial blood. The target ranges for oxygenation and ventilation of neonates differ according to the disease process and gestational age (Table 107-2). No clear relationship has been established between specific partial pressure of arterial oxygen values and adequate tissue oxygenation. It is acceptable to use pulse oximetry alone to guide fraction of inspired oxygen. The overall goal during transport should be to deliver the minimum required fraction of inspired oxygen to maintain adequate tissue oxygenation. The blending of oxygen and air to deliver the minimum fraction of inspired oxygen required to achieve adequate oxygenation is essential in premature infants because of the known retinal and pulmonary toxicities of oxygen.24,25
RESPIRATORY DISTRESS SYNDROME
Premature infants with respiratory distress syndrome present with progressively worsening retractions, tachypnea, and oxygen requirements because their lungs are too immature to synthesize surfactant. This disease has a characteristic radiographic pattern that includes "ground glass" opacities in the lung parenchyma and prominent air bronchograms (Figure 107-2). Initial therapy for respiratory distress syndrome involves continuous positive airway pressure to stent open airways, thereby reducing collapse of alveoli and limiting further damage. Continuous positive airway pressure can be administered during transport through specially designed nasal cannula–type devices (with a continuous pressure of 4 to 6 cm of water) in the nonintubated patient with mild respiratory distress. A similar strategy should be used in the intubated patient by adjusting the ventilator to provide a positive end-expiratory pressure of 4 or 5 cm of water such that there is never a period of negative pressure during passive exhalation. For intubated infants with respiratory distress syndrome, administer surfactant through the endotracheal tube. This procedure can result in rapid changes in pulmonary compliance, can cause transient airway obstruction, and can be associated with pulmonary hemorrhage. For these reasons, only experienced personnel should administer surfactant. When an infant needs surfactant but the referring institution is unable to administer it, transport personnel to administer surfactant as soon as they arrive on site, thereby minimizing further treatment delay.
Chest radiograph of intubated infant illustrating classic findings of respiratory distress syndrome. Note the granular or "ground glass" appearance of the lung parenchyma, the poor inflation, the lack of focal opacities, and the prominent air bronchograms.
PERSISTENT PULMONARY HYPERTENSION
Pulmonary circulation is attenuated in the fetus by high intrinsic vascular resistance in the pulmonary arterioles and bypass shunting around the lungs via the ductus arteriosus. The rapid transition from fetal to newborn circulation includes a precipitous drop in pulmonary vascular resistance concomitant with lung expansion, followed by increased pulmonary blood flow in the first minutes of life and a gradual closing of the ductus arteriosus over the next 48 hours. Unfortunately, there are several common conditions that can disrupt this progression, including meconium aspiration, hypothermia, sepsis, and birth depression. Early diagnosis of persistent pulmonary hypertension is essential to prevent patient morbidity.
Infants with persistent pulmonary hypertension demonstrate labile oxygenation despite adequate ventilation due to right-to-left shunting of blood through the ductus arteriosus (Figure 107-3) or patent foramen ovale. This usually can be detected by placing a pulse oximetry probe on the right hand (preductal) and a second probe on a foot (postductal). Shunting is suggested by a preductal saturation greater than postductal by >10% in a newborn. With shunting exclusively at the atrial level, saturations are low, but the preductal to postductal saturation difference will not be observed.
Homunculus illustrating right-to-left shunting through the ductus arteriosus due to persistent pulmonary hypertension of the newborn.
Initial management of severe persistent pulmonary hypertension includes intubation, administration of 100% oxygen (a pulmonary vasodilator), optimization of ventilation to promote lung recruitment (Table 107-2), correction of acidosis, maintenance of high-normal blood pressures (with fluid boluses and inotropic agents if necessary), maintenance of a normal hematocrit, correction of metabolic abnormalities (hypocalcemia, hypoglycemia), sedation, and sometimes paralysis (to minimize intrathoracic pressure). These therapies may transiently stabilize critically ill infants with persistent pulmonary hypertension but are damaging in the long term. Inhaled nitric oxide is a potent pulmonary vasodilator that can be used after conventional therapies are optimized. Some neonatal transport teams carry portable inhaled nitric oxide tanks. When possible, transport of a neonate with persistent pulmonary hypertension should be performed by a team that can administer inhaled nitric oxide, thus minimizing the time to treatment. Infants who do not respond to conventional therapy or inhaled nitric oxide are likely to require extracorporeal membrane oxygenation for survival. For this reason, infants with severe persistent pulmonary hypertension should be transported preferentially to extracorporeal membrane oxygenation centers.
Because fetal oxygenation occurs through the placenta, cyanotic heart lesions usually are asymptomatic in the fetus, and a number of cyanotic heart lesions dependent on the ductus arteriosus for pulmonary blood flow at birth remain clinically silent until the time of ductal closure. This sequence of events can result in delayed diagnosis of cyanotic heart disease and a subsequent need for emergency management. The presentation and management of congenital heart disease is discussed in chapter 126, Congenital and Acquired Pediatric Heart Disease, and includes (1) supportive interim management and (2) reopening and maintaining ductus arteriosus patency with a prostaglandin E1 infusion. Prostaglandin E1 typically is started by the transport team at 0.05 microgram/kg/min and titrated according to oxygen saturation up to 0.1 microgram/kg/min when trying to reopen the ductus in a severely ill patient. Patients with previously undiagnosed cyanotic heart lesions should be transferred to a tertiary facility that can perform pediatric cardiovascular surgery.
Neonatal hypotension is defined as a systolic blood pressure less than 60 mm Hg. In newborns, hypotension occurs secondary to hypovolemia (intrapartum or postpartum hemorrhage), cardiogenic failure, sepsis, or a combination of these conditions. Physical examination findings of hypotension include weak peripheral pulses, cyanosis, poor perfusion (represented as a capillary refill time >3 seconds), pallor, and cool and mottled skin. Treatment for neonates with hypovolemic shock relies on volume resuscitation initially with normal saline at 10 mL/kg, as larger volumes may be associated with increased risk for intraventricular hemorrhage. In the presence of hypovolemic shock and anemia, administer cross-matched packed red blood cells. Treat cardiogenic failure with inotropic agents (dopamine at 2.5 micrograms/kg/min titrated to desired blood pressure up to 20 micrograms/kg/min).16 In septic shock, capillary leak and the ongoing third space losses will require volume replacement, and the cardiac effects will require inotropic support. Requiring large amounts of volume replacement is not uncommon for infants in septic shock.
To provide volume and inotropes, peripheral venous access must be obtained, and this may be technically challenging. Consider emergent cannulation of the umbilical vessels or use of intraosseous lines (see chapter 112, Intravenous and Intraosseous Access in Infants and Children).
Signs and symptoms of infection in a neonate are often nonspecific and may be indistinguishable from those associated with other diseases. See chapter 116, Fever and Serious Bacterial Illness in Infants and Children, for details on the evaluation and management of neonates and infants with fever, and consider empiric administration of broad-spectrum antibiotics including meningitic dosages of ampicillin (50 milligrams/kg) and gentamicin (2.5 milligrams/kg).26 A third-generation cephalosporin should be added or substituted for gentamicin when gram-negative meningitis is suspected or confirmed on a cerebrospinal fluid gram stain.27 Sick neonates require stabilization and rapid administration of empiric antibiotics, which should not wait for diagnostic studies such as lumbar puncture.
INBORN ERRORS OF METABOLISM
Inborn errors of metabolism encompass a complicated set of diseases involved with the metabolism of carbohydrates, fats, or proteins and are discussed in detail in chapter 144, Metabolic Emergencies in Infants and Children. Regardless of which defect is involved, the end result is depletion of ATP stores and the accumulation of toxic metabolites. Common presentation includes nonspecific symptoms such as vomiting, lethargy, and poor feeding. Fortunately, the principles of management for all emergent presentations of metabolic disease are the same: stop feedings, provide dextrose, and facilitate removal of the toxic metabolites. Stabilization therapy is 10% dextrose in normal saline at 5 mL/kg/h. Additional therapies are discussed in chapter 144, Hypoglycemia and Metabolic Emergencies in Infants and Children.
Delivery of premature infants who are at the limits of viability is not an uncommon occurrence in the ED. The first priority of the physician caring for the infant is to determine whether resuscitation is justified. In the United States, an infant born at a gestational age of <23 weeks, weighing <400 grams, and with gelatinous/translucent skin generally should not be resuscitated or transported. According to the 2010 guidelines,23 when congenital anomalies are associated with almost certain death or an unacceptable high morbidity is likely among survivors, resuscitation is not indicated. Infants born after 23 weeks of completed gestation and without a congenital anomaly associated with a high rate of mortality or unacceptable morbidity are capable of relatively good outcomes and should be supported aggressively after birth. The decision to initiate support must be made immediately because any delay can have a deleterious effect on the infant's prognosis. If the decision is not clear or there is a condition associated with borderline survival and a high rate of morbidity, medical control should be contacted for further directions. The parents' views on resuscitation should be sought and supported. In a newly born baby with no detectable heart rate after 10 minutes of resuscitation, it is acceptable and appropriate to consider stopping resuscitation at that point.23
The death of a newborn judged to be nonviable often does not occur rapidly, even in the absence of spontaneous respiration. After a decision has been made to withhold interventional care, it is important that the staff remain supportive and available to the parents. Additional support, such as family members, friends, or members of the clergy, should be identified and contacted. If the parents desire, the child can be held in a quiet place with a physician checking periodically to determine the time of death. This period, around the time of death, may be emotionally difficult for the staff as well as for the family. Futile efforts at resuscitation or interfacility transport should not be a substitute for compassionate support without medical intervention.