NEONATAL INTENSIVE CARE

PERINATAL RESUSCITATION

Perinatal resuscitation consists of the steps taken by the obstetrician to support the infant during labor and delivery as well as the traditional resuscitative steps taken by the pediatrician after delivery. Intrapartum support includes maintaining maternal blood pressure with volume expanders if needed, maternal oxygen therapy, positioning the mother to improve placental perfusion, readjusting oxytocin infusions or administering a tocolytic if appropriate, minimizing trauma to the infant (particularly important in infants of very low birth weight), suctioning the nasopharynx upon delivery of the head if meconium is present in the amniotic fluid, obtaining all necessary cord blood samples, and completing an examination of the placenta.
Steps taken by the pediatrician or neonatologist focus on temperature support, initiation and maintenance of effective ventilation, maintenance of perfusion and hydration, and glucose regulation.
A number of conditions associated with pregnancy, labor, and delivery place the infant at risk for birth asphyxia: (1) maternal diseases such as diabetes, pregnancy-induced hypertension, heart and renal disease, and collagen-vascular disease; (2) fetal conditions such as prematurity, multiple births, growth retardation, and fetal anomalies; and (3) labor and delivery conditions, including fetal distress with or without meconium in the amniotic fluid and administration of anesthetics and opioid analgesics.

Physiology of Birth Asphyxia
Birth asphyxia can be the result of several mechanisms: (1) acute interruption of umbilical blood flow (eg, prolapsed cord with cord compression), (2) premature placental separation, (3) maternal hypotension or hypoxia, (4) chronic placental insufficiency, and (5) failure to execute newborn resuscitation properly.
The neonatal response to asphyxia follows a predictable pattern that has been demonstrated in a variety of species (Figure 1–3). The initial response to hypoxia is an increase in frequency of respiration and a rise in heart rate and blood pressure. Respirations then cease (primary apnea) as heart rate and blood pressure begin to fall. This initial period of apnea lasts 30–60 seconds. Gasping respirations (3–6/min) then begin, while heart rate and blood pressure gradually decline. Secondary or terminal apnea then ensues, with further decline in heart rate and blood pressure. The longer the duration of secondary apnea, the greater the risk for hypoxic organ injury. A cardinal feature of the defense against hypoxia is the underperfusion of certain tissue beds (eg, skin, muscle, kidneys, gastrointestinal tract), which allows the perfusion of core organs (ie, heart, brain, adrenals) to be maintained.
The response to resuscitation also follows a predictable pattern. During the period of primary apnea, almost any physical stimulus causes the baby to initiate respirations. Infants in secondary apnea require positive-pressure ventilation. The first sign of recovery is an increase in heart rate, followed by an increase in blood pressure with improved perfusion. The time required for rhythmic, spontaneous respirations to occur is related to the duration of the secondary apnea. As a rough rule, for each 1 minute past the last gasp, 2 minutes of positive-pressure breathing is required before gasping begins, and 4 minutes is required to reach rhythmic breathing. These times can vary depending on the degree and duration of intrauterine asphyxia. Not until some time later do spinal and corneal reflexes return. Muscle tone gradually improves over the course of several hours.

Delivery Room Management
When asphyxia is anticipated, a resuscitation team of two persons should be present—one to manage the airway and one to monitor the heartbeat and provide assistance.



A. Steps in the Resuscitation:

1. Dry the infant well, and place it under the radiant heat source.
2. Gently suction the mouth, then the nose.
3. Quickly assess the infant’s condition. The best criteria are the infant’s respiratory effort (apneic, gasping, regular) and heart rate (> 100 or <>
4. Infants who are breathing and have heart rates over 100 beats/min usually require no further intervention. Infants with heart rates less than 100 beats/min and apnea or irregular respiratory efforts should be stimulated vigorously. The baby’s back should be rubbed with a towel while oxygen is provided near the baby’s face.
5. If the baby fails to respond to tactile stimulation within a few seconds, begin bag and mask ventilation, using a soft mask that seals well around the mouth and nose. For the initial inflations, pressures of 30–40 cm H2O may be necessary to overcome surface-active forces in the lungs. Adequacy of ventilation is assessed by observing expansion of the infant’s chest accompanied by an improvement in heart rate, perfusion, and color. After the first few breaths, lower the peak pressure to 15–20 cm H2O. The baby’s chest movement should resemble that of an easy breath rather than a deep sigh. The rate of bagging should be 40–60 breaths per minute.
6. Most neonates can be resuscitated effectively with a bag and mask. If the infant does not respond to bag and mask ventilation, try to reposition the head (slight extension), reapply the mask to achieve a good seal, consider suctioning the mouth and the oropharynx, and try ventilating with the mouth open. If the infant does not respond within 30 seconds, intubation is appropriate. Failure to respond to intubation and ventilation can result from (1) mechanical difficulties (Table 1–17), (2) profound asphyxia with myocardial depression, and (3) inadequate circulating blood volume. Quickly rule out the mechanical causes listed in Table 1–17. Check to be sure the endotracheal tube passes through the vocal cords. Occlusion of the tube should be suspected when there is resistance to bagging and no chest wall movement. Very few neonates (approximately 0.1%) require either cardiac massage or drugs during resuscitation. Almost all newborns respond to ventilation with 100% oxygen if done effectively.
7. If mechanical causes are ruled out and the heart rate remains below 80 beats/min and is not increasing after intubation and positive-pressure ventilation for 30 seconds, cardiac compression should be initiated. Simultaneous delivery of chest compressions and positive-pressure ventilation is likely to decrease the efficiency of ventilation. Therefore, chest compressions should be interspersed with ventilation at a 3:1 ratio (90 compressions and 30 breaths per minute).
8. If drugs are needed (rarely), the drug and dose of choice is epinephrine, 1:10,000 solution, 0.1–0.3 mL/kg given via the endotracheal tube or through an umbilical venous line. Some children and adults who do not respond to standard doses will respond to high-dose epinephrine (ten times the ineffective amount), but the safety and efficacy of such a dose have not been adequately evaluated in the newborn infant and it is thus not currently recommended. Sodium bicarbonate, 1–2 mEq/kg of the neonatal dilution (0.5 mEq/mL), can be used in prolonged resuscitation efforts in which the response to other measures is poor. If volume loss is suspected, 10 mL/kg of a volume expander (5% albumin, normal saline) should be administered through an umbilical vein line.

B. Continued Resuscitative Measures: The appropriateness of continued resuscitative efforts should be reevaluated in an infant who fails to respond to the above efforts. In current practice, resuscitative efforts are made even in apparent stillbirths (ie, infants whose Apgar score at 1 minute is 0–1). Modern resuscitative techniques have led to an increasing survival rate for these infants, with 60% of survivors showing normal development. It is clear from a number of studies that initial resuscitation of these infants should proceed; however, subsequent continued support must depend on response to resuscitation. All studies emphasize that if the Apgar score is not improving markedly over the first 10–15 minutes of life, the mortality rate and the incidence of severe developmental handicaps among survivors are high.

C. Special Considerations:

1. Preterm infants—

• Minimizing heat loss improves survival, so prewarmed towels should be available. The environmental temperature of the delivery suite should be raised to > 25°C (especially for infants weighing <>
• In the extremely low birth weight infant (<>
• Volume expanders and sodium bicarbonate (if needed) should be infused slowly to avoid rapid swings in blood pressure and serum osmolality.

2. Narcotic depression—In the case of opioid administration to the mother during labor, perform the resuscitation as described above. When the baby is stable with good heart rate, color, and perfusion but still has poor respiratory effort, a trial of naloxone (0.1 mg/kg intramuscularly, subcutaneously, intravenously, or intratracheally) is indicated. Naloxone should not be administered in place of positive-pressure ventilation. Naloxone should not be used in the infant of an opioid-addicted mother because it will precipitate withdrawal.

3. Meconium-stained amniotic fluid—

• The obstetrician carefully suctions the oropharynx and the nasopharynx after delivery of the head with a suction apparatus attached to wall suction.
• The delivery is then completed, and the baby is given to the resuscitation team.
• If the baby is active and breathing, requiring no resuscitation, and if obstetric suctioning has been performed, the airway need not be inspected—only further suctioning of the mouth and nasopharynx is required.
• The airway of any depressed infant requiring ventilation must be checked and cleared (by passage of a tube below the vocal cords) before positive-pressure ventilation is instituted. Special adapters are available for use with regulated wall suction to allow suction to be applied directly to the endotracheal tube.

4. Universal precautions should always be observed in the delivery room.

Management of the Asphyxiated Infant
Asphyxia is manifested by multiorgan dysfunction, seizures and hypoxic-ischemic encephalopathy, and metabolic acidemia. The infant who has experienced a significant episode of perinatal hypoxia and ischemia is at risk for dysfunction of multiple end organs (Table 1–18). The organ of greatest concern is the brain.
The clinical features of hypoxic-ischemic encephalopathy progress over time: birth to 12 hours, decreased level of consciousness, poor tone, decreased spontaneous movement, periodic breathing or apnea, and possible seizures; 12–24 hours, more seizures, apneic spells, jitteriness, and weakness; after 24 hours, decreased level of consciousness, further respiratory abnormalities (progressive apnea), onset of brainstem signs (oculomotor and pupillary disturbances), poor feeding, and hypotonia.
The severity of clinical signs and the length of time the signs persist correlate with the severity of the insult. Other evaluations helpful in assessing severity in the term infant include electroencephalogram (EEG), computed tomography (CT) scan, and evoked responses. As experience in the use of magnetic resonance imaging (MRI) is gained, this technique may also prove useful. Markedly abnormal EEGs with voltage suppression and slowing evolving into a burst-suppression pattern are associated with severe clinical symptomatology. A CT scan early in the course may demonstrate diffuse hypodensity, whereas later scans may demonstrate brain atrophy and focal ischemic lesions. Visual and somatosensory evoked potentials provide information about function. In most instances, it is not necessary to use all of these tests, but some are obtained to confirm an ominous prognosis. Management is directed at supportive care and treatment of specific abnormalities. Fluids should be restricted initially to 60–80 mL/kg/d; oxygenation should be maintained (with mechanical ventilation if necessary); blood pressure should be supported with judicious volume expansion (if hypovolemic) and pressors; and glucose should be in the normal range of 40–100 mg/dL. Hypocalcemia, coagulation abnormalities, and metabolic acidemia should be corrected and seizures treated with intravenous phenobarbital (20 mg/kg as loading dose, with total initial 24-hour dosing up to 40 mg/kg). Phenobarbital in large doses (40mg/kg intravenously 1–6 hours after the event) given as a neuroprotective therapy is associated with improvement in neurologic outcome with minimal adverse effects on blood pressure, respirations, or blood gases. Other anticonvulsants should be reserved for refractory seizures. The role of hypothermia (in particular, selective head cooling), free oxygen radical scavengers, excitatory amino acid antagonists, and calcium channel blockers in minimizing cerebral injury after asphyxia is under active investigation.

Birth Asphyxia: Long-Term Outcome
Fetal heart rate tracings, cord pH, and 1-minute and 5-minute Apgar scores are imprecise predictors of long-term outcome. Apgar scores of 0–3 at 5 minutes in term infants result in an 8% risk of death in the first year of life and a 1% risk of cerebral palsy among survivors. A 10-minute Apgar score of 0–3 predicts death in the first year in 18% of cases and cerebral palsy among survivors in 5%; at 15 minutes, the rates are 48% and 9%, respectively; and at 20 minutes, 59% and 57%, respectively. The single best predictor of outcome is the severity of clinical hypoxic-ischemic encephalopathy (severe symptomatology carries a 75% chance of death and a 100% rate of neurologic sequelae among survivors). The major sequela of hypoxic-ischemic encephalopathy is cerebral palsy with or without associated mental retardation and epilepsy. Other prognostic features include prolonged seizures refractory to therapy, markedly abnormal EEGs, and CT scans with evidence of major ischemic injury. Other clinical features required to support perinatal hypoxia as the cause of cerebral palsy include the presence of fetal distress prior to birth, a low cord pH of < 7.00, and evidence of other end organ dysfunction.