Epidemiology

Between 5 and 10% of newborns require some assistance to begin breathing at birth and, in developed countries, approximately 1% need intensive resuscitative measures to restore cardiorespiratory function. It has been estimated that birth asphyxia significantly contributes to approximately 20% of the five million neonatal deaths that occur worldwide each year; outcome might therefore be improved for more than one million newborns per year through effective resuscitation at birth.

Neonatal resuscitation is unique in that it is required at a time when the newborn is undergoing a predetermined process of transition from a liquid filled intrauterine environment to spontaneous breathing of room air. There is an accompanying sequence of dramatic alterations in physiology, each of which may be altered and require correction.

There are two important caveats in this process. First, the achievement of lung expansion with an appropriate oxygen-containing gas leading to establishment of a functional residual capacity and adequate spontaneous ventilation is of primary importance. Second, the significance of a vital sign abnormality depends greatly on the time since birth and the time during which effective resuscitation measures have been administered. For instance, bradycardia immediately after birth prior to any resuscitative manoeuvres likely indicates an intrapartum stress. The same heart rate after 1 to 2 minutes of adequate ventilation suggests a different range of aetiologies and requires a different resuscitative response.

The majority of circumstances where newborn resuscitation is needed can be predicted, allowing opportunity for preparation of appropriate equipment and personnel. Factors placing the newborn at high risk for neonatal resuscitation include those listed in Table 2.6.1, due to maternal, fetal and intrapartum circumstances.

IUGR, intrauterine growth retardation.

Artificial ventilation

Various bag and mask systems are available for neonatal resuscitation. T-piece mechanical devices designed to regulate pressure, self-inflating bag or flow-inflating bag are all recognised as acceptable devices for ventilating newborn infants either via a face mask or endotracheal tube. Target inflation pressures, continuous positive airway pressure (CPAP) and long inspiratory times are achieved more consistently using T-piece devices than when using bags but the ability to achieve an increased inspiratory pressure when required in response to altered compliance (even for a few breaths) is greatest with the self-inflating bag. It is suggested in fact that the invariable success of rescue breathing at birth is because the FRC is established by an induced inspiratory effort via Head’s paradoxical reflex (inspiratory effort induced by any lung inflation). The corollary is that face mask rescue breathing is unlikely to be effective in the severely asphyxiated infant.

Regardless of these issues, it is generally accepted that higher inflation pressures (>30 cmH₂O) and longer inflation times (>1.5 seconds) may be required for the first several (≈5) breaths. Initial peak inflating pressures required are variable and unpredictable. In general, the minimum pressure required to achieve an increase in the heart rate should be used. Visible chest wall movement and an increase in the heart rate are the best indicators of adequate ventilation. Ventilations should be administered at a rate of 40–60 min^–1 and after 30 seconds of effective ventilation, the heart rate should be evaluated.

Compression technique

If required, compressions should be instituted using the two-hand-encircling technique (preferred if greater than one rescuer) or two-finger technique (if only one rescuer or if access to the umbilicus is required). The lower third of the sternum (just below an imaginary intermammary line) should be depressed one third of the depth of the chest. These should be coordinated with ventilations (to avoid simultaneous delivery) in a ratio of 3:1 with about 90 compressions and 30 breaths each minute. The xiphoid portion of the sternum should not be compressed because such compression may damage the neonate’s liver.

Vascular access

Adrenaline (epinephrine) may be administered by intravenous (IV), intraosseous (IO) or endotracheal (ET) routes. If there is respiratory depression once heart rate and colour have been restored by adequate rescue ventilation, naloxone may be given via the intravenous (IV) or intramuscular (IM) route. The other drugs and volume expansion, detailed below, require emergency vascular access. Once vascular access is achieved, if the child remains in arrest, an adrenaline dose should be immediately administered via the IV route.

The preferred site of the vascular access during neonatal resuscitation is the umbilical vein, the larger thin walled single vessel (in comparison to the paired thicker walled arteries), which appears when the umbilical cord is trimmed 1 cm above the skin. A 3.5 or 5 French catheter flushed with saline (to remove any air in the tubing) should be inserted only until a good blood return is achieved (usually to a depth of 1 to 4 cm below the skin). Peripheral veins on extremities or scalp may be attempted or alternatively an intraosseous cannula may be placed on the medial aspect of the tibia just below the tibial tuberosity, if umbilical or other direct venous access is not readily obtainable.

Adrenaline (epinephrine)

Adrenaline is administered with the aim of producing α-adrenergic mediated vasoconstriction, an increase in coronary perfusion pressure and myocardial blood flow. Adrenaline is indicated if the heart rate remains less than 60 beats per minute after a minimum of 30 seconds of adequate ventilation and 30 seconds of combined ventilation and chest compressions. The recommended IV dose is 0.1–0.3 mL kg^–1 of a 1:10000 solution (10–30 mcg kg^–1) repeated every 3 to 5 minutes as indicated. ET delivery, though of unproven efficacy, can be considered and requires a higher dose (up to 100 mcg kg^–1); it should be followed by 1 mL of normal saline and several good inflations to achieve optimal delivery to the pulmonary vascular bed. Most infant animal experimental dosing data supporting adrenaline’s efficacy have been obtained in VF models and as such their value may not be directly applicable to the apparent preterminal bradyarrhythmia in an asphyxiated newborn with markedly elevated PCO₂.

Through the early 1990s some experimental and human data showed that higher intravenous doses of adrenaline (100 mcg kg^–1) were capable of achieving higher plasma adrenaline levels as well as greater myocardial and cerebral blood flow. However, several subsequent adult and paediatric studies showed no ultimate clinical benefit in survival or neurological outcome, with a significant risk of adverse effects from the higher dose (myocardial dysfunction or necrosis, hyperadrenergic states, reduced cerebral cortical blood flow). Specifically, there is an increase in potential risk of intraventricular haemorrhages (IVH) in preterm infants. For these reasons, the currently recommended initial IV dose remains 10 mcg kg^–1 in neonates.

The ET route is likely to be the most accessible route for initial doses of adrenaline. Again, there is a paucity of both experimental and human data regarding dosage and efficacy of ET adrenaline in neonates. There are data to suggest a slower onset with a more prolonged and variable effect at higher dosages. For these reasons the dose recommended is 30–100 μg kg^–1 every 3–5 minutes during arrest.

Bicarbonate

Although correcting acidosis during cardiac arrest to improve both myocardial function and adrenaline’s effectiveness makes theoretic sense, there are few supportive experimental data. Most adult studies have found either no difference or that bicarbonate had deleterious effects on myocardial performance. There are no neonatal animal or human studies specifically examining this question. Bicarbonate administration has multiple possible adverse effects (metabolic alkalosis compromising peripheral tissue oxygen delivery, paradoxical intracellular hypercarbic acidosis). Pertinent to neonates are studies demonstrating large increases in plasma osmolality and reductions in cerebral blood flow, both of which may increase the risk of IVH in newborns. Therefore, bicarbonate administration is only recommended during prolonged arrests unresponsive to other therapy after establishment of adequate ventilation and perfusion. The dose is 1–2 mEq kg^–1 of 4.2% solution by slow IV push over at least 2 minutes.

Naloxone

Naloxone is a narcotic antagonist, recommended for the neonate with respiratory depression secondary to narcotics given to the mother within 4 hours of delivery. Prompt institution of adequate ventilation is the first priority in such a situation and naloxone is not recommended for newborns whose mothers are suspected narcotic abusers as abrupt withdrawal may be precipitated. Following IV administration, onset of action occurs in 1–2 minutes and is variable in duration. The recommended IV dose is 0.1 mg kg^–1. Since the duration of action of narcotics may exceed that of naloxone, continued surveillance and repeat administration are often required. Naloxone may be administered IM, with some adult data suggesting slower onset and more prolonged duration of action via this route. There are no studies examining the ET route of administration in the neonate.

Dextrose

Hypoglycaemia is a potential problem for all stressed and asphyxiated babies and should be treated by using a slow bolus of 5 mL kg^–1 of 10% dextrose IV, avoiding high blood sugar levels which have been shown to worsen CNS injury, at least in adults.

Volume expansion

If hypovolaemia is present because of known or suspected blood loss or loss of vascular tone following asphyxia, volume expansion may be appropriate. Isotonic non-dextrose containing crystalloid (normal saline or Ringer’s lactate) 10 mL kg^–1 intravenously over 5–10 minutes is recommended. Group O negative packed red cells may be indicated for replacement of large volume blood loss. Albumin-containing solutions are used less frequently because of limited availability, risk of infectious disease and an observed association with increased mortality. A recent randomised controlled comparison of albumin versus normal saline for hypotension in premature newborns showed that those who received albumin required significantly more volume expander to maintain normal blood pressure and had a higher mean percentage weight gain in the first 48 hours after birth.³

Premature neonate

Preterm newborns have an increased likelihood of respiratory depression requiring assisted ventilation at birth. This occurs because of diminished lung compliance, weak respiratory muscles and immature respiratory drive and may make it difficult to establish and maintain an adequate FRC. For these reasons, infants born at or before 32 weeks gestation should receive face mask resuscitation by 30 seconds and be intubated at 60 seconds after birth if the onset of adequate spontaneous respirations is delayed. A recent study has shown that CPAP applied promptly to premature babies who breathe at birth may be effective in reducing need for ventilation. Also, because preterm infants often have low body fat and a high body surface area to mass ratio, they are more difficult to keep warm and therefore at increased risk of cold stress. For this reason babies <1500 g should be covered in food-grade heat-resistant plastic wrapping or placed in a polyethylene bag with the head excluded and a hat placed on the head. Rapid boluses of volume expander and use of hyperosmolar solutions may produce large fluctuations in blood pressure or osmolarity and therefore are not recommended.³

Meconium aspiration

Approximately one in 20 infants born through meconium-stained amniotic fluid (MSAF) develop meconium aspiration syndrome (MAS) due to aspiration into the distal airways either in utero or with the initial breaths following birth. However, of these, 25–50% require mechanical ventilation and 5% die. Although a long established practice, it is no longer recommended that infants delivered through MSAF undergo intrapartum suctioning of the oro- and nasopharynx once the head is delivered, prior to delivery of chest or shoulders. If the baby born through MSAF is not vigorous after delivery (depressed respirations, muscle tone or heart rate less than 100 min^–1) direct intratracheal suctioning (using continuous suction directly applied to the tracheal tube as it is withdrawn) should be performed. If meconium is recovered, the procedure should be repeated (if the heart rate is greater than 60 min^–1) before proceeding with resuscitation.

Congenital heart disease

Central cyanosis at birth apparently unresponsive to 100% oxygen particularly in a vigorous baby with adequate spontaneous respiratory effort and minimal respiratory distress may indicate duct-dependent cyanotic congenital heart disease (primarily right heart obstructive lesions, transposition of the great vessels and anomalous pulmonary venous return with complete atrial admixture). The major differential diagnoses are primary pulmonary hypertension or major pulmonary structural abnormalities (e.g. congenital diaphragmatic hernia). In such a circumstance ventilatory support requirement should be dictated by degree of respiratory distress with a target PaCO₂ of 35–40 mmHg.

Detailed cardiac auscultation should be attempted though there may be no abnormal murmurs audible; simultaneous pre- and postductal oximetry measurements should be performed. If a cyanotic cardiac abnormality is strongly suspected, documentation of preductal PaO₂ after breathing 100% oxygen for several minutes (hyperoxia test) will give the best indication of the presence and size of a significant intracardiac right to left shunt (see Chapter 5.1). An urgent bedside echocardiogram, if available, is indicated to delineate the cardiac anatomy. Where this is not available, one should consult with the local tertiary neonatal unit. If a diagnosis of a duct-dependent cyanotic cardiac lesion is confirmed on echocardiogram, IV alprostadil (PGE₁) 25–50 ng kg^–1 min^–1 restores and maintains ductal patency until definitive decisions regarding surgical correction can be made. The main side effects of this medication are flushing, fever and possibly apnoea if respiratory support is not already in place.

Alternatively, babies with duct-dependent systemic circulation usually due to some structural problem with left ventricular outflow (e.g. critical aortic stenosis, severe coarctation, hypoplastic left heart syndrome) may present in the first few days of life with heart failure and poor peripheral perfusion triggered by ductal closure. The most reliable physical signs of heart failure are tachycardia, tachypnoea and hepatomegaly. If shock is present (poor pulse volume, pallor, altered conscious state) respiratory support and fluid volume expansion may be required to restore the circulation. Subsequently, alprostadil or inotrope infusion and continuing judicious fluid administration may be required. The most important steps in restoring systemic circulation in this situation are artificial ventilation to normocapnia, together with re-establishing and maintaining ductal patency (see Chapter 5.5).