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© Springer Nature Switzerland AG 2020
Craig Sims, Dana Weber and Chris Johnson (eds.) A Guide to Pediatric

14.  Neonatal Anesthesia

Chris Johnson1   and Dan Durack2  

Formerly Department of Anaesthesia and Pain Management, Princess Margaret Hospital for Children, Subiaco, WA, Australia

Department of Anaesthesia and Pain Management, Perth Children’s Hospital, Nedlands, WA, Australia



Chris Johnson (Corresponding author)


Dan Durack


Endotracheal intubation, neonateTracheo-esophageal fistula, anesthesiaNeonatal apnea and anesthesiaNeonatal pharmacologyNeonatal laparotomy anesthesia

This chapter outlines differences between the neonate and older patients, some common neonatal conditions, and some aspects to consider in the care of the preterm neonate so that trainees will have some background knowledge if they are involved with these patients.

14.1 The Neonate

A neonate is a baby in the first 4 weeks of life. Preterm neonates are those born at less than 37 weeks gestation. Several terms are used to describe the age of former preterm infants (Table 14.1). The neonatal period is when physiological and pharmacological changes are greatest and technical and equipment needs most specialized. Great changes and differences occur even within the neonatal period, particularly in the first few days of life when the changes from birth are stabilizing.

Table 14.1

Various terms used to describe the age of preterm neonates



Gestational age

Time between the first day of the last menstrual period and delivery. A term baby is 37–40 weeks gestation

Chronological age

(Post-natal age)

Time since birth. A baby celebrates its first birthday 52 weeks after birth

Postmenstrual age (PMA) or Post-conceptual age (PCA)

Gestational age + chronological age. A 6 week old baby born at 35 weeks gestation has a PMA of 41 weeks

Corrected age

Chronological age minus the number of weeks born before 40 weeks of gestation. A 6 week old baby born at 35 weeks has a corrected age of 1 week

Postconceptual age is no longer used

14.2 The Neonatal Cardiovascular System

When based on weight, the neonate has twice the metabolic rate of an adult. As a result, neonates have twice the oxygen consumption, twice the minute ventilation and twice the cardiac output of an adult (Table 14.2). As the cardiac output in a neonate is already high, there is less ability to increase it in response to illness. Other differences of the cardiovascular system of neonates are listed in Table 14.3. Term neonates have a heart rate of 100–160 bpm and normal systolic blood pressure of approximately 60–70 mmHg. Preterm neonates have a lower blood pressure.

Table 14.2

Respiratory and cardiovascular differences between neonate and adult




Oxygen consumption

7 mL/kg/min

3 mL/kg/min

RR (breaths/min)




220 mL/kg/min

100 mL/kg/min

Tidal volume

6 mL/kg

7 mL/kg


30 mL/kg

34 mL/kg

Anatomical dead space

2.2 mL/kg

2.2 mL/kg

Cardiac output

200 mL/kg/min

70 mL/kg/min

Note increased oxygen consumption, cardiac output and increased minute ventilation achieved by increased respiratory rate

Table 14.3

Characteristics of the cardiovascular system in neonates

Cardiovascular system characteristics


Contractility dependent on extracellular calcium concentration

Poorly developed sarcoplasmic reticulum

Rate dependent cardiac output

Relatively fixed stroke volume from non- compliant ventricle

Poorly developed sympathetic nervous system

Unable to increase systemic vascular resistance

Parasympathetic nervous system predominance

Prone to bradycardia

14.2.1 Patent Ductus Arteriosus (PDA)

The ductus arteriosus is a vascular communication between the pulmonary artery and descending aorta, and is an essential component of fetal life. It generally closes soon after birth but in some types of congenital heart disease, ongoing patency may be essential for survival. A small PDA is usually benign and NSAIDs may be used to promote closure. Left-to-right shunting through a large PDA risks pulmonary overload and congestive heart failure. This is managed with fluid restriction and diuretics. Surgical closure may be required, either by cardiac catheter or by thoracotomy.

14.3 The Neonatal Airway

Differences in the airway (Table 14.4) (see also Chap. 4) make the larynx appear anterior at laryngoscopy and have the potential to make intubation more difficult. However, intubation is readily achieved in most neonates with a straight Miller blade laryngoscope and laryngeal pressure. The routine use of a videolaryngoscope for intubation of neonates is also a reasonable approach nowadays.

Table 14.4

Summary of airway differences

Neonatal airway features

Occiput relatively large—more difficult to position for optimal intubating conditions

Obligate nasal breathing, most resistance in nose, don’t cope with nasal obstruction. 40% of term babies can convert to oral breathing if nasal obstruction

Underdeveloped mandible with little space in mouth for tongue

Larynx higher in neck with fewer vertebral joints above larynx that can flex

Long, floppy, U-shaped epiglottis

Larynx appears to be more anterior at laryngoscopy

Vocal cords angled forward (more likely to catch ETT on anterior commissure)

Short trachea makes right endobronchial intubation more likely


Positioning for intubation is different in neonates compared to adults: A head ring to stabilize the relatively large head; a small roll under the shoulders if the head is particularly large; mild head extension (too much and the epiglottis may be pushed against the tongue base); no neck flexion needed because of their high larynx.

14.4 The Neonatal Respiratory System

Neonates have several differences that place them at risk of respiratory and ventilatory failure.

14.4.1 Lung Development

The lung is underdeveloped at birth—alveoli develop late in gestation and lung development continues after birth. A preterm baby has only terminal sacs with underdeveloped alveolar ducts. Term babies have 20–50 million alveoli and the number increases to the adult number of 300 million by 8 years. Surfactant production begins around 23 weeks gestation and sufficient levels are present from early in the third trimester through to birth. Surfactant deficiency is a problem in preterm neonates, resulting in reduced compliance, atelectasis and respiratory distress syndrome (RDS). Surfactant is so important for lung function in neonates that antenatal steroids are given to mothers to stimulate surfactant production if delivering at 34 weeks or less. Preterm neonates born at less than 30 weeks gestation are given surfactant via an ETT. Bronchopulmonary dysplasia (BPD) refers to lung damage caused by mechanical ventilation and subsequent inflammatory reaction.

14.4.2 Airway and Respiratory Mechanics

Respiration is less efficient and the work of breathing higher because of the characteristics of the chest wall, diaphragm and tracheobronchial tree (Table 14.5). The neonatal larynx is high in the neck and the posterior oral airway is potentially obstructed by the high and long epiglottis in proximity to the soft palate and tongue. This allows simultaneous feeding and breathing, but in combination with immature coordination between respiratory and pharyngeal muscles, neonates and young infants preferentially breathe through their nose. Only about 40% of term babies can convert to oral breathing if the nose is obstructed, but nearly all can convert by the age of 5 months.

Table 14.5

List of the major differences in respiratory physiology in neonates compared to children and adults

Respiratory physiology in neonate

Horizontal ribs rather than ‘bucket handle’

Piston-like, diaphragmatic breathing which is compromised by gastric or abdominal distension

Diaphragm has less type I muscle fibers (25% vs adult 60%; adult levels by 9 months) and copes with increased work of breathing poorly. Diaphragm is flatter and develops less pressure for any given muscle tension

Compliant rib cage which in-draws if upper airway obstruction

Small diameter, poorly supported airways

Immature respiratory control


Neonates and infants younger than 3 months are termed ‘obligate nasal breathers’ because less than half can quickly convert to breathing through their mouth if their nose is obstructed.

14.4.3 Control of Respiration

The respiratory center in the brain stem of the neonate is immature, and respiratory control is not fully developed. Neonates have periodic breathing- the respiratory rate varies and includes periods of self-correcting apnea lasting 5 or 10 s. Neonates also have a biphasic response to hypoxia—they increase ventilation initially, but then become apneic. After about 3 weeks of age the response to hypoxia is sustained hyperventilation as in children and adults. Neonates also have a reduced response to hypercarbia compared with children and adults. Finally, neonates have increased sensitivity to stimulation in the superior laryngeal nerve territory and respond with hypoventilation, apnea or bradycardia.

14.4.4 Apnea and Anesthesia in Neonates

As a further indication of their immature respiratory control, neonates, and especially preterm neonates, are prone to apnea after anesthesia. An apnea is considered significant if it lasts longer than 15 s, or is associated with oxygen desaturation <90% or bradycardia (<100 bpm). They usually occur in the first 2 h after anesthesia, but may occur anytime during the first 12 h. The incidence of apnea after anesthesia increases with increasing prematurity—7% of neonates born at 34–35 weeks will have apneas, but 80% born at less than 30 weeks will have apneas. Anesthesia or sedation may cause apnea even if the infant wasn’t having them before. These apneas are not self-correcting and are a life-threatening risk of anesthesia in preterm infants. It is the reason for overnight admission even after minor surgery (Table 14.6). Apneas are often seen in these infants immediately after anesthesia while still in the OR (sometimes while still intubated and awaiting extubation). They sometimes respond to stimulation, and sometimes need IPPV briefly. Apnea in the PACU indicates a higher risk of apnea later on the ward. Overall, 6–10% of preterm neonates aged 44 weeks PMA or less will have apnea after anesthesia.

Table 14.6

Summary of apnea in infants after anesthesia and sedation

Key features



Longer then 15 s, or 10 s if associated desaturation or bradycardia

Usually within first few hours after anesthesia

Risk period extends to 12 h post op

Usually responds to stimulation; some require IPPV

Risk groups

Other preterm baby (less than 35 weeks) until 52 weeks PMA

Mildly preterm baby (35–37 weeks) until 48 weeks PMA

Term baby until 44 weeks PMA

Other risk factors in preterm infants

Co-morbidities (especially neurological, respiratory)

Intraoperative opioids or sedatives

Anesthesia technique and agents



Analgesia without opioids

Light GA with low-solubility volatile and regional analgesia

Caffeine base 10 mg/kg

Spinal anesthesia

PMA post menstrual age Risk Factors for Apnea After Anesthesia

Preterm infants aged less than 52 weeks PMA are at risk of apnea after anesthesia or sedation. The risk declines with age, is very low after 46 weeks PMA and is negligible after 52 weeks PMA. Preterm infants under 44 weeks PMA are most at risk. The degree of prematurity at birth also affects the risk—infants born mildly preterm at 35–37 weeks have a lower risk of apnea than neonates born before 35 weeks. Term neonates (born at 37 weeks gestation or more) are at a lower risk of apnea than preterm neonates, but a risk exists until 44 weeks PMA. Co-morbidities including anemia (Hb <100 g/L), lung disease, neurological problems and pre-existing apnea increase the risk of postop apnea.


Term neonates require admission and monitoring for postoperative apnea until a postmenstrual age of 44 weeks, and preterm infants until 52 weeks (some centers still use 60 weeks). Prevention Strategies to Reduce Apnea

The risk of postoperative apnea can be reduced by postponing elective surgery until the infant is older. Term infants should not have day-stay surgery until they are 44 weeks PMA (that is, 4 weeks old if born at 40 weeks gestation, 7 weeks old if born at 37 weeks). Preterm infants should not have day-stay surgery until they are 52 weeks PMA (some centers use 60 weeks). The risk in infants born mildly preterm (35–37 weeks) is lower and some centers allow day-stay surgery after 48 weeks PMA in these infants if there are no other risk factors. This last group still needs to be monitored for 6–8 apnea-free hours before discharge. Although anemia increases apnea risk, many centers accept mild anemia unless there are other reasons for transfusion.

General anesthesia can be modified to reduce the risk. Regional or local anesthesia should be used in place of opioids, allowing a light plane of anesthesia with relatively insoluble agents such as sevoflurane. Longer acting drugs of all classes should be avoided.

Spinal anesthesia was thought to greatly reduce the risk of postop apnea. More recent work suggests spinal anesthesia does not reduce the overall incidence of apnea compared to general anesthesia. However, it does reduce the number of infants needing any intervention greater than stimulation to resolve their apnea, and the number of apneas in the PACU. Spinal anesthesia is discussed in Chap. 10, Sect. 10.​5.​4. In summary, its disadvantages are technical difficulties with lumbar puncture in small infants, and the short duration of spinal anesthesia in infants.

IV caffeine during anesthesia reduces the incidence of postop apnea. Preterm infants at high risk (44 weeks PMA or less) are given caffeine base 10 mg/kg IV (equivalent to caffeine citrate 20 mg/kg) during anesthesia to prevent apnea. Caffeine is also used in the neonatal nursery to prevent apnea in premature neonates, so it is important to check the baby has not already been given caffeine. Aminophylline can be used if IV caffeine is not available, although it has more cardiovascular side effects.


Spinal anesthesia was thought to greatly reduce the risk of postop apnea. It is now realized it does not affect the overall incidence of postop apnea, but does reduce the severity of apneas and incidence of early apneas. Monitoring for Apnea

Detection of apnea prevents hypoxia or hypoxic cardiac arrest. An ‘apnea monitor’ is used, usually in combination with pulse oximetry. The monitor uses ECG leads on the chest and detects respiratory movement via the impedance between the leads and measures heart rate via the ECG. It will not detect obstructive apnea (chest moving but no air flow) until bradycardia develops. Most apnea begins in the first few of hours after anesthesia. The risk diminishes with time and monitoring is ceased when there has been no apnea for 12 h.

Apneas nearly always respond to stimulation alone and rarely require bag-mask ventilation. Groups of infants that require monitoring are those in the ‘risk group’ of Table 14.6.

14.5 Fluid and Glucose Requirements

Neonates have a greater proportion of their bodies as water, a larger blood volume and higher fluid, glucose and sodium requirements than older children and adults (Table 14.7). Body water makes up 80% of weight at birth, falling to 60% at age 1 year. The extracellular fluid volume is larger than the intracellular fluid volume (the opposite of children) until about 3 months of age. Fluid requirements are low for the first few days after birth while lung water is reabsorbed, and then high in keeping with the neonate’s high metabolic rate.

Table 14.7

Differences in body fluid compartments and fluid requirements between neonate and adult

Fluid compartment



Total body water



Extracellular fluid volume



Blood volume

90 mL/kg

70 mL/kg

Sodium requirement

3 mmol/kg/day


Glucose requirement

6–8 mg/kg/min


Fluid requirements

Day 1

60 mL/kg/24/h

Day 2


Day 3


Day 4


Day 5


Day 7 onwards


Fluid requirements are low initially because fluid is being absorbed from the lungs after birth. Based on data from Newborn clinical guidelines, Starship Children’s

Glucose requirements are high in neonates to match their metabolic rate and limited gluconeogenesis. A commonly used maintenance fluid is 10% glucose with 0.2% saline. Hypoglycemia is defined as <2.6 mmol/L in neonates (4.0 mmol/L in children). In the neonatal unit, hypoglycemia is corrected gradually by increasing feeds or the rate of glucose administration. Boluses of glucose are avoided and very rarely used. Renal function is immature at birth with reduced glomerular filtration rate (GFR) and poor concentrating ability. GFR reaches 50% of the adult level by 48 weeks PMA, 90% of the adult rate by 1 year, and reaches the adult rate by 2 years (Fig. 14.1).


Fig. 14.1

Glomerular filtration rate (GFR) at birth is roughly one quarter of the adult, but reaches the adult level at 2 years of age. Modified from Anderson BJ, Holford NHG. Negligible impact of birth on renal function and drug metabolism. Pediatr Anesth 2018;28: 1015–21

14.5.1 Neonatal Blood

The neonate has predominantly fetal hemoglobin (HbF) which has an oxygen dissociation curve shifted to the left—oxygen extraction at the tissue level is impaired due to the higher venous oxygen levels after birth. The hemoglobin level at birth is variable, but commonly about 16 g/dL. Adult hemoglobin (HbA) is produced from birth, but red cell production is inadequate and the hemoglobin falls, reaching a low point of 8–11 g/dL at 2–3 months (called the ‘physiological anemia’). Nearly all of the hemoglobin at this stage is HbA, and so tissue oxygen delivery is actually improved compared to earlier with HbF.


The presence of HbF in neonates is a key reason for a higher transfusion-trigger hemoglobin in neonates than children.

The coagulation system of the neonate is immature and does not reach adult levels until about 6 months of age. The coagulation changes are due to reduced levels of the vitamin K dependent factors and reduced levels of coagulation inhibitors (Antithrombin III, Protein C and S). Vitamin K is often given to neonates because of this coagulopathy. Platelet numbers are normal, but they do not reach adult activity until the neonate is 2 weeks old. Neonates do not have blood group antibodies in their plasma apart from some transferred through the placenta from the mother. Cross match of blood is performed on maternal serum.

14.6 Temperature

Neonates can only control body temperature over narrow range of environmental temperatures compared to children and adults. Their thermoneutral temperature depends on the age and weight of the baby, but for a naked term baby it is 32–35 °C. Methods to maintain body temperature are during surgery are described in Sect. 14.9.2.

14.6.1 Heat Loss and Production

Neonates have large heat losses and a decreased ability to generate heat, so are at great risk of hypothermia during transport and while in theatre. Losses are through the skin, particularly by convection and radiation. Evaporation is also an important source of heat loss in preterm infants because of their thin skin. Heat losses are high because of the neonate’s large surface area to weight ratio and poor insulation from subcutaneous fat. The head (20% of surface area) is a significant site of heat loss and should be kept covered.

Heat production is limited—neonates do not shiver, or at least not enough to generate any heat. They do however have brown fat that is rich in mitochondria located around the great vessels in the neck and thorax, and also in the axilla and between the scapulae. This fat is used for non-shivering thermogenesis, which can double heat production in neonates and infants until 2 years of age. Non-shivering thermogenesis is inhibited by anesthesia, as is shivering in older children and adults.


Think of heat loss when you uncover an infant to insert an IV.

Consider underbody or overhead warming, covering patient with a clear plastic sheet, insulating cap for the head.

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Nov 27, 2021 | Posted by in ANESTHESIA | Comments Off on Anesthesia
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