Abstract
Children are not simply ‘small adults’. The anatomical and physiological differences between children and adults have a significant impact on their anaesthetic management.
Children are not simply ‘small adults’. The anatomical and physiological differences between children and adults have a significant impact on their anaesthetic management.
Childhood is classified into the following age groups.
Neonate: the first 28 days of life (or, more precisely, a baby under 44 weeks in terms of post-conceptual age);
Infant: 28 days to 1 year;
Child: 1–12 years;
Adolescent: 13–17 years.
Describe the main anatomical and physiological differences between children and adults
The differences between children and adults are most evident below the age of 1 year. System by system, key features are as follows.
– Relatively large head with a prominent occiput; relatively short neck and large tongue. Optimal head position is ‘neutral’ rather than the ‘sniffing the morning air’ position of the adult.
– Neonates and infants are obligate nasal breathers. Nasal obstruction with secretions or nasogastric tubes can significantly impact breathing. This risk diminishes beyond the age of 4 months.
– Large ‘U’-shaped epiglottis. A straight-bladed laryngoscope may be required.
– A more cephalad larynx. The larynx is at vertebral level C3 in the neonate and C4 in the child, compared with C5 or C6 in adults.
– A short trachea (as little as 4 cm). This increases the risk of accidental endobronchial intubation. Intubation of the left main bronchus is as likely as the right, as the angle at the carina is similar. This is in contrast to the situation in the adult, where the left bronchus takes a more acute angle than the right, making the right bronchus more susceptible to endobronchial intubation. The endotracheal tube (ETT) should be positioned at least 1 cm above the carina and should be fixed to the maxilla (otherwise accidental endobronchial intubation may occur with intraoperative head and jaw movement).
– The narrowest part of the trachea is the cricoid ring in prepubescent children. The mucosa here is loosely bound, pseudostratified ciliated epithelium that, following airway trauma, is very prone to developing oedema.
In young children, the trachea is very narrow. Even a small amount of oedema will have a significant impact on the radius of the trachea and therefore the resistance to airflow: the Hagen–Poiseuille equation indicates that resistance to flow is inversely proportional to the fourth power of the radius (see Chapter 21).
Traditionally, smaller versions of the adult high-pressure, low-volume cuff ETTs were used in children. Pressure on the tracheal mucosa caused oedema, which had the potential to cause airway obstruction following extubation. Therefore, uncuffed ETTs were used for children below the age of 10, whose tracheas were the narrowest, with the ETT size calculated using the following formula: (age/4) + 4. When inserted, a correctly sized, uncuffed ETT should not feel tight and there should be an air leak when positive pressure is applied. However, getting the right-sized ETT for a particular patient sometimes required multiple changes of ETT in order to find one that was not too tight and did not have a large air leak.
More recently, ETTs designed for use in children have been developed with low-pressure, high-volume cuffs. Cuffed ETTs are sized using the following formula: (age/4) + 3.5 (i.e. half a size smaller than an uncuffed ETT). The use of a cuffed ETT means that the large air leaks (and resultant suboptimal ventilation) associated with uncuffed ETTs are avoided. However, the reduced internal diameter of a cuffed ETT inevitably leads to greater airways resistance, meaning that a spontaneous breathing technique may not be possible.
Respiratory physiology. Children (especially neonates and infants) have limited respiratory reserve.
– High O2 consumption. Arguably the most important feature of paediatric physiology is a high basal metabolic rate (BMR), resulting in increased O2 consumption in relation to body mass: a neonate has an O2 consumption double that of an adult: 6 mL kg–1 min–1 versus 3 mL kg–1 min–1.
– Increased alveolar ventilation. As a result of their high BMR, CO2 production in children is increased. PaCO2 remains within the normal range due to increased V̇A.
– Increased respiratory rate (RR). VT is 6–8 mL/kg; that is, similar to adults. The increased V̇A is achieved by increasing RR rather than VT.
– The diaphragm is the main muscle of inspiration. Ribs are soft and aligned horizontally; the ‘bucket-handle’ mechanism of the thoracic cage does not occur. VT is fairly static; high intrapleural pressure results in intercostal recession rather than lung expansion, especially in neonates and infants. An acute abdomen or gas insufflation of the stomach splints the diaphragm, impairing ventilation.
– Reduced functional residual capacity (FRC). Their soft ribs mean that chest wall compliance is increased in children. The elastic recoil of the lung is only slightly less than that of an adult. Overall, FRC (the point at which inward lung elastic forces match the outward elastic recoil of the chest wall) is reduced. As FRC is the O2 reservoir of the lung, rapid desaturation may occur during periods of apnoea, such as following induction of anaesthesia. FRC is further reduced during general anaesthesia: the physiological mechanisms that maintain FRC (partial adduction of the vocal cords during expiration and inspiratory muscle tone) are abolished.
– Closing capacity (CC) exceeds FRC. The increase in chest wall compliance and lower lung volumes mean that small airways collapse easily: CC exceeds FRC in neonates, leading to a significant V̇/Q̇ mismatch.
– The muscles of respiration are easily fatigued. The work of breathing is higher due to lower lung volumes, excessive chest wall compliance and the inadequacy of the bucket-handle mechanism. The diaphragm and intercostal muscles fatigue easily due to a lack of type I muscle fibres.
Cardiovascular physiology. The cardiovascular differences between children and adults are most stark in neonates, becoming more adult-like with age.
– Cardiac index (i.e. cardiac output (CO) corrected for body surface area) is increased by 30–60% in neonates. The high CO is required to increase O2-carrying capacity so that the high metabolic demands of the neonate are met.
– The Frank–Starling response is limited. The neonatal myocardium has a lower proportion of contractile proteins. The ventricles generate less tension during contraction and cannot increase their tension in response to increased preload. The end result is a relatively fixed stroke volume; CO is largely heart rate (HR) dependent. As a result, bradycardia is poorly tolerated: a neonatal HR of <60 bpm is an indication for cardiopulmonary resuscitation.
– HR decreases with age, from a typical value of 120 bpm in neonates to 75 bpm in adults.
– Sinus arrhythmia, the variation of HR with breathing, which, despite its name, is not pathological. It is thought to be due to suppression of vagal tone on inspiration leading to an increase in HR, and vice versa on expiration. It is often seen on the electrocardiogram of children below teenage years as a sinusoidal variation in R–R interval. In adults, sinus arrhythmia may be preserved in athletes who have a higher vagal tone.
– Blood pressure increases with age, from typical systolic values of 70 mmHg in neonates to 120 mmHg in adults.
– Autonomic nervous system reflexes. The parasympathetic nervous system and baroreceptor reflexes are mature in neonates, but the sympathetic nervous system is relatively immature. The neonatal response to stress (e.g. hypoxia) is therefore predominantly parasympathetic, resulting in bradycardia. Bradycardia associated with hypoxia should be initially treated with O2 and ventilation rather than atropine!
Central nervous system. Key features are:
– Intracranial pressure (ICP). Neonates and infants have a large anterior fontanelle. Raised ICP can be partially compensated for by expansion of the fontanelle and separation of the cranial sutures; palpation of the fontanelle can be used to assess ICP.
– The blood–brain barrier (BBB) is immature and incomplete in neonates. Bilirubin and drugs (e.g. opioids and barbiturates) cross the BBB more easily. This explains the increased sensitivity of neonates to respiratory depressants.
– Spinal cord. The spinal cord ends at the level of L3 in neonates and L2/3 at 1 year of age. The adult level of L1/2 is reached at around the age of 8. Incomplete myelination of nerves results in better penetration of local anaesthetic; doses may be reduced slightly. The immaturity of the sympathetic nervous system means that central neuraxial blockade is well tolerated, with hypotension being uncommon.
Renal physiology. The neonatal kidneys are immature. Renal function gradually reaches adult levels by 2 years of age:
– Glomerular filtration rate in infants is around half that of the adult (65 mL/min compared with 120 mL/min).
– Tubular function is immature and concentrating ability is reduced, especially in the first week of life; a dehydrated infant has a limited ability to conserve water.
– Preterm neonates are unable to significantly increase their Na+ excretion if excessive volumes of crystalloid are administered.
Haematology.
– At birth, foetal haemoglobin (HbF) predominates. By 3 months of age, 95% of Hb is adult HbA.
– During foetal life, the HbF concentration is high (around 180 g/L) to maximise O2 carriage. In the days following birth, Hb concentration rises by 10–20 g/L as fluid loss results in haemoconcentration. Over the first 3 months of life, Hb concentration falls to 100 g/L, before it rises slowly to adult levels by puberty.
– During foetal life, vitamin K (a fat-soluble vitamin) barely crosses the placenta. Neonates are relatively vitamin K deficient, leading to impaired hepatic synthesis of clotting factors II, VII, IX and X, with the potential for bleeding exemplified by haemorrhagic disease of the newborn. Breast milk is low in vitamin K; this is why neonates are routinely given prophylactic vitamin K shortly after birth.
– Blood volume is approximately 90 mL/kg in the neonate and 80 mL/kg at 6 months. By 1 year of age, blood volume reaches the adult value of 70 mL/kg.
Hepatic physiology. The neonatal liver has impaired enzymatic function:
– The function of glucuronosyltransferase, which catalyses the glucuronidation of bilirubin, is especially poor. Plasma unconjugated bilirubin increases and crosses the immature BBB, predisposing to kernicterus.
– Drugs that undergo hepatic metabolism by phase 1 and 2 reactions have prolonged action, such as barbiturates and opioids.
– Neonatal BMR is double that of an adult (50 kcal/kg per day versus 25 kcal/kg per day), resulting in increased O2 consumption and CO2 production. This is due to the metabolic demands of growth and thermoregulation. Neonatal BMR is higher than foetal BMR; the neonate must expend energy to achieve gas exchange (up to 25% of BMR), a process that was performed passively by the placenta in foetal life.
– Neonates are prone to hypoglycaemia due to their high BMR coupled with both low liver glycogen stores and immature gluconeogenesis enzymes. Neonates should therefore not be fasted excessively prior to surgery, and most centres would commence an intravenous glucose infusion.
Thermoregulation. Neonates and infants are prone to heat loss due to:
– A large surface area-to-body weight ratio;
– Minimal insulating subcutaneous tissue;
– Poorly developed shivering and vasoconstriction mechanisms.
Hypothermia in neonates is associated with acidosis, respiratory depression and decreased CO. Under general anaesthesia, the main mechanism of heat loss is radiation. In addition to the usual measures to prevent heat loss (forced-air warming blankets, heat and moisture exchangers, etc.), ambient theatre temperature should be increased for younger children.
– Neonatal total body water is 75% of body weight, compared with 60% in an adult. Premature neonates have an even higher proportion of body water: up to 85%.
– Extracellular fluid is 40% of total body weight in the neonate, compared with 20% of total body weight in an adult.
– When nil-by-mouth, dehydration occurs more rapidly in neonates than in adults owing to:
▪ Increased evaporative losses due to the neonate’s high surface area-to-body weight ratio.
▪ Increased respiratory loss of water vapour due to higher V̇E.
▪ Impaired ability to concentrate urine.
