Paediatric anaesthesia

Respiratory system

Cardiovascular system

Fetal circulation and cardiorespiratory changes at birth

The fetal circulation features several adaptations to the intrauterine environment that preferentially deliver oxygenated blood from the placenta to the developing brain ( Fig. 33.1 ). Significant physiological changes occur at and soon after birth, allowing a transition to the normal adult circulation; an understanding of these processes is fundamental to providing safe anaesthesia for neonates.

In utero

• Oxygenated blood returns from the placenta via the single umbilical vein, passing to the inferior vena cava (IVC). A proportion of this bypasses the liver via the ductus venosus.

• The Eustachian valve lies at the junction of the IVC and right atrium and streams this oxygenated blood across the foramen ovale to the left atrium.

• Oxygen-rich blood then passes via the left ventricle to the ascending aorta and to the brain.

• In contrast, desaturated venous blood from the head and neck returns to the heart via the superior vena cava (SVC); this passes to the right atrium, right ventricle and pulmonary artery.

• Approximately 90% of the right ventricular output is directed via the ductus arteriosus to the descending aorta because of the high pulmonary vascular resistance (PVR) of the non-aerated lungs.

• In this way, relatively oxygenated blood is conserved for the developing brain and coronary circulation, with less oxygenated blood delivered to the rest of the body.

• Fetal haemoglobin (HbF) has a low P50 (see Chapter 10 ) to reflect the relatively low oxygen tension in utero and to facilitate oxygen uptake at the fetal side of the placenta ( Fig. 33.2 ). However, this is at the cost of HbF being poorer at releasing oxygen to the tissues; to allow adequate tissue oxygen delivery to occur a higher haemoglobin concentration is needed, typically up to 200 g L ^–1 (see later).

  

• Deoxygenated blood returns to the placenta via the paired umbilical arteries (each arising from the internal iliac arteries).

At birth

• Placental blood flow ceases and systemic vascular resistance (SVR) increases.

• At the same time PVR falls rapidly because of expansion of the lungs, increased oxygen tension and increase in nitric oxide and prostacyclin concentrations.

• As a result, pulmonary perfusion increases dramatically, right-sided heart pressures fall and left-sided heart pressures increase, which results in closure of the flap valve over the foramen ovale.

• After the initial rapid fall at birth the PVR continues to decline more slowly to reach adult values by 4–6 weeks of age.

• The ductus arteriosus starts to constrict after birth as a result of oxygen-mediated vasoconstriction and metabolism of prostaglandins that maintain ductal patency in utero.

• There is usually no right-to-left shunting across the duct by about day 2 of life in healthy infants, with anatomical closure as a result of intimal fibrosis within 2–3 weeks.

Importantly, functional closure of the arterial duct is reversible in the first weeks of life, and neonates may revert to a persistent fetal circulation if the PVR remains high (e.g. because of hypoxia, acidosis, meconium aspiration, sepsis or congenital diaphragmatic hernia), with right-to-left shunting across the ductus arteriosus and reduced pulmonary blood flow. This is termed persistent pulmonary hypertension of the newborn and is demonstrated by the presence of differential cyanosis, with lower oxygen saturations in the lower limbs (postductal) than right upper limb (preductal). This is the basis of oxygen saturation screening for congenital heart disease in newborns.

In some congenital cardiac lesions, continued ductal patency may be required for survival, to allow blood flow to either systemic circulation (e.g. in severe aortic coarctation) or pulmonary circulation (e.g. in pulmonary atresia). A prostaglandin infusion may be required to keep the arterial duct open in these duct-dependent circulations until a more definitive intervention can be performed.

Central nervous system

Several features of the developing nervous system are of relevance to the anaesthetist. The neonatal blood–brain barrier is anatomically and functionally incomplete; this contributes to increased sensitivity to opioids and other sedatives, as well as to increased vulnerability to local anaesthetic toxicity.

At birth the brain occupies a much larger proportion of total body weight than in the adult (10%–15% vs. 2%). The cerebral metabolic requirement for oxygen (CMRO ₂ ) is also higher (~5 ml 100 g ^–1 min ^–1 vs. 3.5 ml 100 g ^–1 min ^–1 ). Autoregulation of blood flow is present at term; however, preterm neonates are vulnerable to changes in blood pressure causing intracranial haemorrhage, particularly affecting the periventricular germinal matrix.

The spinal cord in the fetus initially occupies the entire length of the spinal canal, the termination subsequently moving cranially because of differential growth of the spine and spinal cord. The spinal cord terminates at S1 at 28 weeks gestation, L3 at term, and L1–2 by early adolescence. The sacral hiatus is relatively large in the infant and child and is not ossified, hence allowing ease of access to the epidural space via the caudal route. Furthermore, the epidural fat is less densely packed than in adults, which facilitates spread of local anaesthetic injected into the caudal space to the thoracic region.

The long-term effect of exposure to anaesthetic drugs in infancy and early childhood is an area of active research. Neurotoxicity with persistent cognitive deficit has been demonstrated after exposure to anaesthetic agents in animal studies, but the clinical significance of this in humans is unknown. Initial data from prospective randomised trials suggest that a single short general anaesthetic in infancy has no impact on early cognitive development. At present there is insufficient evidence to alter current anaesthetic and surgical practice, although deferral of non-urgent procedures requiring general anaesthesia (e.g. cosmetic procedures, non-urgent imaging) to older than 3 years of age has been suggested.

Liver function and drug metabolism

Liver function is immature at birth, and hepatic phase I and II processes (except for sulphation) are not fully functional. Immature glucuronidation combined with high red cell turnover in neonates may lead to kernicterus if unconjugated hyperbilirubinaemia is left untreated. Hepatic metabolism and clearance of drugs is reduced, and drugs cleared by this means have a longer duration of effect. Hepatic function accelerates rapidly after birth, reaching adult levels by 2–3 months in normal infants. Relevant examples include morphine and the aminosteroid non-depolarising neuromuscular blocking agents (NMBAs), such as vecuronium and rocuronium. A single dose of these drugs in neonates and young infants will have longer duration of action than in older children because of reduced clearance.

Hepatic synthetic function is also immature in neonates. Vitamin K–dependent clotting factors (II, VII, IX and X) are deficient at birth, and all neonates should receive vitamin K at or soon after delivery. Reduced glycogen stores and impaired gluconeogenesis (combined with a high metabolic rate) increase vulnerability to hypoglycaemia, particularly during starvation. Lower plasma protein concentrations (e.g. albumin and α ₁ -acid glycoprotein) result in reduced protein binding of drugs (e.g. morphine, lidocaine and bupivacaine) and therefore higher proportion of free drug and increased risk of drug toxicity.

Renal function

Renal blood flow is low in the neonatal period (because of high renal vascular resistance), rising from about 6% of cardiac output to the adult level of approximately 20% by age 1 month. Antidiuretic hormone (ADH) concentrations are high at birth, resulting in low urine output and fluid requirements. A significant diuresis occurs as ADH concentrations fall during the first week of life, and fluid requirements rise. For this reason maintenance i.v. fluids should be restricted in the first few days of life until the postnatal diuresis has occurred ( Table 33.2 ).

Although nephrogenesis is complete by 34 weeks gestation, both tubular excretory and concentrating ability are limited in the first few weeks of life. Neonates do not tolerate dehydration, fluid loading and electrolyte or acid–base derangements well. They are particularly at risk for acute kidney injury, hyponatraemia and metabolic acidosis.

Temperature regulation

Thermal homeostasis is immature in neonates and small children, and hypothermia is a particular risk during anaesthesia. Heat losses are high because of increased surface area/body mass ratio, insensible evaporative losses via the respiratory tract and thermal conductance. Compensatory mechanisms such as shivering and vasoconstrictive responses are less effective in neonates and only partially compensated for by non-shivering thermogenesis (metabolism of adipose tissue around the base of the neck, scapulae and back). This situation is reflected in the differing thermoneutral temperature for neonates and adults, the ambient temperature at which metabolic expenditure is minimal – 34 ^o C for a preterm neonate, 32 ^o C for a term neonate and 28 ^o C for an adult.

Preoperative assessment

As with adult practice (see Chapter 19 ) the goals of preoperative assessment in children include obtaining relevant history and clinical data to anticipate anaesthetic complications (e.g. difficult tracheal intubation), assess the risk of anaesthesia and surgery and inform the appropriate anaesthetic and perioperative plan. In addition, it is important to establish rapport with the patient and parents, to obtain consent for anaesthesia and to agree on a mode of induction; clear and honest communication is crucial, as is providing appropriate reassurance. Where possible, children should be involved in these discussions (see Chapter 21 ).

History and examination should include assessment of:

• problems with previous anaesthetics (e.g. anxiety, nausea and vomiting, airway difficulties).

• prematurity and its consequences (e.g. gestational age at birth and current corrected age, previous need for invasive ventilation and evidence of ongoing lung disease). Apnoea monitoring and pulse oximetry are recommended for 24 h after surgery in preterm neonates younger than 60 weeks postconceptual age.

• respiratory morbidity (e.g. asthma, including severity and current status; obstructive sleep apnoea; and active upper respiratory tract infection, or URTI).

  • The last of these is a common dilemma for anaesthetists, particularly in elective surgery. On the one hand, perioperative respiratory complications (e.g. laryngospasm, bronchospasm, desaturation or airway obstruction) are more common in children with active symptoms or within 2 weeks of a URTI. On the other hand, mild URTIs are extremely common (and may also be part of the underlying surgical pathophysiology), and deferring surgery until a child is symptom-free may be not be feasible. In practice, minor elective surgery may usually proceed if there are only mild coryzal symptoms without systemic features (e.g. fever, anorexia, difficulty sleeping) or signs of lower respiratory tract infection (e.g. tachypnoea, inspiratory crepitations, purulent sputum). It is sensible to avoid airway surgery in a child with an active URTI. However, these are often not straightforward decisions, and a discussion with the parents, with senior anaesthetic and surgical input, is essential. If you proceed with surgery in a child with airway symptoms the risk of airway complications is lower with i.v. induction of anaesthesia, using inhalational agents for maintenance, use of a face mask rather than tracheal intubation and in the presence of a more experienced anaesthetist. If surgery is deferred because of a URTI the consensus for the minimum period of deferral is 2–4 weeks.

• cardiovascular morbidity, particularly high-risk cardiac conditions requiring expert management in a specialist centre, such as cardiomyopathy, pulmonary hypertension, single ventricle circulations and ventricular outflow tract obstruction (left or right). Detection of a previously undiagnosed heart murmur during preassessment is relatively common; in most cases the murmur is innocent, but in some it may indicate significant disease requiring specialist management before surgery. Features suggestive of a significant lesion include signs and symptoms of heart failure, such as failure to thrive; dyspnoea, tachypnoea or diaphoresis during exertion or feeding; recurrent respiratory tract infections; unexplained collapse; or cyanosis/cyanotic episodes. The index of suspicion should be higher in those with a syndrome associated with cardiac disease (e.g. Down's, DiGeorge's, CHARGE ( c oloboma, h eart defect, a tresia choanae, r estricted growth and development, g enital abnormality and e ar abnormality) and VACTERL ( v ertebral defects, a nal atresia, c ardiac defects, t racheo-o e sophageal fistula, r enal anomalies and l imb abnormalities) associations). Although most congenital cardiac disease is detected before 3 months of age, all infants (<1 year old) with a newly detected murmur should be referred to a paediatric cardiologist for assessment before surgery if possible as significant lesions may be asymptomatic in this age group. An older child who is asymptomatic but has an abnormal 12-lead ECG (e.g. with evidence of left ventricular hypertrophy) should also be referred before surgery. Defer investigation of other children with a murmur until after surgery.

• other comorbidity, drug history and allergies. Exacerbation of asthma with NSAIDs is very rare in children, but a history of safe NSAID use is usually sought and documented before prescribing them.

• family history of relevant inherited disorders (e.g. plasma cholinesterase deficiency, malignant hyperpyrexia, sickle-cell disease). Children born in the UK are routinely screened for sickle-cell disease at birth.

• airway assessment. Clinical features associated with difficult airway management (e.g. micrognathia/retrognathia, reduced mouth opening and thyromental distance) or specific syndromes (e.g. Pierre Robin, Crouzon, Treacher Collins, Down's).

• weight. An accurate measure should be obtained to guide drug dosing and fluid management. If this is not possible, weight may be estimated using the formulae in Table 33.3 .

  Table 33.3

  Formulae for estimating children's weights

  Age	Estimated weight (kg)
  <1 month	~3 kg
  1–12 months	(0.5 × age in months) + 4
  1–5 years	(2 × age in years) + 8
  6–12 years	(3 × age in years) + 7
  >12 years	Highly variable