Paediatrics

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Chapter 9 Paediatrics

General Paediatrics

Definitions

• Neonate – first 28 days of life or <44 weeks post-conception

• Infant – 1 month to 1 year

• Child – >1 year to adolescence

• Low birth weight – 2500 g at birth

• Premature – less than 37 weeks.

Physiological changes at birth

• Tactile stimulus triggers respiratory centre. Inflation of lungs reduces pulmonary vascular resistance.

• Increased flow to lungs increases left atrial pressure, closing the foramen ovale.

• Cessation of placental flow increases SVR. Combined with decreased PVR, flow through ductus arteriosus reverses. High P_aO₂ causes ductal smooth muscle to constrict, and closure occurs (reversible for several days).

Fetal circulation is shown in Figure 9.1.

Figure 9.1 Fetal circulation.

Neonatal physiology

CVS

• Tendency to revert to fetal circulation for 2 weeks is triggered by acidosis and ↑ P_aCO₂.

• Relatively little contractile tissue in heart (30%), so increased cardiac output achieved by increased heart rate rather than stroke volume. Ventricular thickness equal by 6 months.

• Cardiac index is 2–3 times that of an adult.

• Heart rate at term is 120/min. Rises to 160/min by 1 month and decreases to adult rates by 15 years.

• PNS more developed than SNS. Therefore there is a tendency to bradycardia. Response to adrenergic drugs is diminished.

• Ductus arteriosus reopens following fluid overload.

Respiratory

• Obligatory nasal breathing until 5 months. Nasal passages account for 30–50% of airway resistance. May be unable to convert to mouth breathing if there is nasal obstruction.

• Large tongue obstructs the airway and makes laryngoscopy difficult. Epiglottis is longer, narrower and angled away from the axis of the trachea.

• Larynx is higher (C₃–C₄) and more anterior than in adults (C₄–C₅).

• Narrowest part of upper airway is cricoid cartilage. Even minimal oedema causes a large increase in airway resistance (Hagen–Poiseuille law).

• Short trachea at term: ≈︀4 cm.

• Tendency to apnoea if <50 weeks post-conceptual age, due to immature respiratory centre.

• Negative pressure of 40–80 cmH₂O is required for initial lung expansion.

• Surfactant produced from 32 weeks by type II alveolar pneumocytes.

• No bucket handle rib movement, therefore increased minute volume is achieved by increasing respiratory rate.

• Diaphragmatic > intercostal respiration. Fewer type I muscle fibres used in prolonged work so earlier diaphragm fatigue.

• Rapid respiratory rate of 32 breaths/min.

• FRC <CC due to decreased outward recoil of chest wall.

• Small FRC, high O₂ consumption; therefore rapid desaturation.

• Increased laryngeal irritability with susceptibility to laryngospasm.

• Increased susceptibility to respiratory infection.

GI

• Acute gastric dilatation is common, so consider a NG tube.

• Lower oesophageal sphincter incompetence predisposes to aspiration pneumonia.

• Immature hepatic function and reduced blood flow, increasing half-life of drugs excreted by hepatic metabolism. Phase I reactions attain adult levels within 1 week; phase II reactions within 3–4 months.

Renal

• Immature renal function with reduced GFR; therefore reduced ability to excrete drugs, dependent upon renal clearance.

• Reduced concentrating ability.

• 50% N₂ forms new tissue; therefore less renal N₂ load.

CNS

• Immature blood–brain barrier with increased permeability to lipid-soluble drugs.

• Motor nerve endings differentiate to form end plates at 26–28 weeks, but process still incomplete at term.

• Increased risk of intraventricular haemorrhage, particularly with abrupt fluctuations in cerebral blood flow and CVP, due to underdeveloped perivascular connective tissue.

• Increased proportion of low-affinity μ₂ opiate receptors (mediate respiratory depression).

• Increased sensitivity to volatiles due to increased progesterone, increased β-endorphins, immature blood–brain barrier and decreased protein binding.

Blood

• 70% HbF at term; P₅₀ = 2.7 kPa (3.5–4.0 kPa in adult) with leftward shift of O₂ dissociation curve.

• Blood volume 80 mL.kg⁻¹ at term.

• Physiological anaemia is greatest at 3–4 months, with Hb = 10 g.dL⁻¹.

Change of haematocrit with age is shown in Figure 9.2.

Figure 9.2 Changes in haematocrit with age.

Temperature

• Increased surface area:body weight ratio. Therefore increased heat loss.

• Thermoneutral temperature at term = 33°C.

• Noradrenaline > adrenaline released with stress to trigger non-shivering thermogenesis in brown fat. Brown fat stores are limited. Shivering does not occur before 3 months.

• Immature thermoregulatory mechanisms, further inhibited by GA.

• Hypothermia causes acidosis, persistent fetal circulation, hypoxia, diaphragm fatigue, intraventricular haemorrhage and coagulopathy.

Glucose

• Minimal glycogen reserves for gluconeogenesis.

• Poorly developed glucose homeostasis.

• High glucose requirements at term. Tendency to hypoglycaemia in small-for-dates babies, infants of diabetic mothers and sick neonates.

Pharmacokinetic and pharmacodynamic differences

• Decreased lean body mass.

• Increased total body water (increased central volume by 50%).

• Decreased total body fat. Therefore, increased V_D of water-soluble drugs, decreased V_D of fat-soluble drugs.

• Decreased protein binding.

General anaesthesia

NCEPOD RECOMMENDATIONS FOR PAEDIATRIC ANAESTHESIA

• Anaesthetist must have sufficient paediatric experience

• One anaesthetist in each hospital must be responsible for paediatric anaesthesia

• Most problems occur in children <3 years

• Neonates (<28 days) must be anaesthetized in specialist units.

Weight (kg)

• 1–8 years = (age + 4) × 2

• >9 years = age × 3

Preoperative fasting

Half-life of gastric fluid (saline) is 11 min, prolonged by fat and glucose. Recent studies show that prolonged fasting may actually decrease gastric pH and increase volume. Clear fluids administered 2–3 h preoperatively do not alter gastric residual volume and cause less distress. See Association of Paediatric Anaesthetists Guidelines 2007 (below) for preoperative fasting guidelines.

CONSENSUS GUIDELINE ON PERIOPERATIVE FLUID MANAGEMENT IN CHILDREN, V1.1

Association of Paediatric Anaesthetists of Great Britain and Ireland 2007

Executive summary

1. Children can safely be allowed clear fluids 2 h before surgery without increasing the risk of aspiration.

2. Food should normally be withheld for 6 h prior to surgery in children aged 6 months or older.

3. In children under 6 months of age it is probably safe to allow a breast milk feed up to 4 h before surgery.

4. Dehydration without signs of hypovolaemia should be corrected slowly.

5. Hypovolaemia should be corrected rapidly to maintain cardiac output and organ perfusion.

6. In the child, a fall in blood pressure is a late sign of hypovolaemia.

7. Maintenance fluid requirements should be calculated using the formula of Holliday and Segar

Body weight	Daily fluid requirement
0–10 kg	4 mL/kg per h
10–20 kg	40 mL/h + 2 mL/kg per h above 10 kg
>20 kg	60 mL/h + 1 mL/kg per h above 20 kg

8. A fluid management plan for any child should address three key issues:

i. any fluid deficit which is present

ii. maintenance fluid requirements

iii. any losses due to surgery, e.g. blood loss, 3rd space losses.

9. During surgery, all of these requirements should be managed by giving isotonic fluid in all children over 1 month of age.

10. The majority of children over 1 month of age will maintain a normal blood sugar if given non-dextrose containing fluid during surgery.

11. Children at risk of hypoglycaemia if non-dextrose containing fluid is given are those on parenteral nutrition or a dextrose containing solution prior to theatre, children of low body weight (<3rd centile) or having surgery of more than 3 h duration and children having extensive regional anaesthesia. These children at risk should be given dextrose containing solutions or have their blood glucose monitored during surgery.

12. Blood loss during surgery should be replaced initially with crystalloid or colloid, and then with blood once the haematocrit has fallen to 25%. Children with cyanotic congenital heart disease and neonates may need a higher haematocrit to maintain oxygenation.

13. Fluid therapy should be monitored by daily electrolyte estimation, use of a fluid input/output chart and daily weighing if feasible.

14. Acute dilutional hyponatraemia is a medical emergency and should be managed in paediatric intensive care.

Preoperative assessment

Examine for congenital defects, cardiorespiratory pathology due to prematurity, hypoglycaemia and hypocalcaemia.

Premedication

Bradycardia secondary to cholinergic effects of drugs (halothane, suxamethonium) and upper airway stimulation is reduced with anticholinergic premedication.

Intubation

• Tracheal tube size (>1 year) = age/4 + 4 mm

• Tracheal tube length = age/2 + 12 cm.

Volatiles

MAC is lower in the neonate, but increases to a peak at 6 months before declining. Age-related change in MAC of sevoflurane is less pronounced. Gas induction is fast because alveolar ventilation is large compared with FRC, high cardiac output and lower blood:gas solubility of volatiles in neonates. Sevoflurane produces less laryngeal irritation than desflurane and is more suitable for gas induction. Baroreflex response is maintained with isoflurane and sevoflurane but not with halothane or desflurane.

Volatiles depress respiration, depress intercostal muscles and ventilation becomes diaphragmatic. Therefore, intubate if <5 kg or <44 weeks post-conceptual age. Volatiles reduce SVR, worsening a right-to-left shunt if persistent fetal circulation is present.

MAC of nitrous oxide is not related to age. N₂O may cause marked cardiovascular depression in neonates and diffusion into bowel may impair ventilation.

Variation in MAC of isoflurane with age is shown in Figure 9.3.

Figure 9.3 Variation in the MAC of isoflurane with age.

Barbiturates

Reduced V_D of lipid-soluble drugs reduces redistribution of thiopentone thus prolonging recovery. Induction doses: 2–4 mg/kg in neonates; 7–8 mg/kg in infants; 5–6 mg/kg in older children.

Propofol

Pain on induction, more excitatory phenomenon and less postoperative nausea and vomiting than with thiopentone. Greater depression of laryngopharyngeal reflexes than with thiopentone so more suitable for use with laryngeal mask. Larger V_D, faster metabolism and clearance. Therefore, a larger induction dose of 2.5–3.5 mg/kg is required.

Only licensed as an induction agent in children >3 years because of case reports of a syndrome of lactic acidaemia, bradyarrhythmias, hypotension, lipaemia and oliguria.

Benzodiazepines

Opioids

Increased sensitivity due to immature blood–brain barrier, reduced protein binding and decreased glucuronidation. Reduced clearance of all opioids. High doses reduce stress response and prevent pulmonary hypertension associated with airway instrumentation.

Muscle relaxants

Depolarizing. Decreased plasma cholinesterase but minimal effect on hydrolysis. Decreased sensitivity to suxamethonium due to increased V_D and immature neuromuscular junction. Therefore use a higher dose of 2 mg/kg.

Non-depolarizing. Atracurium has an increased V_D but increased clearance, so elimination half-life is unchanged and thus little change in overall pharmacokinetics. Sensitivity to, and action of, vecuronium is increased in children <1 year.

Ensure complete reversal before extubation with glycopyrrolate 0.01 mg/kg.

Local anaesthetics

Reduced protein binding and reduced metabolism increase risk of toxic side-effects.

Oxygen toxicity

Neonates <2 kg or <35 weeks are particularly susceptible to retinal damage by exposure to high P_aO₂. It is related to the level and duration of raised oxygen tension. Other risk factors are prematurity, twins, hypoxaemia, hyper/hypocarbia, sepsis and transfusion. S_ao₂ of 90–94% is considered optimal.

Fluid management

Insensible losses are greater due to:

• increased surface area:body ratio, increasing evaporation

• immature skin – loses more water

• increased alveolar ventilation – increases water lost via the lungs

• kidneys less able to concentrate urine.

Short operations <1 h in healthy children do not usually require fluids if preoperative fasting was not excessive. For longer procedures, an i.v. infusion is necessary. When calculating perioperative fluid requirements, add fluid lost during preoperative fasting to the operative regime. Maintain haematocrit >0.30.

Analgesia in neonates

Significant pain is not only unacceptable, but will produce a ‘pain memory’ with an exaggerated response to subsequent pain for as long as 6 months. Neonates and infants mount a graded hormonal stress response to surgery and adequate analgesia modifies the stress response and reduces morbidity and mortality. Multi-modal analgesia, using local anaesthetics, opioids, non-steroidal anti-inflammatory drugs (NSAIDs), and paracetamol is an effective approach for most infants. A local/regional analgesic technique should be used in all cases unless specifically contraindicated.

Opioids

Avoid painful i.m. injections. Subcutaneous delivery via cannula may be useful in some patients. Use of i.v. techniques is tempered by the risk of respiratory depression. Monitoring of respiratory frequency is an insensitive indicator of respiratory depression, and pulse oximetry in a high-dependency unit should be used when administering i.v. opioids. Patient-controlled analgesia has been used successfully in children as young as 5 years of age. Use of NSAIDs and regional/local blocks with their opioid-sparing effects is becoming much more widespread.

Table 9.1 Opioids: relative potency and dosing

Non-steroidal anti-inflammatory drugs

These appear to provide analgesia in children as young as 3 years. Ketorolac, indometacin, diclofenac and ibuprofen have all been shown to reduce postoperative opioid requirements. The degree of gastric irritation, renal impairment and fluid retention is not known. Immature renal and hepatic function may impair excretion. Caution is required in those with asthma, severe eczema, multiple allergies and those with nasal polyps.

Regional techniques

Nerves are less myelinated, resulting in a faster onset of block and an adequate block at lower concentrations of LA. Reduced plasma protein results in higher blood levels of LA. All routes cause less hypotension than in adults because of an immature SNS and less developed capacitance vessels. Postoperative numbness over wide areas may cause confusion and restlessness (3% of patients).

Spinal cord ends at L₃; dura ends at S₄.

	Single bolus injection	Continuous postoperative infusion
	Maximum dosage	Maximum infusion rate
Neonates	2 mg.kg⁻¹	0.2 mg.kg⁻¹.h⁻¹
Children	2.5 mg.kg⁻¹	0.4 mg.kg⁻¹.h⁻¹

GUIDELINES ON THE PREVENTION OF POSTOPERATIVE VOMITING (POV) IN CHILDREN

The Association of Paediatric Anaesthetists of Great Britain and Ireland, Spring 2007

Children at high risk of POV

• POV risk increases markedly at >3 years old and continues to rise throughout early childhood and into adolescence.

• Previous history of motion sickness is likely an independent risk factor of subsequent POV.

• Previous history of POV is an independent risk factor of subsequent POV in children.

• Post-pubertal girls have an increased incidence of POV.

Surgical procedures associated with high risk of POV

• Strabismus surgery

• Tonsillectomy ± adenoidectomy

• Surgical procedures >30 min duration.

What anaesthetic factors affect POV in children?

• Volatile anaesthesia is associated with increased POV risk, particularly in children with other risk factors.

• Opioids are associated with increased POV risk, particularly if longer-acting agents are used postoperatively.

• Mandating oral fluids may be associated with increased POV risk. Intraoperative i.v. fluids may reduce POV risk.

• N₂O is not associated with a high risk of POV.

• Anticholinesterases may be associated with an increased POV risk.

Recommendations for prevention of POV in children

• Children at increased risk of POV should be given i.v. ondansetron 0.15 mg.kg⁻¹ prophylactically.

• Children at high risk of POV should be given prophylactically i.v. ondansetron 0.05 mg.kg⁻¹ and i.v. dexamethasone 0.15 mg.kg⁻¹.

• Adenotonsillectomy or strabismus surgery: consider i.v. anaesthesia and alternatives to opioid analgesia in children at high risk of POV.

Recommendations for the treatment of established POV in children

• Ondansetron i.v. 0.15 mg.kg⁻¹ should be given to children who have not already been given ondansetron for prophylaxis of POV.

• For children who have already been given ondansetron, a second antiemetic from another class should be given, such as dexamethasone i.v. 0.15 mg.kg⁻¹ injected slowly.

Prematurity (37 weeks)

Associated with:

• Aspiration pneumonia, respiratory distress syndrome

• Apnoea

• Hypoglycaemia, hypocalcaemia, hypomagnesaemia

• Congenital defects.

Ex-premature baby for surgery

Preoperative assessment should include respiratory system, venous access and frequency of any apnoeic attacks. Assess gestational and chronological age.

Pulmonary function is often abnormal, with a higher respiratory rate, lower compliance and impaired gas exchange which may persist for several years. Risk of life-threatening apnoea is present until 45 weeks post-conceptual age. Use apnoea alarm for at least 24 h postoperatively.

Risk of postoperative apnoea in 30–40% of babies due to immature respiratory control mechanisms, impaired respiratory function, airway obstruction, anaemia and the residual effects of anaesthetic gases (reduced chemoreceptor response to hypoxia, increased paradoxical chest wall movement, depressed intercostal muscle activity). Caffeine 10 mg/kg i.v. at induction may reduce the risk of apnoea. Regional anaesthesia reduces but does not remove the risk of postoperative respiratory depression and apnoea.

Infections and sudden death more common.

Tracheo-oesophageal fistula (Fig. 9.4)

Presentation

Incidence of 1:3000 live births. Presents as excess oral secretions causing frothing at mouth, regurgitation of first feed and later as recurrent pneumonia; 30% are born prematurely, and 25% with major CVS abnormalities.

Figure 9.4 Anatomical variants of tracheo-oesophageal fistulae.

Associated with VATER syndrome (Vertebral abnormalities, Anal atresia, Tracheo-oEsophageal fistula, Radius abnormalities) and musculoskeletal and craniofacial malformation.

Diagnosis

• Inability to pass NG tube

• Barium swallow.

Preoperative

• Nurse head-up to reduce risk of aspiration

• Continuous suction of upper oesophageal pouch

• Physiotherapy and antibiotics if there is evidence of aspiration

• Intravenous fluids to correct dehydration and prevent hypoglycaemia

• If IPPV is planned, gastrostomy under LA may be necessary preoperatively.

General anaesthesia

Right-sided thoracotomy. Left precordial stethoscope detects ETT displacement. Awake intubation or gas induction (sevoflurane) with spontaneous respiration avoids IPPV, which causes gastric distension and respiratory impairment. IPPV may also be ineffective in patients with a gastrostomy tube as gas escapes through the tube. Intravenous induction is safe if a fistula is not present because IPPV is effective. If a fistula is present, allow the baby to breathe spontaneously until the fistula is closed.

The opening of the fistula is usually located on the posterior distal wall of the trachea. Intubate the right main bronchus and withdraw the ETT until breath sounds are heard in both lungs so that the tip of the ETT then occludes the fistula.

Aim for early extubation postoperatively to minimize suture line stress. Postoperative respiratory complications (aspiration, pneumonia) are common.

Congenital diaphragmatic hernia

Incidence of 1:3000 live births. Associated with 50% mortality within 6 h. Caused by early gut return or delayed diaphragm closure.

Sites of herniation (Fig. 9.5)

• Posterolateral foramen of Bochdalek (left >> right) – 85%

• Anterior foramen of Morgagni – 10%

• Oesophageal hiatus – <5%.

Figure 9.5 Sites of congenital diaphragmatic herniation.

Embryology of diaphragm

Comprises three structures:

• Septum transversum

• Pleuroperitoneal membrane

• Thoracic myotomes.

Sequelae

Ipsilateral alveolar and bronchial hypoplasia and decreased surfactant. Contralateral lung may also be affected. Usually presents as cyanosis, dyspnoea and cardiac dextroposition. Bowel sounds in thorax with reduced breath sounds.

A total of 23% are associated with cardiovascular abnormalities. Abnormalities of most other organ systems are also described; also trisomy 18 and 21.

Symptoms depend upon degree of hypoplasia:

• Severe – hypoplasia incompatible with life

• Moderate – respiratory distress, tachypnoea and cyanosis

• Mild – less severe symptoms, not always presenting immediately.

Pulmonary hypoplasia and pulmonary artery hypertension worsen any right-to-left shunt and cause respiratory acidosis, which predisposes to persistent fetal circulation. The degree of shunting may be reduced with bicarbonate infusion:

(Dilute in equal volume of 10% glucose prior to i.v. administration.)

General anaesthesia

• Emergency surgery is no longer recommended as mortality is reduced by preoperative resuscitation

• Monitoring: S_ao₂, ECG, invasive BP (one preductal, one post-ductal to assess shunt), urinary catheter

• Good venous access above IVC, which is compressed postoperatively by gut

• NG tube to decompress stomach

• Avoid IPPV which inflates the stomach and worsens respiratory distress. Therefore, awake intubation. Ventilate by hand to detect sudden changes in compliance, e.g. pneumothorax. Barotrauma, will further damage the hypoplastic lung and must be avoided.

• Avoid N₂O, which distends bowel. SNS stimulation worsens pulmonary vasoconstriction and is reduced by opioids, e.g. fentanyl

• Pulmonary vasodilators (tolazoline (α-antagonist), PGE₁, nitroprusside, nitroglycerine) improve oxygenation and acidosis, reducing airway pressure and risk of barotrauma

• Some success with ECMO, but mortality from anticoagulation causing bleeding

• Necessity for postoperative ventilation depends upon severity of abnormalities

• Successful in utero surgical correction reported.

ECMO has been used both as a rescue therapy in those with severe hypoxia after surgical repair and in the preoperative stabilization of infants before surgery. A recent UK study showed that infants who had received ECMO for CDH had a significant mortality in the first year of life, with long-term physical and neurodevelopmental morbidity in the majority of survivors.

Hypertrophic pyloric stenosis

Incidence 1:5000 live births. Occurs in males more than females. Due to hypertrophy of muscularis layer of pylorus. Associated anomalies in 6–20% cases include oesophageal atresia and congenital cardiac abnormalities. Usually presents in weeks 2–6 with non-bilious projectile vomiting.

Results in:

• dehydration

• metabolic disturbance

• aspiration risk.

Characterized by hypochloraemic hypokalaemic metabolic alkalosis with acidic urine. Due to bicarbonate initially excreted with K⁺ and Na⁺. Once K⁺ becomes depleted, the kidneys excrete H⁺ in an attempt to save Na⁺, worsening the alkalosis. Increased urinary H⁺ acidifies the urine. Prerenal renal failure and metabolic acidosis occur in severe cases.

Resuscitate preoperatively with normal saline 0.9% to correct acid–base balance and dehydration:

Aspirate stomach with large-bore NG tube preoperatively.

Gaseous induction risks vomiting and aspiration. Therefore, use awake intubation or rapid sequence induction. Balanced anaesthesia during surgery. Extubate awake.

Upper airway obstruction

Resulting large negative inspiratory intrathoracic pressure may cause pulmonary oedema. If bronchoscopy is required, intubate first to establish airway then exchange ETT for a ventilating bronchoscope. If child desaturates, remove bronchoscope back into trachea and re-oxygenate.

Epiglottitis

Usually 1–7 years. Of rapid onset and progression. Upper airway obstruction (inspiratory stridor, tachypnoea, intercostal recession) and difficulty swallowing with drooling. Systemically unwell.

Usually caused by Haemophilus influenzae type B. Chloramphenicol now superseded by third-generation cephalosporin, e.g. cefuroxime.

Keep the child and parents calm. No preoperative X-ray. Establish i.v. access only if the child is calm. Perform a gas induction in the sitting position with halothane in 100% O₂. Then establish i.v. and give atropine 20 μg.kg⁻¹ before laryngoscopy. Use oral ETT one size smaller than usual. If unable to pass, try intubating bronchoscope or cricothyroidotomy. Change to nasal ETT if easy intubation. Steroids are controversial. Intubate for 24–48 h. Examine larynx before extubation.

Laryngotracheobronchitis (Croup)

Occurs at 6 months–6 years. Slow onset with inspiratory stridor and intercostal recession. Mild pyrexia. Usually viral.

Treat with cool humidified air and O₂; nebulized adrenaline as appropriate (may initially improve, then worsen obstruction). If there is still no improvement, it is probably due to inspissated secretions (6% of cases). If so, treat as for epiglottitis.

Foreign body aspiration

Often a history of coughing, choking or cyanosis while eating. Most foreign bodies are not radiopaque. Hyperinflation and atelectasis on CXR. Specific problems are:

• Potential loss of airway

• Risk of full stomach

• V/

mismatch prolonging gas induction.

Give atropine premedication. Avoid opioids. Gaseous induction as for epiglottitis. Gentle bagging if necessary to avoid driving foreign body distally. Insert Storz ventilating bronchoscope once airway is secured.

Peanut oil causes intense inflammation with rapid airway obstruction if not removed early. Consider the possibility of airway obstruction due to foreign body in oesophagus compressing trachea.

Bibliography

Al-Rawi O., Booker P.D. Oesophageal atresia and tracheo-oesophageal fistula. Contin Edu Anaesth, Crit Care Pain. 2007;7:15-19.

American Society of Anesthesiologists’ Task Force on Preoperative Fasting. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. Anesthesiology. 1999;90:896-905.

Association of Paediatric Anaesthetists of Great Britain and Ireland. APA consensus guideline on perioperative fluid management in children, v1.1. APAGBI, London, 2007. www.apagbi.org.uk.

Association of Paediatric Anaesthetists of Great Britain and Ireland. Guidelines on the prevention of post-operative vomiting in children. APAGBI, London, 2007. www.apagbi.org.uk.

Bingham B. Paediatric anaesthesia: past, present and future. Anaesthesia. 2003;58:1194-1196.

Fell D., Chelliah S. Infantile pyloric stenosis. BJA CEPD Rev. 2001;1:85-88.

Gormley S.M., Crean P.M. Basic principles of anaesthesia for neonates and infants. BJA CEPD Rev. 2001;1:130-134.

Holliday M.A., Segar W.E. The maintenance need for water in parenteral fluid therapy. Pediatrics. 1957;19:823-832.

King H., Booker P.D. Congenital diaphragmatic hernia in the neonate. Contin Edu Anaesth, Crit Care Pain. 2005;5:171-174.

Lönnqvist P.A., Morton N.S. Postoperative analgesia in infants and children. Br J Anaesth. 2005;95:59-68.

Marsh D.F., Hodkinson B. Remifentanil in paediatric anaesthetic practice, Anaesthesia. 2009;64:301-308.

Rowney D.A., Doyle E. Epidural and subarachnoid block in children. Anaesthesia. 1998;53:980-1001.

Paediatric Cardiology

Anaesthesia for congenital cardiovascular disease

Approximately 8000 infants born in the UK each year have some form of congenital heart disease, of which one-third will require cardiac surgery.

• Cyanotic lesions – Fallot’s tetralogy, transposition of great vessels, tricuspid atresia, Eisenmenger’s syndrome.

• Acyanotic lesions – ASD, VSD, PDA, aortic coarctation.

General anaesthesia

General aims

• Maintain adequate perfusion of systemic and pulmonary circulation

• If pulmonary hypertension is present, aim to reduce pulmonary artery pressures

• In the presence of an obstructive lesion, maintain filling pressures, HR and coronary perfusion pressure

• Careful purging of air bubbles from all lines to avoid systemic embolization.

Premedication

• None for babies <6 months or if there is minimal anxiety

• Morphine 0.1 mg/kg is well tolerated

• Glycopyrrolate as an antisialogogue.

Monitoring

• ECG, precordial/oesophageal stethoscope, NIBP, ± arterial line, CVP, temperature, pulse oximeter, capnograph and urinary catheter

• Consider pre- and post-ductal pulse oximeters to detect degree of right-to-left shunt.

Induction

• Intravenous is best for cardiovascular disease

• Gaseous induction risks desaturation, especially with severe disease. Slow if right-to-left shunt. If there is no venous access with severe disease, use 100% O₂, i.m. ketamine and i.m. suxamethonium.

Maintenance

High-dose fentanyl, 100% O₂, pancuronium technique provides good cardiovascular stability and decreases the stress response. (Pancuronium offsets the vagotonic effects of fentanyl.)

Degree of shunting in PDA, ASD and VSD depends upon the pressure difference between the systemic and pulmonary circulations:

• Increase PVR by decreasing F_iO₂, use of PEEP and high P_aCO₂

• Decrease PVR by increasing F_iO₂, no PEEP, alkalosis, decreasing P_aCO₂ and nitric oxide

• Increase SVR by vasoconstrictors and flexing hips

• Decrease SVR by inhalational agents and vasodilators.

IPPV can reverse left-to-right shunt and therefore cause air bubbles to enter the arterial circulation.

Ventricular septal defect (Fig. 9.6)

Commonest congenital heart lesion (2/1000 births); 50% close spontaneously within 1 year. Often associated with more complex lesions. Results in gradually increasing left-to-right shunt as RV pressure falls below LV pressure after birth. High pulmonary blood flow causes heart failure and pulmonary oedema. Treat with digoxin and diuretics or pulmonary artery banding to reduce pulmonary blood flow if severe.

Figure 9.6 Ventricular septal defect – pulmonary blood flow increased by systemic vasoconstriction or pulmonary vasodilation.

Patent ductus arteriosus

Transposition of the great vessels (Fig. 9.7)

Aorta arises from RV and pulmonary artery arises from LV. Unless there is a shunt present (ASD, VSD, PDA), there is no communication between the two circuits and closure of the ductus arteriosus results in death. Balloon septostomy creates an atrial septal defect as a temporary measure. Definitive surgery involves switching PA and aorta or creating shunts to establish single circulation (Blalock shunt followed by Rastelli procedure).

Figure 9.7 Transposition of the great vessels – communication between pulmonary and systemic circulations provided by the ASD and PDA.

Tetralogy of Fallot (Fig. 9.8)

• Overriding aorta

• Right ventricular hypertrophy

• VSD with right-to-left shunt

• Pulmonary stenosis.

Figure 9.8 Tetralogy of Fallot – blood flow showing right-to-left shunt through the VSD.

Both ventricles are at the same (systemic) pressure. Increasing systemic vascular resistance (SVR) reduces right-to-left shunt and increases pulmonary blood flow. Acidosis and hypoxia cause infundibular spasm and worsen shunt. Squatting increases SVR and reduces return of acidotic venous blood from the IVC. Hyperviscosity from raised haematocrit is common. Avoid dehydration, which may cause hypotension and thrombotic complications. Cyanotic spells may be reversed with propanolol 0.025–0.1 mg/kg i.v.

Pulmonary hypertension

Common problem associated with VSD, total anomalous pulmonary venous drainage, truncus arteriosus, atrioventricular septal defect and hypoplastic left heart. Defined as PAP >50% of the systemic pressure. Usually associated with excess pulmonary blood flow and poor arborization of the pulmonary vasculature.

Minimize all stimuli which cause a rise in PAP, e.g. physical contact, suctioning, physiotherapy, hypoxaemia, hypercapnia and metabolic acidosis. Ensure baby is well sedated and paralyse if ventilatory pressures are high. Hyperventilate to achieve a moderate respiratory alkalosis (P_aCO₂ = 3.5 kPa, pH 7.50) and aim for P_aO₂ of 15–25 kPa. The only specific pulmonary vasodilator is nitric oxide (NO) at 2–10 ppm. Other vasodilators (prostacyclins, phenoxybenzamine, milrinone, sildenafil) cause pulmonary > systemic vasodilation.

Bibliography

Greenley W.J., Kern F.H. Anesthesia for pediatric cardiac surgery. In: Miller R.D., editor. Anesthesia. Edinburgh: Churchill Livingstone; 1994:1811-1850.

Javorski J.J., Burrows F.A. Pediatric cardiac anesthesia. Curr Opin Anaesth. 1995;8:62-67.

Long T.J. Pediatric cardiology and cardiac surgery update. Curr Opin Anaesth. 1997;10:221-226.

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Paediatrics

Tracheo-oesophageal fistula (Fig. 9.4)

Sites of herniation (Fig. 9.5)

Ventricular septal defect (Fig. 9.6)

Transposition of the great vessels (Fig. 9.7)

Tetralogy of Fallot (Fig. 9.8)

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