700

Current considerations in neonatal anaesthesia The neonatal period encompasses the first 30 days of post-natal life, the period in which anatomical and physiological differences from the older child and adult are most marked. These differences have important implications in all phases of anaesthetic management. This review will focus on the preoperative assessment of the neonate, on some newer aspects of intraoperative anaesthetic care, and on the postoperative management problems of the neonate.

Pre.operative assessment At the Children's Hospital of Eastern Ontario (CHEO), a special preoperative information sheet (Figure) is used for neonates. The form facilitates preoperative assessment by gathering essential preanaesthetic data in one place for rapid review at a glance, and focuses attention on potential problems. The birth history is of importance to the anaesthetist. Weight and gestational age at birth will help identify certain high risk neonates, like the premature* and the small-for-gestational age (SGA).t Calculation of the conceptual age (gestational age plus postnatal age), may reveal a healthy, "normar' infant to be less than 44 weeks, and therefore, at risk for retrolental fibroplasia, t or less than 46 weeks, and therefore, at risk for postoperative apnoea. 2 Comparison of present weight to birth weight helps to assess nutritional status and, in some instances, to estimate the extent of dehydration. Normal weight gain is calcualted at 20 gm per day in a term infant after the tenth day of life. By reviewing the Apgar score and the delivery history the anaesthetist can be alerted to the possibility of perinatal asphyxia, the effects of which may still be present and of importance to the *Premature - less than 37 weeks gestational age at birth. I'SGA - less than the tenth weight percentile for the gestational age.

CAN ANAESTH SOC .I 1984 / 31:6 / pp700-9

Rachel Waugh MD FRCP(C), Gary G. Johnson MD FRCP(C)

planning of the anaesthetic technique. Asphyxia causes loss of the autoregulatory capacity in the cerebral circulation of the neonate. 3 Sudden increases in systemic arterial blood pressure resulting from awake intubation or inadequate analgesia will then be passively transmitted to the fragile capillaries of the cerebral germinal layer and may have a role in the genesis of intraventricular hemorrhage (1VH). Hypoglycaemia, hypocalcaemia, and clotting disorders may be found in neonates who have survived perinatal asphyxia. 4 Family history is essential as well, especially the maternal drug history. Infants of mothers with alcoholism, diabetes, drug addiction or myasthenia must be identified. There may be persistent foetal circulation in neonates whose mothers took large doses of ASA or acetaminophen prior to delivery. 5 A careful systems review will yield important information with a clinical bearing on anaesthesia. A Centralnervous system

A history of birth asphyxia, hydrocephalus or ventricular taps is significant and may be a clue to glossopharyngeal incoordination and/or defective laryngo-pharyngeal reflexes, with resultant poor protection of the airway before and following anaesthesia. Awake intubation, most inhalation anaesthetic agents, and succinylcholine will all transiently increase intracranial pressure in the premature infant. 6 Neonates receiving phenobarbitone for the treatment of seizures may be assumed to have hepatic enzyme induction. The extent of any neurologic deficit should be documented preoperatively; e.g., the level of the sensory and motor deficit in neonates with myelomeningocoele.

From the Department of Anaesthesia, Children's Hospital of Eastern Ontario, 401 Smyth Road, Ottawa, Ontario, KIH 8LI.

Waugh and Johnson: NEONATAL ANAESTHESIA

701

Children's Hospital of Eastern Ontario HSpital pour enfants de rest de rOntario NEONATAL

INTENSIVE

PREOPERATIVE

CARE

INFORMATION

UNIT SHEET

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PHYSICAL DATA

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7. Glucose

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Temp. (Site)

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Bil ir~bin (Total)

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' Mechanical Ventilation

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0ohthalmology

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702

CANADIAN A N A E S T H E T I S T S ' SOCIETY J O U R N A L

B The cardiovascular system flattens the preterm infant's response to CO2. Neonatal myocardium contains 30 per cent less Premature infants respond to hypoxaemia by an contractile tissue than that of the older child or adult immediate increase (30 sec) and a late decrease (5 and is less distensible. Its sympathetic innervation min) in ventilation. Hypothe~Tnia abolishes the is incomplete and its stores of norepinephrine are initial hyperventilatory response to hypoxaemia. reduced. 7 There is centralisation of blood volume in Oxygen consumption in the neonate per unit of the neonate, and the peripheral vascular response to body weight is twice that of the adult, yet the lung catecholamines is reduced. Thus, the neonate's surface area available in the neonate for gas ability to increase stroke volume is strictly limited, exchange is only equal to that of the adult. The and cardiac output is rate-dependent. For these functional residual capacity (FRC) is smaller and reasons, the neonate is unable to compensate for may be markedly decreased and unstable in the dehydration or blood loss, and it is imperative that premature. Gas trapping is characteristic of the fluid deficits preoperatively be accurately assessed newborn and may persist for weeks or months in the and replaced. Robinson and Gregory found that premature. It is indicative of the small airway hypotension developed during anaesthesia in 75 per closure which occurs within tidal volume range cent of those neonates whose urine specific gravity breathing in the neonate, and produces areas of prior to surgery was greater than 1.009. 8 atelectasis and of low ventilation/perfusion ratios. Knowledge of any structural abnormalities due to Chest wall and diaphragmatic mechanics are congenital heart disease (e.g., ventrieuloseptal de- unfavourable for the neonate as well. io The very fect), prematurity itself (e. g., patent ductus arterio- compliant chest wall and horizontal insertion of the sus (PDA)), will allow anticipation of the effect of diaphragm accentuate rib cage distortion and deintracardiac shunting on the pharmacokinetics of crease the efficiency of diaphragmatic contraction. inhaled agents. The transitional nature of the At the same time, the proportion of high oxidative cardiovascular system in neonates should be appre- capacity fibres in the respiratory muscles at birth is ciated since even in term neonates, increases in only 25 per cent compared to 55 per cent in the pulmonary vascular resistance from surgical retrac- adult. All of these developmental features of the restion, hypoxaemia, hypertension, acidosis, hypothermia or systemic hypotcnsion may lead to piratory system in the neonate predispose him to re-opening of foetal shunts. disturbances of respiratory control, compromise of If there is a history of treatment for heart failure gas exchange and diaphragmatic fatigue, and make with diuretics, and/or fluid restriction (e.g., in careful assessment preoperatively mandatory. PDA), then the anaesthetist should consider the Any history of apnoeic or periodic breathing has likelihood of a chronically contracted blood volume profound implications for the recovery period since with potential intraoperative hypotension. they may recur or be accentuated. 2 For polycythemic neonates with haematocrits Any history of respiratory distress syndrome greater than 0.65, adequate hydration or even (RDS) is likewise significant since even those partial exchange transfusion may be considered to neonates with mild disease treated with only suppleavoid small vessel thrombosis, particularly if any mental oxygen will have a reduced FRC, decreased hypotension is anticipated. dynamic compliance and low PaO2 until two to four months of age. Infants who have developed bronc Respiratory system chopulmonary dysplasia (BPD) during mechanical Breathing pattern disturbances are common in ventilation may show hypoxaemia, hypercarbia and neonates, especially in preterm infants, because of decreased compliance, as well as right heart failure, the immaturity of respiratory control. The ventila- migratory atelectasis and bronchopneumonia. Posttory response to CO2 increases with increasing extubation aphonia, weak cry or stridor following gestational age and postnatal life. 9 Infants with long-term intubation suggest the presence of subperiodic breathing are known to have a depressed glottic granulomata or stenosis, t2,13 control system characterized by a high arterial In the neonate who is still dependent on ventilaPaCO2, a shift in the CO2 response curve to the tory assistance at the time of surgery, the precise right, and a slight decrease in slope. Hypoxaemia level of support should be carefully noted pre-

703

Waugh and Johnson: NEONATAL ANAESTHESIA operatively, especially the FIO2, the peak inspiratory and end-expiratory pressures, the inspiratory/ expiratory ratio and the intermittent mandatory ventilation (IMV) rate, in order that the anaesthetist be able to provide a level of support approximately 20 per cent higher during the anaesthetic. The PaO2 and PaC02 resulting from current respiratory support equally require documentation, The size of the endotracheal tube in place, the degree of leakage around it, and its correct midtracheal position need verification. Any radiologic evidence of interstitial emphysema or mediastinal air is a warning that pneumothorax may occur intraoperatively. To maximize oxygen transport preoperatively, transfusion may be indicated. We transfuse any infant with acute RDS who requires mechanical ventilatory assistance to a haemoglobin level of 14.0g/dl preoperatively. A mature infant with apnoea or growth failure should have a haemoglobin level of at least 12.0g/dl. Prematures who are asymptomatic and healthy, and have attained the age of six weeks preoperatively, should be transfused if their haemoglobin level has fallen below 10.0 g/dl. D Meta bolic

Certain metabolic problems are common in the neonate, and require preanaesthetic correction. Hypocalcaemia is most common in the premature infant in the first 48 hours of life, and in the asphyxiated or sick neonate, t4 Its signs may include hypotension, decreased peripheral perfusion, and irritability, in the premature, a low ionized calcium level may not necessarily be reflected by a low total serum level. Total serum calcium should be kept above 2.0 mmol-1- i (8.0 mg/ml) 6 and lower values should be treated with calcium, 100-200 mg.kg -I preoperatively, since alkalosis resulting from hyperventilation during anaesthesia may reduce ionized calcium levels further. Hypoglycaemia is defined as blood glucose less than 1.1 mmol. 1- l (20 mg" 100 ml- l ) in prematures, less than 1.7mmol'l -I (30mg'100m1-1) in term infants in the first 72 hours of life, and less than 2.2 mmol'l- 1(40 mg- 100 ml i) thereafter. 15 Hypoglycaemia is most commonly found in those infants who have suffered from intrauterine growth retardation, as well as in premature infants and in infants of diabetic mothers. Treatment is begun with glucose before anaesthesia with a bolus of 200 mg.kg- l fol-

lowed by an infusion at a rate of 8 mg'kg-~.min -l. is Hyperglycaemia (blood glucose greater than 6.9-7.8mmo1"1 -~ (125-140mg'100ml-l)) is a metabolic problem of major importance, particularly in the premature infant. The resulting hyperosmolar state can produce intraventricular haemorrhage, and an osmotic diuresis with resultant dehydration and hyponatremia. The anaesthetist should immediately decrease the glucose infusion rate to 4 - 8 mg.kg- i. min- ~, avoid bolus administration of any glucose containing solutions, and monitor blood glucose closely. ~6 In the infant who is receiving intravenous hyperalimentation before surgery, the anaesthetist can continue the infusion at the same rate intraoperatively. Abrupt termination of total parenteral nutrition (TPN) may lead to sudden hypoglycaemia because of the high level of circulating insulin originally stimulated by the hyperalimentation. The TPN fluid should not be used as extracellular fluid replacement during the anaesthetic since this could result in gross serum hypertonicity, and problems similar to those associated with hyperglycaemia. One area of controversy in the preparation of neonates for anaesthesia is the period of fasting. While overnight fasting in children may be associated with asymptomatic hypoglycaemia, 17 no specific data are available in neonates to define the optimal period of preoperative starvation. Because of the reduced hepatic, myocardial and cerebral glycogen stores in neonates and to minimize the risk of dehydration and hypotension, our approach for non-urgent cases is to allow the last milk feed (breast or formula) four hours before surgery and then specifically offer clear fluids two hours preoperatively, i 8

Intraoperative management There are several areas in the intraoperative management of the neonate in which new knowledge and new technology have made important recent contributions to neonatal anaesthesia. A Monitoring

The need for repeated arterial punctures or intermittent sampling from peripheral arterial cannulas in order to obtain blood gases, has decreased with the advent of sophisticated, non-invasive, monitoring devices. Improved heated skin electrodes for measure-

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CANADIAN ANAESTHETISTS' S O C I E T Y

ment of transcutaneous 02 and COz tensions (Ptc O2 and Ptc CO2), provide a reasonable correlation with arterial gas levels if the blood pressure is within two standard deviations of the mean, body temperature exceeds 35.5 degrees Celsius and peripheral circulation is well maintained.19 When transcutaneous electrodes are used for continuous monitoring, hypoxaemia not recognized by intermittent arterial blood gas sampling can be identified. During anaesthesia, correlation with arterial values in neonates is best in the PaO2 range of 4-12 kPa (27-92 mmHg) and poorest in the range of 14-58kPa (105-439mmHg). 2~ Although Ptc 02 does not correlate well with the PaO2 during hyperoxia, it fortunately overestimates the PaO2 in the hyperoxic range and thus allows for avoidance of the dangers associated with administration of high oxygen concentrations. More recent is the introduction of a new, flexible, noninvasive pulse oximeter (Nellcor| It provides a continuous, accurate, digital readout of haemoglobin oxygen saturation without heating or "arterialization" techniques, zj Since the position of the oxy-haemoglobin dissociation curve depends on the proportion of foetal haemoglobin (HbF) to adult haemoglobin, and since the neonate at three weeks has about 70 per cent HbF, then keeping a haemoglobin saturation of 85-95 per cent will maintain the PaO2 in the desirable range of 8-11kPa (60-80 mmHg).~2 Improved automated blood pressure devices based on oscillometry (e.g. Dinamap | or ultrasonic flow detector devices (Arteriosonde| can now provide accurate readouts of arterial blood pressure in the smallest neonate if suitable size cuffs are used. Care must be taken that cycling of these devices is not more often than every 3-4 minutes, to avoid limb ischaemia. Systolic blood pressures reasonably reflect circulating blood volume since the neonatal heart cannot increase stroke volume. Its accurate determination thus serves as a reliable guide to blood replacement. Awareness of the vulnerability of the neonate to hypothermia and vigorous intraoperative defence of core temperature has resulted in the appearance of hyperthermia, although less common, as an intraoperative problem in the neonate. Hyperthermia leads to increased oxygen consumption, accentuation of apnoea, and even hypematremia from increased evaporative fluid losses. Sloughing of the

respiratory mucosa has been reported associated with the use of heaters to warm and humidify inspired fresh gases. These concerns dictate that central temperature should be monitored continuously from two locations (nasopharynx, rectum, oesophagus, or tympanic membrane), that the temperature at the interface between the patient and the warming mattress be continuously verified, and that the temperature of warmed, humidified fresh inspired gases be monitored at the endotracheal tube connector and kept at 32-37 degrees Celsius, to avoid respiratory tract bums.

JOURNAL

B Induction, maintenance and emergence

Although there are some neonates so gravely ill that an endotracheal tube must be placed belore induction of anaesthesia, evidence is available now that awake intubation in the unparalyzed, unanaesthetized neonate is associated with acute arterial hypertension and increases in intracranial

pressure 6 predisposing the neonate to intraventricular haemorrhage, particularly in the premature and the asphyxiated (see above). In addition, even in the preoxygenated neonate, awake intubation can be accompanied by apnoea, obstructed breathing, haemoglobin desaturation, and bradycardia. 23'24 The anaesthetist must then balance knowledge of these hazards with his own familiarity with neonatal intubation. If there is any doubt about possible abnomlalities of the upper airway, or the anaesthetist's ability to secure intubation, then awake intubation becomes the safer approach. Any current technique of induction may be used provided the anaesthetist is experienced and skilled in its use in the neonate. If the common inhalation induction technique using halothane is elected, then respiration must be quickly controlled to avoid apnoea and bradycardia. Succinylcholine (4.0 mg'kg -I) may be gi'r intramuscularly after inhalation induction to shorten the time to intubation, and to reduce exposure to high concentrations of inhalation agents. If intravenous induction is preferred, then thiopentone 1-5 mg.kg -l, is given slowly. In an infant who is to be ventilated postoperatively, fentanyl intravenously (3050 I-tg'kg -1) followed by succinylcholine will attenuate the hypertensive response to intubation. Until recently, the anaesthetic requirement in infants less than six months of age was thought to be greater than at any other time in life. Lerman et al.

Waugh and Johnson: NEONATAL ANAESTHESIA have established that MAC for babies from 0-1 month of age is about 25 percent less than in infants 1-6 months of age. 25 Gregory and Wade reported that the fetal MAC in lambs at least, is even less. 26 Earlier studies 27 demonstrating increased susceptibility to myocardial depression and hypotension in neonates during inhalation anaesthesia may therefore have represented relative "overdose." It appears that for the correct 1.0MAC value of halothane, neonates are no more prone to hypotension and circulatory collapse than older infants. 25 The high ratio of alveolar ventilation of FRC and the greater proportion of the vessel-rich tissue mean that the ratio of end-tidal to inspired concentration (Fe/Fi) more rapidly approaches unity and that high myocardial concentrations are thus more rapidly obtained earlier in the anaesthetic than in older infants, leading to the hypotension and bradycardia commonly seen.2S In neonates, the baroresponse is very markedly blunted by inhaled anaesthetics (halothane 0.5 MAC is thought to produce 90 per cent loss ofbaroresponse in neonates versus a 54 per cent loss in adults). 29'3~ Fentanyl 30-50 ixg.kg-I, intravenously will avoid the hypotension of inhaled anaesthetics, but presupposes postoperative mechanical ventilation. Regardless of the nature of the procedure, there is no place in neonatal anaesthesia for spontaneous ventilation. The decreased FRC and higher closing tidal volume, the doubled oxygen consumption per unit body mass and the frequency of apnoeic breathing patterns demand controlled ventilation at all times. The use of muscle relaxants permits lower concentrations of inhaled anaesthetics to be used. Dosage of both non-depolarizing and depolarizing relaxants in the neonate has long been controversial. It now seems clear that maturation of the neuromuscular junction does not occur until about 12 weeks after birth. 31 Prior to this time, neonates have less neuromuscular reserve than older infants and children. They exhibit failure of neuromuscular transmission at high frequencies and depression of the frequency sweep electromyogram responses with nitrous oxide anaesthesia. 32 Further, monitoring of the neuromuscular transmission in the neonate should be done with a nerve stimulator with 50 Hz capacity since prolonged post-tetanic exhaustion may result if 100 Hz is used. 31 Fisher et al. have shown that the large extracellu-

705 lar volume in the neonate results in a large apparent volume of distribution of curare with smaller concentrations thus being achieved at the motor end plate. At the same time, there is increased sensitivity of the neonatal neuromuscular junction to curare. These two factors combine I0 balance each other so that dose requirements for curare do not vary with age; however, because of the neonate's larger distribution volume, a smaller percentage of the drug is eliminated during each time unit creating a longer elimination half-life. Therefore, in neonates, second and subsequent doses will be required at less frequent intervals and should be given only when indicated by recovery of the twitch response. 33 Goudsouzian and Liu demonstrated that the dose of succinylcholine to produce greater than 90 per cent depression of twitch height is related to age, the requirement being higher in younger infants and diminishing with age; nevertheless, neonates less than ten days old were shown to be extremely variable, so that it is essential to follow their response to succinylcholine with a nerve stimulator. 34 Postanaesthetic management of the neonate

The weakest link in the perioperative care of the neonate may be the early postoperative period. One-quarter of cardiac arrests in paediatric surgical patients occur during or after recovery and involve the respiratory system in the form of airway obstruction (laryngospasm, aspiration, and premature extubation), or respiratory depression and insufficiency (antibiotic administration, inadequate reversal, hypoxaemia). A further ten per cent of these cardiac arrests are related to the cardiovascular system - preoperative anaemia (especially in premature infants), and hypovolemia. 35 Neonates, because of the unique developmental features of their respiratory, cardiovascular and metabolic systems, are at higher risk of compromise in the postanaesthetic period. Some of the most frequent recovery phase complications in the neonate are summarized below, and are listed in the Table. 1 Apnoea The precarious nature of respiratory control in the neonate, especially the preterm neonate, has been described earlier. In the postoperative period, addi-

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CANADIAN ANAESTHETISTS' SOCIETY JOURNAL

TABLE Postanacsthetic complications in Ihe neonate

four months postnatal age. The prematures with a preanaesthetic history of apnoea but who subsequently had a normal recovery were older than 46 weeks conceptual age and four months postnatal age. Even further definition of the infants at risk of developing apnoea following anaesthesia, as well as the duration of the risk period after anaesthesia is needed. It seems clear, however, that prematurely born infants who have not achieved 46 weeks conceptual age at the time of non-urgent surgery should not be permitted to have anaesthesia on a day-care basis. If surgery cannot be delayed until the infant is older than 46 weeks conceptual age, then the infant should be admitted for surgery to a centre where he can be monitored with an apnoea monitor for at least 18 hours after anaesthesia, and where full neonatal mechanical ventilatory support can be provided if needed. It is only by obtaining the birth and perinatal history that the anaesthetist can identify this group of patients at potential risk for this most serious complication.

Apnoea Hypoxaemia Impaired neuromusculartransmission Hypotension Hypothermia Metabolicdisturbances

tional factors may become superimposed upon this immature control system leading to the occurrence or recurrence of apnoeic episodes. Residual low levels of halothane can be expected to further depress the ventilatory response to CO2. Hypothermia may arise during the patient's transport from the operating theatre to the ward, and abolish the initial hyperventilatory phase of the response to hypoxemia. Postoperative discomfort and low levels of halothane will cause tachypnoea, shortening the endurance time of the ventilatory muscles and increasing ventilatory muscle fatigue. Paradoxical movements of the neonate's very compliant chest cage persist into the postoperative period (due to the depressant effect of halothane on intercostal muscle activity), thus increasing diaphragmatic work. In the neonate, diaphragmatic fatigue can be expected to occur rapidly (see above). Jo Nutritional deprivation in the perioperative period may also favour ventilatory muscle fatigue, and thus, apnoea. Of course, all the usual metabolic causes of apnoeic breathing patterns - hypoglycaemia, hypothermia, hypocalcaemia and acidosis may occur after anaesthesia and surgery, and need to be anticipated. Awareness of the alarming incidence of apnoea in preterm infants following anaesthesia has been growing since 1981. Gregory 36 and then Steward 37 reported apnoea in 25 and 12 per cent respectively, of premature infants during the first 12 hours after anaesthesia. Liu et al. attempted to further define which infants were at risk for developing apnoea. They found that prematurely born infants with a preanaesthetic history of apnoea developed apnoea after anaesthesia more frequently than did all other infants, and more frequently than other premature infants without a history of apnoea. Further anlaysis revealed that those prematures with a history of apnoea who developed postoperative apnoea were all less than 41 weeks conceptual age and less than

2 Hypoxaemia Hypoxaemia is the second most common postanaesthetic complication in the neonate. The unfavourable position of the neonate in providing gas exchange to meet his increased metabolic requirements has been discussed earlier. Any additional increase in oxygen consumption postoperatively, for example, due to hypothermia, sepsis, fever, or acidosis may lead to inadequate tissue oxygenation. Haemoglobin F is poorly suited to the demands of postoperative stress since it is unable to respond to hypoxia by significantly increasing oxygen unloading capacity. The reduction in the small, unstable FRC of the neonate which will follow anaesthetic induction and persist postoperatively will be even more critical in him, since small airway closure is already occurring within tidal volume range breathing. Most neonates then will require an increased FIO2 postoperatively, for 24 hours, and this need should be guided by regular and frequent blood gas determinations or continuous haemoglobin oxygen saturation monitoring with the aim of maintaining PaO2 at 60-80 torr or SaO2 of 85-95 per cent. In those infants with anticipated unusually great postoperative compromise of FRC (e.g., peritonitis, lengthy surgery, massive transfusions, correction of omphalocoele or gastroschisis), then

Waugh and Johnson: NEONATAL ANAESTHESIA as a minimum, constant positive airway pressure (CPAP) should be provided postoperatively. Neonates with preoperative, borderline pulmonary function, such as infants who may have broncho-pulmonary dysplasia (BPD), and who have been previously weaned from mechanical support will demonstrate a temporary increase in oxygen dependency and need for mechanical support postoperatively. It should likewise be anticipated that those neonates who are already receiving mechanical ventilatory support preoperatively will require an increase of 10-20 per cent in the level of CPAP or positive end-expiratory pressure (PEEP) postoperatively, along with similar increases in FrO2 and IMV rates over previous preoperative requirements. In general, about 20-35 per cent of neonates will require mechanical ventilatory support after noncardiac surgical operations. In some centres, elective ventilation is used after all operations in the neonate, while others confine this approach to high risk groups.

707

neonates and well with adequate reversal of muscle relaxants3s to permit extubation.

4 Hypotension

The developmental features of the neonatal cardiovascular system (see above) combined with the characteristics of the postsurgical state predispose to hypotension. The blunting effect of halothane on the baroreceptor reflex of the neonate may persist into the postoperative period, making the infant even less able to respond to blood loss. Maintenance of blood volume is critical postoperatively, as is recognition of the need to replace continuing losses. In any neonatal surgical procedure where there has been blind or blunt dissection (e.g., ventriculo-perltoneal shunting, skin undermining for flaps for closure of myelomeningocoele, subcutaneous tunnelling with trocars for permanent central venous feeding lines), there will be continued postoperative hidden bleeding. Sudden hypotension may be a reflection of hypovolemia due to this concealed haemorrhage. After extensive abdominal procedures there will be continued third space fluid or translocation losses which may re3 Impaired neuromuscular transmission The decreased margin of safety for neuromuscular quire as much as 80 cc.kg -I acutely, or 300 cc.kg -~ transmission in the neonate has been described in 24 hours for replacement. above. Any slight reduction in neuromuscular transmission in the postoperative phase may greatly 5 Metabolic complications In the jittery, twitching, postoperative neonate, diminish the patient's ventilatory capacity. The longer elimination half-life for curare (DTC) both hypocalcaemia and hypoglycaemia should be in neonates33 means that if neonates are given ruled out as discussed earlier. Hyperglycaemia, on repeated doses of DTC at the same intervals as the other hand, is frequently seen in stressed, adults, neuromuscular blockade may be prolonged premature infants recovering from surgery, and and persist into the postoperative period. Neostig- since the incidence of death and intracranial haemine or edrophonium may improve neuromuscular morrhage is higher in the hyper- vs the normotransmission sufficiently to permit the patient to glycemic infant, it should be corrected early. breathe, but cannot fully restore neuromuscular transIt is in the postoperative period that hypothermia mission. If hypothermia, acidosis, hypocalcaemia or has its most dangerous effects, leading indirectly to hypoperfusion are present, reversal may be difficult. increased metabolic rate and oxygen consumption The interaction between muscle relaxants and and resulting in hypoxaemia, acidosis, and apnoea, antibiotics may continue into the postoperative The actions of many drugs, particularly the muscle period because of continuing absorption of the anti- relaxants and anaesthetic agents will be prolonged if biotics, especially the aminoglycosides. Amino- hypothermia is present. Extubation is not conglycosides and/or hypermagnesemia (e.g., in in- sidered unless core temperature is greater than fants born to pre-eclamptic mothers treated with 35.5~ magnesium) superimposed on residual neuromuscular blockade may precipitate postoperative res- Conclusions piratory failure in the neonate. This paper has presented and discussed aspects of Leg lift corresponds with a maximum inspiratory current clinical importance to the anaesthetist who pressure of at least - 3 k P a ( - 3 2 c m H20) in may be confronted with neonatal patients in his/her

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CANADIAN ANAESTHETISTS' SOCIETY JOURNAL

practice. Emphasis has been placed on the identification and anticipation of the wide body of problems that are special in the neonatal period. Considerations in the preoperative assessment have been outlined to emphasize their clinical importance to subsequent anaesthesia. Highlights of aspects of the anaesthetic management in neonates have been presented with some emphasis on newer monitoring. The final section of this review has dealt with the numerous serious problems presenting or persisting into the postoperative period. The postoperative period represents an extremely unstable period for the neonate and awareness of the pitfalls in this period will hopefully lead to their avoidance, or anticipation and successful management.

11 Bryan HM, Hardie MJ, Reilly BJ, Swyer PR. Pulmonary function studies during the first year of life in infants recovering from the respiratory distress syndrome. Pediatrics 1973; 52: 169-78. 12 Leland LF, Flynn JW, Pathak DR, Madden WA. Predictive value of stridor in detecting laryngeal injury in extubated neonates. Crit Care Med 1982; 10: 453-5. 13 Hengerer AS, Strome M, Jaffe BF. Injuries to the neonatal larynx from long term endotracheal tube intubadon and suggested tube modification for prevention. Ann Otol 1975; 84: 764-70. 14 Hatch J, Sumner E. Neonatal Anaesthesia. Year Book Medical Publishers, 1981 : 58. 15 Gregory GA. Pediatric Anesthesia. ChurchillLivingstone, New York. 1983: 209-12. 16 Idem 195-8. 17 Bevan JC, Burn MC. Acid-base and blood glucose levels of pediatric cases at induction of anaesthesia. Br J Anaesth 1973; 45:115. 18 Berry FA. Fluid and electrolyte therapy in the pediatric patient. ASA Annual Refresher Course Lectures 1979: 105. 19 Peabody JL, Gregory GA, Willis MM, Tooley WH. Transcutaneous oxygen tension in sick infants. Am Rev Respir Dis 1978;118: 83-7. 20 Venus B, Kanchen CP, Pratap KS, Konchigeri H, Vidyasagar D. Transcutaneous PO2 monitoring during pediatric surgery. Crit Care Med 1981; 9: 714-6. 21 Yelderman M, New W. Evaluation of pulse oximetry. Anesthesiology 1983; 59: 349-52. 22 Delivoria-Papadopoulos M, Roncevic NP, Oski FA. Postnatal changes in oxygen transport of term premature and sick infants: the role of red cell 2,3diphosphoglycerate and adult hemoglobin. Pediatr Res 1971; 5: 235-45. 23 Marshall TA, Deeder R, Pai S, Berkowitz GP, Austin TL. Physiologic changes.associated with endotracheal intubation in preterm infants. Crit Care Meal 1984; 12: 501-3. 24 Hinkle AJ. Awake neonatal laryngoscopy: preoxygenation alone versus continuous oxygenation. Anesthesiology 1983; 59: A437. 25 Lerman J, Robinson S, Willis MM, Gregory GA. Anesthetic requirements for halothane in young children 0-1 month and 1-6 months of age. Anesthesiology 1983; 59: 421-4.

References 1 Quinn GE, Betts EK, Diamond GR, Schaeffer DB. Neonatal age at retinal maturation. Anesthesiology 1981; 55: A326. 2 Liu LMP, Cote CJ, Goudsouzian NG et al. Lifethreatening apnea in infants recovering from anesthesia. Anesthesiology 1983; 59: 506-10. 3 Lou HC, Lassen AA, Friis-Hansen B. Impaired autoregulation of cerebral blood flow in the distressed newborn infant. J Pediatr 1979; 94:118-21. 4 Gregory GA. Pediatric anesthesia. ChurchillLivingstone, New York. 1983: 595. 5 Perkin RM, Levin DL. Clark R. Serum salicylate levels and right-to-left ductus shunts in newborn infants with persistent pulmonary hypertension. J Pediatr 1980; 96: 721-6. 6 Raju TNK, Vi~vasagar D, Tortes C, Grundy D, Bennett EJ. lntracranial pressure during intubation and anesthesia in infants. J Pediatr 1980; 96: 860-2. 7 Friedman WF. The intrinsic physiologic properties of the developing heart. Progress in Cardiovascular Disease 1972; 15:87-111. g Robinson S, Gregory GA. Urine specific gravity as a predictor of hypovolemic and hypotensive response to halothane anesthesia in the newborn. American Society of Anesthesiologists Abstracts of Scientific Papers pp. 37, 1977. 9 Rigatto H. Respiratory control and apnoea in the newborn infant. Crit Care Med 1977; 5: 2-9. 10 Muller NL, Bryan AC. Chest wall mechanics and respiratory muscles in infants. Ped Clin N Am 1979; 26: 503-16.

Waugh and Johnson: NEONATAL ANAESTHESIA 26 Gregory GA, Wade JC, Biehl D, Ong BY, Sitar DS, Fetal anesthetic requirements (MAC) for halothane. Anesth Analg 1983; 62: 9-14. 27 Barash PG, Glanz S, Katz JD, Taunt RT. Talner NS. Ventricular function in children during halothane anesthesia: An echocardiographic evaluation. Anesthesiology 1978; 49: 79-85, 28 Brandon BW, Brandon RB, Cook DR. Uptake and distribution of halothane in infants. Anesth Analg 1983; 62: 404-10. 29 Wear R, Robinson S, Gregory GA. The effect of halothane on the baroresponse of adult and baby rabbits. Anesthesiology 1982; 56: 188-91. 30 Gregory G. The baroresponses of pretcrm infants during halothane anesthesia. Can Anaesth Soc J 1982; 29: 105-7. 31 GoudsouzianNG. Maturation of neuromuscular transmission in infants. Br J Anaesth 1980; 52: 205-13. 32 Crumrine RS, Yodlowski Ell. Assessment of neuromuscular function in the infant. Anesthesiology 1981; 54: 29-32. 33 Fisher DM, O'Keeffe C, Stanski DR, Cronnelly R, Miller RD, Gregory GA. Pharmacokiuetics and pharmacodynamics of d-tubocurarine in infants, children and adults. Anesthesiology 1982; 57: 203-8. 34 Goudsouzian NG, Liu LMP. The neuromuscular response of infants to a continuous infusion of succinylcholine. Anesthesiology 1984; 60: 97-10 I. 35 Salem MR, Bennett EF, Schweiss JF et al. Cardiac arrest related to anesthesia: contributing factors in infants and children. JAMA 1975; 233: 238-41. 36 Gregory GA. Outpatient Anesthesia, Anesthesia. Ed. Miller RD. New York, Churchill-Livingstone, 1981: 1329. 37 Steward DJ. Preterm infants are more prone to complications following minor surgery than are term infants. Anesthesiology 1982; 56: 304-6. 38 Mason LJ, Betts EK. Leg lift and maximum inspiratory force, clinical signs of neuromuscular blockade reversal in neonates and infants. Anesthesiology 1980; 52: 441-2.

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