w a update in anaesthesia - smile train · paediatric anaesthesia covering the basics of anatomy,...

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UPDATE INANAESTHESIA

1

Editors: Drs Iain Wilson, Roger Eltringham Sub Editors: Drs Henry Bulwirwa (Uganda), David Conn,Mike Dobson, Frank Walters and Mr Mike Yeats Distribution: Dr Ray Sinclair, Department of Anaesthesia, Royal

Truro Hospital (Treliske), Truro, Cornwall Designed and Typeset by : Angela Frost

A journal for anaesthetists in developing countries

WORLD ANAESTHESIANo 8 1998

Millions of children are anaesthetised eachyear. Some are fortunate enough to be lookedafter in dedicated paediatric centres, undergoingsurgery and anaesthesia with fully trainedspecialists. At the other end of the spectrumthere are places where children do not receivesurgery because of a lack of trained anaesthetistsor suitable equipment.

Almost all anaesthetists, particularly thoseworking in developing countries, expect to carefor children regularly. This edition of Update inAnaesthesia contains a review of paediatricanaesthesia which we hope will prove practical.It discusses the differences betweenanaesthetising children and adults and detailssome of the techniques and equipment required.There is also an article on caudal anaesthesia, acommonly used regional technique to reducepostoperative pain.

We know that our readers work in a variety ofcircumstances, and we are anxious to ensurethat our topics are covered at a realistic level.We would be delighted to receivecorrespondence regarding our reviews,particularly where specific techniques can bedescribed or recommended for those workingwith minimal resources.

Update in Anaesthesia is now available on theinternet and can be accessed as described onp24. The articles can be downloaded directly to

EDITORIAL ISSN 1353-4882

Contents: No 8

l Editorial

l Paediatric Anaesthesia Review

l Caudal Anaesthesia

l Neurophysiology

l General Anaesthesia for OphthalmicSurgery

l Anaesthesia in Children Using the EMOSystem

l Equipment - Oxford Minature

Vaporisers

l 'Update' on the Internet

your computer and you can use any of thematerial for teaching or studying purposes.When doing this please acknowledge Update inAnaesthesia.

We have recently made a few alterations in theway Update is produced and hope to publishevery six months in the future. There will besome changes in the way material is presentedand we would appreciate feedback on whichareas of anaesthesia should be covered. Thereare many experienced anaesthetists who readour publication and we would benefit fromyour comments.

Iain WilsonRoger Eltringham

WORLDANAESTHESIA

WORLDANAESTHESIA

AW

Update in Anaesthesia2

PAEDIATRIC ANAESTHESIA REVIEW

Dr Lyn RusyMedical College of Wisconsin AnaesthesiaDepartment, Childrens Hospital of Wisconsin9000 W Wisconsin Ave PO1997Milwaukee WI 53201USA

Dr Elmira Usaleva,Research Institute of Obstetrics & Paediatrics,Rostov on Don, Russia

This article outlines the essential principles of safepaediatric anaesthesia covering the basics ofanatomy, physiology and pharmacologyemphasising the differences which exist betweenadults and children. It assesses how principles usedin adult anaesthesia may be adapted to paediatricanaesthesia and includes suggested techniques,monitoring methods, regimens for fluidmanagement and new advances in paediatric painmanagement. It is divided into three sections;physiology, pharmacology and practicalconsiderations.

PHYSIOLOGYOne of the most important differences betweenpaediatric and adult patients is oxygen consumptionwhich, in infants may exceed 6 ml/kg/min, twicethat of adults. There are physiological adaptationsin paediatric cardiac and respiratory systems tomeet this increased demand.

Cardiovascular. The cardiac index (defined as thecardiac output related to the body surface area toallow a comparison between different sizes ofpatients) is increased by 30-60 percent in neonatesand infants to help meet the increased oxygenconsumption. Fetal haemoglobin (which is presentin fetal life and up to 3 months following birth) isnot able to deliver oxygen to the tissues as efficientlyas normal haemoglobin because the oxy-haemoglobin dissociation curve is shifted to the leftcausing oxygen to be released less readily. Neonateshave a higher haemoglobin concentration (17 g/dl)and blood volume and this together with theincreased cardiac output compensates for thedecreased release of oxygen from haemoglobin inthe tissues. Replacement of fetal haemoglobin withadult haemoglobin begins at 2-3 months of age andthis period is known as physiological anaemia as

haemoglobin concentrations may fall to 11 g/dl.Anaemia sufficient to jeopardise oxygen carryingcapacity of the blood is possible if the haemoglobinconcentration is less than 13 g/dl in the newbornand less than 10 g/dl in the infant under 6 months ofage.

Neonatal myocardium has a large supply ofmitochondria, nuclei and endoplasmic reticulum tosupport cell growth and protein synthesis but theseare non-contractile tissues which render themyocardium stiff and non-compliant. This mayimpair filling of the left ventricle and limit theability to increase the cardiac output by increasingstroke volume (Frank Starling mechanism). Strokevolume is therefore relatively fixed and the onlyway of increasing cardiac output is by increasingheart rate.

The sympathetic nervous system is not welldeveloped predisposing the neonatal heart tobradycardia. Anatomical closure of the foramenovale occurs between 3 months and one year of age.Arterial blood pressure increases with age.

Table 1 depicts many of these cardiovasculardifferences.

Age Neonate Infant 1yr 5yr Adult

02 Consumption

(ml/kg/min) 6 5 5 4 3

Systolic BP(mmHg) 65 90 95 95 120

Heart Rate(beats/min) 130 120 120 90 77

Blood Volume(ml/kg) 85 80 80 75 70

Haemoglobin(g/dl) 17 11 12 13 14

Respiratory. There are some special featurespeculiar to the paediatric airway. The head isrelatively large with a prominent occiput, the neckis short and the tongue is large. The airway is proneto obstruction because of these differences. Infantsand neonates breathe mainly through their nasalairway, although their nostrils are small and easilyobstructed. The larynx is higher in the neck (morecephalad), being at the level of C3 in a prematureinfant and C4 in a child compared to C5-6 in theadult.

Update in Anaesthesia 3

The epiglottis is large, floppy and U shaped. Thetrachea is short (approximately 4-9 cm) directeddownward and posterior and the right main bronchusis less angled than the left. Right mainstemintubations are therefore more likely. The glotticopening (laryngeal opening) is more anterior andthe narrowest part of the airway is at the cricoidring. (In the adult airway the narrowest point is thevocal cords). The diameter of the trachea in thenewborn is 4-5mm. Since the resistance to airflowthrough a tube is directly related to the tube lengthand inversely related to the fourth power of theradius of the tube, tracheal oedema of just 1mm candramatically increase resistance to breathing.

The size of the endotracheal tube is critical, as onethat is too large will exert pressure on the internalsurface of the cricoid cartilage resulting in oedemawhich could lead to airway obstruction when thetube is removed. An uncuffed endotracheal tubewhich has an air leak around it when positivepressure is applied to it should be used in childrenunder 10 years of age. An uncuffed tube provides alarger internal diameter compared with a cuffedtube. In general the internal diameter of endotrachealtube related to age is as follows:

Because of the higher position of the larynx and theshape of the epiglottis intubation may be easier ininfants and young children using a straight bladedlaryngoscope to elevate the epiglottis rather than acurved Mackintosh blade in the vallecula. Althoughthe length of the trachea varies, in most infants upto one year of age, if the 10cm mark of theendotracheal tube is at the alveolar ridge (gums),the tip of the tube is just above the carina. Witholder children an easy formula of

Age + 12 will provide a guide to which mark

should be at the lips. After intubation the tubeshould be secured carefully to the maxilla ratherthan the mandible which is mobile and the positionof the tube checked by auscultation and capnographyif this is available.

Alveolar minute ventilation is increased to meet theincreased oxygen demands. Carbon dioxideproduction is also increased in neonates but anormal PaCO

2 level (blood CO

2 level) is maintained

by the increased alveolar ventilation. Tidal volumeis similar for adults and children on a ml/kg basis,so that the increased alveolar ventilation is achievedby an increase in respiratory rate. All of thesefactors give the lungs less reserve of oxygen so thata well oxygenated infant with upper airwayobstruction can become cyanotic in a matter ofseconds. Control of ventilation is immature inneonates and responses to hypoxic conditions areunpredictable, sometimes resulting in periods ofapnoea. Ex-premature babies are at risk of apnoeafollowing general anaesthesia up to 52 weeksgestational age and should be closely observed for24 hours post operatively.

Infants have relatively soft chest walls comparedwith the more rigid chest wall of older children andadults. This results in intercostal and sternalrecession in small children with airway obstruction.The diaphragm is responsible for most of theventilation in this group and anything tending todecrease its efficiency, such as a distended abdomen,may cause respiratory problems for the infant.

Renal system and fluid balance. The neonatalkidney is characterised by a decrease in glomerularfiltration rate, sodium excretion and concentratingability. These values slowly approach those of theadult by 12 months of age. Consequently, the infantcannot handle a large water load and may be unableto excrete electrolytes.

The extracellular fluid volume (ECF) is equivalentto about 40% of the body weight in neonates asopposed to 20% in adults. This difference hasdisappeared by the age of two years. The increasedmetabolic rate of infants results in a faster turnoverof extracellular fluid. An interruption of the normalfluid intake can therefore rapidly lead to dehydrationand careful attention to intra-operative fluids ismandatory. Fluid requirements can be consideredas maintenance fluids and replacement fluids.

Premature 2.5 - 3.0 mm

Neonate to 6 months 3.0 - 3.5 mm

6 months - 1 year 3.5 - 4.0 mm

1 - 2 years 4.0 - 5.0 mm

> 2 yearsUse the formula 4 + Age

4

2


Maintenance fluid requirements are calculatedon an hourly basis depending on the body weight.A suitable way of working this out is as follows: 4ml/kg for the first 10 kg, adding 2 ml/kg for thesecond 10 kg and 1 ml/kg for each kg over 20kg.

The maintenance fluid replaces the fluid that thechild would normally have been drinking. Aftermost minor or moderate surgery children will returnto drinking fairly quickly and make up any deficit.However after major surgery or when there are pre-existing fluid deficits intravenous maintenancefluids will be required. A regimen with 30% of thefluid as normal saline and 70% as dextrose 5% issuitable for this purpose. Alternatively 4% glucosein 0.18% saline may be used.

Replacement fluids. Patients undergoing surgerymay also need intravenous fluid to replace abnormallosses of fluid from bleeding or “third space” lossand any pre-existing deficits. “Third space” lossrefers to fluid which is lost from the circulationduring surgery. Some of this fluid forms oedema inthe area of the operation, some may be lost into thebowel and there may also be losses from evaporation.In general the more major the surgery the morereplacement fluid will be required. These lossesare commonly replaced by balanced salt solutionssuch as Hartmanns solution. Colloid solutions aresometimes used when losses are heavy.

Body surface surgery (eg a hernia), or surgeryinvolving a distal extremity will result in onlyminor fluid losses and replacement fluids will onlybe needed in the event of significant blood loss.Abdominal or chest surgery will have much greaterrequirements for fluids and possibly blood. In

Example of maintenance fluid calculation:

8kg child8kg X 4mls/kg = 32mls/hour maintenance

12kg child (is 10kg + 2kg)10kg X 4mls/kg = 40mls/hr+2kg X 2mls/kg = 4mls/hrTotal = 40 + 4 = 44mls/hour maintenance

25kg child (is 10kg + 10kg + 5kg)10kg X 4mls/kg = 40mls/hr+10kg X 2mls/kg = 20mls/hr+ 5kg X 1ml/kg = 5mls/hrTotal = 40+20+5= 65mls/hr maintenance

general abdominal surgery will need extra fluid toreplace these third space losses at around 10mls/kg/hour for each hour of surgery.

Pre-existing deficit. Patients who are already fluiddepleted preoperatively need replacement in avolume proportional to the degree of dehydrationestimated on the basis of the history and clinicalsigns: Dry skin and mucus membranes represents a5% deficit. Cool peripheries and loss of skinelasticity, depressed fontanelles and eyeballs andoliguria represents a 10% deficit. A hypotensivemoribund patient, unresponsive to pain representsa 15% deficit. The volume required to replace thisdeficit is calculated as the percent deficit times10mls/kg. Whenever possible fluid deficits shouldbe corrected prior to surgery, though time is alwayslimited with emergency or urgent surgery. If venousaccess is impossible fluids can be administered viathe intra-osseous route (Update in AnaesthesiaNumber 5, page 17).

Replacement of blood. Blood volume variesaccording to age (Table 1). In general bloodreplacement is required when the haematocrit dropsbelow 25% (around a Hb of 8g/dl) or when theestimated blood loss exceeds 20% of the calculatedblood volume. Lesser degrees of blood loss can bereplaced by colloid, such as gelatin, dextran oralbumin or crystalloid solutions. If crystalloid isused then a volume of three times the estimatedblood loss should be given, usually in the form oflactated Ringers (Hartmanns solution) or 0.9%saline. Try to warm iv fluids for children in theatreif they are receiving replacement fluids.

Calculation of blood loss is best done by collectingand measuring suction blood during the procedure.Swabs may be weighed on a simple pair of kitchentype scales. If the weight of the dry swabs issubtracted from the total weight then the extragrams can be taken to indicate the number of mls ofblood on the swab. The swabs should be weighedbefore they dry, because of inaccuracies due toevaporation.

Temperature regulation. Maintenance of bodytemperature may be a major problem even in warmcountries. Neonates and infants have a large surfacearea to volume ratio and therefore a greater area forheat loss, especially from the head. There is anincreased metabolic rate but insufficient body fatfor insulation and heat is lost more rapidly. Infants


less than three months of age do not shiver and relyprimarily on non-shivering thermogenesis togenerate heat. The heat is produced in the brown fatand occurs only in infants. The fat is locatedprimarily around the scapula, in the mediastinumand around the adrenal glands and kidneys. It isimportant to maintain a warm environment tominimise heat loss. For the very small neonate,operating room temperatures must be increasedmuch to the dismay of the surgeon in heavy operatingroom scrub suits! In addition to warming theenvironment, heat loss may be reduced by wrappingthe limbs and head in wool or foil, placing the childin a heating blanket, warming and humidificationof inspired gases and warming of intravenous fluids.Very occasionally, in a hot theatre environment,children may become too hot, particularly if theywere pyrexial preoperatively. Atropine or etheranaesthesia may increase this tendancy. Thetemperature can be measured in theatre using asimple thermometer.

PHARMACOLOGYChanging factors during development determinethe response of the paediatric patient to variousdrugs. These include those affecting pharma-cokinetics (absorption, distribution and elimination)and those affecting pharmacodynamics (the effectof the drug on the body).

Inhalational agents. Both induction and emergencefrom anaesthesia are more rapid in children than inadults. This is probably because of a smaller lungfunctional residual capacity per unit body weightand a greater tissue blood flow, especially to thevessel rich group (brain, heart, liver and kidney).The vessel rich group in adults is 10 percent of bodyweight versus 22 percent in neonates.

Anaesthetic potency has traditionally been measuredby the minimal alveolar concentration (MAC)required to prevent response to a surgical incision.The anaesthetic requirements of paediatric patientsvary according to age. In general the MAC ofinhalational agents are greatest in the young anddecrease with age. However neonates require lowerconcentrations of volatile anaesthetics than infants.For example the MAC in preterm neonates forhalothane is 0.87 percent compared to 1.20 in olderinfants. MAC decreases to 0.9 by 3 years of age andthen progressively declines with age reaching 0.76in adults. There are slight increases at the time of

puberty. The reasons for this apparently greateranaesthetic requirement in infants are unclear, butmay reflect interaction of many factors such asresidual elevated progesterone and/or endorphinlevels as well as an immature central nervoussystem. Thus, there is nearly a 30 percent greateranaesthetic requirement for infants to obtain thesame depth of anaesthesia. It should be emphasisedthat there is a smaller margin of safety betweenadequate anaesthesia and severe cardiovasculardepression for the infant and child compared to theadult. This is because the cardiac output in infantsis largely dependent on heart rate. Some of themyocardial depression of volatile anaesthetics canbe offset by the administration of vagolytic agentssuch as atropine.

Nitrous Oxide is used as a carrier gas to supplementmore potent inhalational agents. It is virtuallyodourless and makes the introduction of morepungent agents more acceptable. As it is relativelyinsoluble it rapidly achieves equilibrium withalveolar concentration leading to rapid inductionand recovery. In the recovery period rapid diffusioninto the alveoli may reduce alveolar concentrationsof oxygen (diffusion hypoxia) and highconcentrations of oxygen should be given for 5 - 10minutes following its administration. Because it isvery diffusible it rapidly equilibrates with gas filledbody cavities and should be avoided in suchconditions as pneumothorax.

Brief Review of Halothane. Halothane is ahalogenated hydrocarbon. The carbon-fluoridebonds are responsible for its non-flammable andnon-explosive nature. During preparation it is mixedwith thymol as a preservative and is stored in ambercolored bottles to retard spontaneous oxidativedecomposition. It has a MAC of 0.76 and vaporpressure of 243mmHg. Circulatory effects includedose dependent reductions in blood pressure andcardiac output often associated with reductions inheart rate. It is non-pungent and therefore allowsfor a smooth inhalational induction. Halothanecauses an increased respiratory rate and decreasedtidal volume which results a rise in PaCO

2.

Halothane increases the susceptibly of the heart tothe arrhythmic effects of adrenaline (epinephrine)injected by the surgeon. Although children are lesslikely that adults to exhibit this effect, doses ofadrenaline should be kept under 10mcg/kg whenusing halothane.


Around 20% of halothane is metabolised byoxidative metabolism in the liver. Rarely hepaticdysfunction (sometimes known as “halothanehepatitis”) is diagnosed when other causes of hepaticimpairment have been excluded. Certain factorsincrease susceptibility, including repeatedexposures to halothane and obesity. Extremelyrarely, severe and occasionally fatal liver damagemay occur. However, in patients with liverproblems, halothane has undoubtedly been wronglyincriminated in many patients when a more detailedinvestigation would have cleared the anaestheticfrom any blame. The mechanism of hepaticdysfunction in unknown but several theories exists,including metabolic, hepatic oxygen deprivationand immunological.

Enflurane is less useful as an induction agent as itmay cause breath holding, coughing andlaryngospasm. It may cause cardiovascular andrespiratory depression and should be avoided inepileptic patients especially when controlledventilation is used as it lowers the threshold forseizures.

Isoflurane has a pungent odour and induction ischaracterised by breath holding, coughing andlaryngeal irritation. It is more useful for maintenanceof anaesthesia and causes ventilatory andcardiovascular depression similar to halothane.

Sevoflurane is a recently introduced inhalationalagent which has the advantage of a pleasant non-irritating odour and a low blood/gas solubilitycoefficient. Consequently induction is both rapidand smooth and it is an ideal agent for inhalationalinduction but is considerably more expensive thanhalothane.

Ether has a high blood gas solubility ratio and apungent odour. Consequently inhalational inductiontakes a long time and may be associated withrespiratory irritation. It causes minimal respiratoryand cardiovascular depression and is thereforeextremely safe. It is flammable in air and explosivein oxygen.

Intravenous Anaesthetics. An immature bloodbrain barrier and decreased ability to metabolisedrugs may increase the neonate’s sensitivity tobarbiturates and opioids. Lower doses may berequired to produce the desired pharmacologicaleffects. Children less than 6 months old are

susceptible to the respiratory depressant effect ofopioids and when used, the infant's breathing shouldbe monitored. On the other hand, older, healthychildren require higher doses of thiopentone toachieve intravenous induction of anaesthesia (5-7mg/kg in children versus 3-5 mg/kg in adults).

Propofol is a new intravenous anaesthetic agentthat is being used in paediatric anaesthesia. It isdissolved in a soyabean emulsion and is associatedwith rapid recovery and reduced nausea and istherefore popular for daycase anaesthesia. Inductionof anaesthesia may be associated with pain oninjection which can be prevented by mixinglignocaine with the propofol. Induction doses of 2-5 mg/kg may be associated with apnoea, a reductionin arterial blood pressure and cardiac output, similarto thiopentone. As always, with use of such drugs,cardiac and respiratory function need to bemonitored. Propofol is safe for patients with acuteintermittent porphyria and does not triggermalignant hyperthermia.

Ketamine is a phencyclidine derivative that iswidely used in paediatric anaesthesia. An inductiondose of 1-2mg/kg produces dissociative anaesthesiacharacterised by open eyes and nystagmus. Muscletone is preserved but not sufficiently to maintainlaryngeal reflexes. Blood pressure is maintaineddue to sympathetic stimulation and it is the agent ofchoice in shocked patients. It does not producesignificant depression of ventilation, upper airwaytone is well maintained and it causes bronchodilationand is recommended for asthmatics. It causes a risein intra-ocular and intracranial pressure.Hallucinations may occur in the recovery periodbut these can be minimized by the administration ofbenzodiazepines and the provision of a quietrecovery environment. It causes salivation inchildren, and should be used in combination withan antisialogogue such as atropine 0.02mg/kg. Itcan also be given intramuscularly in a dose of 5-10mg/kg. (See also Update No4 for a full review ofketamine.)

Muscle Relaxants. Neonates and infants are moresensitive than adults to non-depolarising musclerelaxants. Initial doses, however are similar in bothage groups because the increased extracellular fluidvolume and volume of distribution in youngerpatients means that less drug actually reaches theneuromuscular junction. This increased sensitivity


combined with decreased glomerular filtration rateand hepatic clearance can result in prolongedduration of muscle relaxants in neonates. The doseof neostigmine per kg required for antagonism ofnon-depolarising muscle relaxants is similar inchildren to adults. A combination of either atropine0.02mg/kg or glycopyrrolate 0.01mg/kg withneostigmine 0.05mg/kg is suitable.

Neonates and infants require more suxamethoniumon a body weight basis to produce comparabledegrees of skeletal muscle paralysis, 2 mg/kg forinfants versus 1 mg/kg for adults to obtain acceptableconditions for intubation. Again, this change indrug requirement reflects dilutional effects of theincreased extra cellular fluid volume and volume ofdistribution of younger patients. Whensuxamethonium is contraindicated, one of the newernon-depolarising agents, rocuronium, allowsintubation almost as rapidly.

Table of drug doses

Thiopentone 5-6mg/kgstandard induction dose

Suxamethonium 1-2mg/kg (2mg/kg in infants)Atropine 0.02mg/kgKetamine 1-2mg/kg IV

3-5mg/kg IM “sedation”8-10mg/kg IM anaesthetic dose8mg/kg rectally

Curare 0.5 mg/kgAtracurium 0.5 mg/kgPancuronium 0.1 mg/kgVecuronium 0.1 mg/kgNeostigmine 0.05mg/kg

PRACTICAL CONSIDERATIONSPreoperative Assessment. Every patient shouldbe visited by the anaesthetist prior to surgery,preferably in the presence of the parents in order toobtain a history, perform a physical examinationand evaluate laboratory data in addition to estimatingthe patient’s response to hospitalisation. Parentalanxiety and fears concerning surgery andanaesthesia are very real and may be transmitted tothe patient. To prepare the child psychologicallyfor elective surgery, educational booklets and aclear explanation are useful. Parents are informedof what to expect, possible risks and the anaesthetic

plan. If a parent wishes to accompany the child tothe induction room they should be warned in advancewhat to expect and arrangements made for someoneto escort them from the room once induction ofanaesthesia has occurred.

Fasting. Safe anaesthesia depends on the patientbeing fasted. However, numerous studies haveshown that the traditional prolonged period withoutclear liquids prior to anaesthesia is unnecessary.Fasting periods can safely be shortened in normalinfants and children who feed frequently during theday. A baby who is used to feeding every two hourswill come to surgery less distressed and betterhydrated if he or she has been allowed to have clearliquids closer to the time of surgery. Most hospitalshave developed more liberal fasting guidelinesalong the following lines:

Newborn to 12 months:No formula or breast milk 4 hours before surgeryClear liquids up to 2 hours before surgery

Over 1 year:No formula, milk or solid food 6 hours beforesurgeryClear liquids up to 2 hours before surgery

(A clear fluid is defined as a fluid through whichprint can be seen. Remember breast milk is not aclear fluid.)

Common conditions relevant to anaesthesiaWhat is the anaesthetist to do if the parents tell youthe child “has a cold” (upper respiratory tractinfection)? Children, especially those having ENTtype procedures such as ear tubes or tonsillectomy,often have clear rhinorrhea (nasal discharge) andprocedures should not be cancelled on this basisalone. Purulent rhinorrhea, productive cough andfever indicate the cold is a more systemic problemand elective surgery is better postponed for one totwo weeks. Ask the parents how the child with acold has been acting. Is he or she eating and playingnormally or is it associated with general malaiseand fatigue? These are the cases best postponed.Performing an anaesthetic in the presence of asystemic upper respiratory tract infection may resultin laryngospasm and ventilatory problems withhypoxia, all easily avoided if the procedure issimply postponed until the child is well.

Asthma is a common disorder (3-5% of thepopulation) resulting in airway hyperreactivity in


response to a variety of stimuli. Active bronchialasthma is usually characterised by reversiblenarrowing of airways resulting in audible wheezingon auscultation of the chest. Obstruction of airflowleads to changes in lung volumes, chest wallmechanics, and altered distribution of ventilationand perfusion resulting in hypoxemia andhypercarbia. Pulmonary function tests show theratio of FEV1:FVC is less than 80 percent.

The sympathetic nervous system plays a major rolein maintaining normal bronchial tone and treatmentoften includes beta-adrenergic agonists,theophylline, anticholinergics, glucocorticoids (insevere cases) and cromoglycate. Beta-adrenergicagents are usually given in the form of inhalers ornebulisers producing bronchodilatation byactivation of beta-2 receptors thus avoiding theundesirable beta-1 cardiac effects.

Theophylline and aminophylline producebronchodilation by inhibiting phosphodiesterase,the enzyme that breaks down cyclic AMP.Anticholinergics produce bronchodilation throughtheir antimuscarinic action and also dry up airwaysecretions. Glucocorticoids (steroids) have anti-inflammatory effects as well as membranestabilization and are used in severe cases.Beclomethasone is used as an inhaled steroid andproduces fewer systemic side effects.

Management of anaesthesia for the asthmatic patientincludes preoperative assessment to determine theseverity of the asthma. Elective cases are bestavoided in the presence of active wheezing. Thegoal during induction and maintenance ofanaesthesia in the asthmatic is to avoid unnecessarystimulation of the non-anaesthetised airway whichmay result in bronchospasm. Regional anaesthesiais a good choice as any manipulation of the airwayis avoided but is often not practical in children. Ifgeneral anaesthesia is needed, a smooth inductionand emergence is the goal, using drugs such as thevolatile anaesthetics, non-histamine releasingopioids or ketamine to establish a depth ofanaesthesia that will depress hyperreactivity of theairway. Ketamine is the only intravenous agentwith bronchodilating properties.

Intraoperative wheezing should be treated bydeepening the anaesthetic and by using inhaledbeta-2 agonists by aerosol (salbutamol / terbutaline).Severe bronchospasm can be treated with

intravenous aminophylline using a 6mg/kg loadingdose followed by 0.5-0.9mg/kg/hour by infusion.Cardiac dysrhythmias during aminophylline needto be carefully monitored. With refractorybronchospasm, adrenaline may be required - in thissituation halothane should be turned off.Hydrocortisone (3mg/kg 6 hourly) may also proveuseful but acts slowly producing an effect afterabout 2 hours.

Epilepsy. Seizures represent abnormalsynchronisation of electrical activity of the brainand may be localised or generalised. Grand malseizures are most common and are characterised byloss of consciousness followed by clonic/tonic motoractivity. The condition is usually controlled withdaily doses of anticonvulsants including phenytoin,phenobarbitone, carbamazepine and valproic acid.

Preoperatively, the anaesthetist needs to determinehow active the disease is, i.e., is it well controlledon medications and when was the last seizure?Adverse side effects of the medications can bedetermined clinically (ataxia, dizziness, confusionand sedation). Anticonvulsants should be ideallycontinued pre and post operatively to maintaintherapeutic levels. Fortunately, most have aprolonged half-life so missing one or two doses isnot critical.

Anaesthetic agents which may provoke epilepsyinclude ketamine, enflurane and methohexitone.Phenytoin and carbamazepine may increase thedose requirements for non-depolarising musclerelaxants due to hepatic microsomal enzymeinduction.

Sickle Cell Disease is an inherited disorder resultingfrom the formation of abnormal haemoglobin (HbS).HbS differs from normal adult haemoglobin (HbA)in the substitution of valine for glutamic acid at thesixth position of the beta chain of haemoglobin.HbS has lower affinity for oxygen as well asdecreased solubility. Upon deoxygenating, HbSpolymerizes, causing the cells to take on a sickleshape and obstruct vessels.

Painful vaso-occlusive crises result which arethought to be due to micro infarcts in various tissuesresulting in joint pain, chest pain and abdominalpain. Aplastic crises can produce profound anemiawhen red cell production is exhausted. The red cellsurvival is only 10-20 days compared to the 120


depth of anaesthesia is often judged by changes inheart rate, the resultant tachycardia from atropinemay make it more difficult for the anaesthetist.Flushing of the face, delirium, restlessness andagitation may occasionally occur in the recoveryroom following atropine or scopolamine (hyoscine).

A recent advance is EMLA (a Eutectic Mixture ofLocal Anaesthetic) prepared with prilocaine andlignocaine as an emulsion in a white cream. Itproduces skin anaesthesia after it has been in placefor one hour under an occlusive dressing and hasproved useful for painless venous puncture even invery young children. Systemic absorption of thedrug is well below toxic levels even after extensiveapplication of the cream. However, methaemo-globinaemia may be produced by the metabolismof prilocaine in the young infant or the older infantafter repeated application or where it has beenplaced on broken skin. Another local anaestheticcream has recently been introduced based onamethocaine (Ametop).

Basic Anaesthetic TechniquesThe induction room. There are advantages inanaesthetising children in a dedicated inductionroom outside the operating theatre away fromdistracting sights and sounds. Anxiety may bereduced if a parent accompanies the child.Anaesthesia can frequently be induced with thechild sitting on the parent’s lap. When induction isover the child can then be transferred to the tableand the parents escorted from the room by a nurse.Equipment checks. Since children can deterioraterapidly during anaesthesia it is especially importantto check that all drugs and apparatus are readyprior to induction. In particular there should be twolaryngoscopes, suction apparatus, a range ofendotracheal tubes and masks. The Rendell-Bakermask is designed to fit closely around the face tominimise the dead space although some anaesthetistsprefer to use a clear mask which allows the child’scolour to be checked during induction. Atropineand suxamethonium should be instantly availablein case unexpected laryngospasm or other airwayproblems develop causing hypoxia and bradycardia.

Induction of anaesthesia is generally by intravenousor inhalational methods. Since the introduction oftopical local anaesthetic preparations intravenousinduction has increased in popularity.

In the absence of suitable veins induction can

days of a normal red cell, resulting in chronicanaemia. The diagnosis is confirmed withhaemoglobin electrophoresis. Update inAnaesthesia No. 4 contains a full discussion ofSickle Cell disease.

Optimal preoperative preparation includeshydration, control of infections and ensuring anacceptable haemoglobin concentration.Preoperative simple or exchange transfusion maybe necessary to achieve a haemoglobinconcentration of 10g/dl or greater with 40-50% ofnormal HbA present.

Intraoperative problems that might promote sicklingshould be avoided including dehydration,hypothermia, hypoxaemia, hypotension andacidosis. An inspired oxygen tension of 50 percentis desirable, if possible. Many clinicians also avoidthe use of tourniquets as these may enhance sicklingdistal to the tourniquet. The same principles applyin the postoperative period. Supplemental oxygen,optimal pain control, pulmonary physiotherapy,hydration and early ambulation are all desirable.

Pre-medication should be prescribed according tothe needs of the patient. Providing that a goodrapport has been established with the child andparents most children do not require pre-medication.Sedatives should be reserved for those who areunduly anxious. Oral midazolam 0.75mg/kgadministered 30 minutes prior to induction is verysuitable. When prepared from the parenteral formthe bitter taste can be reduced by adding ateaspoonful of paracetamol elixir. Other commonlyprescribed pre-medications are oral trimeprazine3mg/kg and diazepam 0.25mg/kg. Intramuscularpre-medications are traumatic for children andshould be avoided whenever possible

Atropine or glycopyrrolate can be administeredorally (or intramuscularly) preoperatively or giveniv on induction of anaesthesia. Certain anaestheticdrugs, particularly suxamethonium and halothanemay cause vagally induced bradycardia. This effectis more prominent in infants under three months ofage. A vagolytic dose of atropine (0.03 mg/kg)provides complete protection against vagal cardiacslowing or other cardiac arrhythmias in infantsunder 6 months of age. These seemingly largedoses are well tolerated by infants. In general, ifatropine is needed, many anaesthetists prefer togive it intravenously in the operating room. As


generally be achieved rapidly using one of thepotent inhalational agents. Nitrous oxide may beadded to oxygen as the carrier gas to speed inductionbut the proportion of oxygen must be kept at >30%to reduce the possibility of hypoxia. The applicationof a face mask may be unacceptable to the patientin which case the anaesthetic can be graduallyintroduced via the cupped hand of the anaesthetistheld initially away from the patients face.

An inhalational induction of anaesthesia is usuallyvery easy to perform with halothane which is notirritating to the airway. The induction is startedwith 70% nitrous oxide (if available) and 30%oxygen for a few breaths. The volatile anaestheticis then gradually introduced, increasing a halfpercent with every three breaths. More rapidincreases should be avoided as coughing or evenlaryngospasm may develop. A calm voice is helpfulfrom the anaesthetist. Once anaesthesia is obtained,an intravenous cannula or needle may be insertedand drugs can be administered as needed for thesurgery. Muscle relaxants are often used to facilitateintubation. If laryngospasm occurs before anintravenous catheter is placed, positive airwaypressure should first be used in an attempt to curethe spasm. If this is not successful and hypoxiadevelops, suxamethonium administered sub-lingually 2mg/kg or intramuscularly 4mg/kg(preceeded by atropine if possible to preventbradycardia) should be used.

Once anaesthesia has been induced veins usuallybecome more prominent and an indwellingintravenous cannula should be inserted as soon aspossible. In babies and children less than six monthsintubation is advisable due to the difficulty ofmaintaining an airway. Because of the problems ofabsorption atelectasis, falling functional residualcapacity and hypercapnia it is common practice toventilate all children under 20kg for anything butvery short procedures. The laryngeal mask airwayis now manufactured in paediatric sizes and providesan alternative form of airway management but theyare not suitable for controlled ventilation in smallchildren because of the danger of gastric dilatation.

Muscle relaxants are often used to facilitateintubation. If suxamethonium is selected atropinemust be drawn up ready to administer in case ofbradycardia. If a second dose of suxamethonium isrequired it should always be preceded by atropine

(0.02mg/kg) since bradycardia is common withrepeat administrations.

It is important to flush an indwelling intravenouscannula with saline following the administration ofany drug to prevent any residue in the dead space ofthe cannula being inadvertently injected when thecannula is next used.

Occasionally the anaesthetist is confronted by anunruly and hysterical child who will not co-operatewith either of the above methods of induction.While an IM injection of ketamine (3-5 mg/kg) ispossible, it is often easier and less traumatic togown up the parent and bring them to the inductionor operating room with you to be present with thechild until an inhalational induction is performed.However, there must be sufficient staff to allowsomeone to escort the parent out of the operatingroom after anaesthesia is induced. If intramuscularketamine is the only option, secretions in the airwaycan be kept to a minimum if glycopyrolate (0.01mg/kg) is added to the injection. Alternatively atropinemay be given after anaesthesia develops.

Anaesthesia Breathing Systems

Many anaesthesia ventilators designed for adultscannot reliably provide the low tidal volumes andrapid respiratory rates required for infants andsmall children. Unintentional delivery of large tidalvolumes to a small child can generate large airwaypressures and cause barotrauma (damage to thelungs due to excessive inspiratory pressure).

Spirometers are less accurate at small volumes anddelivered tidal volumes may be reduced when adultanaesthesia breathing systems are used due tocompression of the gas in long breathing tubes withhigh compliance. Dedicated paediatric anaesthesiatubing is usually shorter and stiffer and the smallertidal volumes can be better delivered manuallywith a 500ml or 1000ml breathing bag.

The efficiency of breathing circuits is measured bythe fresh gas flow required to eliminate CO

2

rebreathing. Mapleson circuits are lightweight, andinexpensive. The Mapleson A circuit (Magill circuit)is very efficient during spontaneous ventilation iffresh gas flow is equal to the patients minuteventilation. It is inefficient during controlledventilation and requires a high gas flow to preventrebreathing. The Mapleson D is more efficient thanthe A system with controlled ventilation requiring


a fresh gas flow of 1 to 2 times minute ventilation.The Bain circuit is a co-axial Mapleson D system.

The Ayres T-Piece (Mapleson E) functions in asimilar way to the Mapleson D circuit, but becausethere are no valves and very little resistance tobreathing it has proved very suitable for childrenunder 20kg. The version most commonly used isthe Jackson-Rees modification which has an openbag attached to the expiratory limb (classified as aMapleson F system). Fresh gas flows of 2-3 timesminute volume should be used to prevent rebreathingduring spontaneous ventilation, with a minimumflow of 3 litres/min. During controlled ventilationthe litres of fresh gas required per minute can becalculated by giving 1000 ml + 100 mls/kg. Theminimum flow should be 3 litres/min. (A fulldiscussion of breathing systems can be found inUpdate No. 7.)

In general circle systems are bulky with increasedresistance making them less suitable forspontaneously breathing children.

Drawover systems have slightly increasedrespiratory resistance compared with standardcontinuous flow apparatus. There are 2 ways ofusing drawover apparatus for small children.

The systems can be converted to continuous flowby connecting a continuous flow of oxygen to theupstream side of the vaporiser. A T piece can thenbe connected in the normal fashion. Ensure thatthere are no leaks.

There are differences in the performance of thedifferent drawover vaporisers when supplied witha continuous flow of gas. In this mode, the OxfordMiniature Vaporiser (OMV) requires 4 - 6 litres /minute of fresh gas flow to work efficiently. TheEMO requires 8 - 10 litres /minute flow to performpredictably. Lower flows should not be used withthis technique.

An alternative technique when using the OMV is tomake a paediatric drawover circuit using a AMBUPaedivalve and small AMBU inflating bag. Thechild’s respiration should be supported or controlledthroughout, but this vaporiser has been reported towork well at small tidal and minute volumes.

Monitoring techniques for paediatric patientsshould be similar to those of adults undergoingcomparable types of surgery. Standard monitoring

includes close observation by the anaesthetist,precordial or oesophageal stethoscope and bloodpressure. Where facilities allow the presence ofmore advanced monitors increases the safety ofanaesthesia. These include non-invasive bloodpressure, pulse oximetry, temperature, end tidalCO

2 and ECG, all of which should be placed on

induction of anaesthesia . There is no doubt that thebest monitor available is the pulse oximeter whichwas discussed in detail in the 5th edition of Updatein Anaesthesia.

The stethoscope (precordial or oesophageal) is amost valuable monitoring device and should beused continually in all paediatric patients. It isinexpensive, reliable, does not require any externalsource of power or maintenance. It providesinformation on the cardiovascular system (heartrate and rhythm, intensity of heart sounds) andrespiratory system (respiratory rate, the presence ofsecretions, pulmonary oedema and bronchospasm).It also gives instant warning of ventilatordisconnection.

Blood pressure measurement requires the correctsize of the cuff. A cuff that is too large will giveartificially low readings and one that is too smallwill give readings that are falsely high.

In seriously ill children who are undergoing moreextensive surgery with potential for fluid losses,blood pressure should be closely monitored. Thecentral venous pressure may be assessed to helpdetermine the blood volume status. Hourly, urinaryoutput with a Foley catheter is also useful andshould exceed 0.5 ml/kg/hr. Hypoglycemia occursfrequently in seriously ill children or very younginfants and should be treated with 1-3 ml/kg of a20% glucose solution intravenously over 5 minutes.Excessive glucose replacement should be avoidedas an osmotic diuresis resulting in dehydration mayresult from hyperglycemia.

All monitors as well as a reliable intravenousinfusion should be secured in position before thecommencement of surgery after which access tothe patient may be difficult.

A Common Intra-operative ProblemBradycardia in paediatrics often means hypoxiaand restoring adequate ventilation and oxygenationmay be all that is needed to restore heart rate.Bradycardia from vagal influence, as seen in eye


muscle surgery, can be treated by asking the surgeonto relieve tension on the eye muscle and givingintravenous atropine. Bradycardia resulting fromincreased intracranial pressure is treated withhyperventilation, diuretics and surgical release ofthe pressure.

Basic Postoperative CareInfants and children generally recover faster thanadults from anaesthesia and surgery. The immediatepostoperative care is as critical as the intra-operativecare and the child should be taken to a recoveryarea with trained staff. The anaesthetist shouldreport to the recovery room personnel any intra-operative problems that occurred. The airway shouldbe maintained to assure adequacy of ventilationand oxygenation and any unexpected findingsreported to the anaesthetist. Vital signs should betaken frequently in the first hour and pain treated.The child may return to the ward when theobservations are stable, he is fully conscious andhis pain is controlled.

Occasionally croup or subglottic oedema afterendotracheal anaesthesia manifests itself in thefirst few hours after extubation. Mild croup resultsin a hoarse cough, more severe croup may causelabored respiration, sternal recession, anxiety andinadequate ventilation. Mild cases will resolveover time and may only require extra observationand possibly some humidified oxygen. Nebulisedadrenaline (5mg) by facemask is used in moresevere cases. It is the vasoconstrictor effect of theadrenaline that relieves the oedema but the effectmay be short lived. The patient should be monitoredvery closely as it may recur after the treatment andmay require a second dose. Steroids may or may notbe useful and a single, large dose of i.v. dexa-methasone (4mg for infants, 8mg for children) canbe used. If the above treatment is ineffective,preparations should be made for reintubation usinga smaller endotracheal tube. This complicationmay be prevented by using the correct size ofendotracheal tube at induction of anaesthesia.

Post operative pain managementMethods of treating postoperative pain in childreninclude the use of systemic analgesics and localanaesthetic agents. The systemic analgesics can bedivided into non-opioids and opioids. This areawas discussed more fully in Update No 7.

1. Non-opioid analgesics (for mild or moderatepain)a) paracetamol (acetaminophen) 15mg/kg 6 hourly

b) NSAIDS - this group of drugs has becomeextremely popular for treating post operative painin children as they are effective with few sideeffects and produce an opioid sparing action. Theyshould be avoided in patients with coagulopathy(because of a tendency to prolong postoperativebleeding), nephropathy, gastropathy and asthma.Diclofenac 1-3mg/kg per day in divided doses iswidely used. It is also available as a suppository.NB: Aspirin should not be used for children under12 years because of the association with Reye’ssyndrome.

2. Opioids (for severe pain)Opioids may be administered by IM, IV or oralroutes. Children are sensitive to opioids and dosesshould be reduced accordingly. They should not begiven to children <5kg.

Suggested doses intramuscularly:Morphine: 0.1-0.2mg/kg 4 hourly (may be givensubcutaneously also)

Pethidine: 1 - 1.5mg/kg 4 hourly

Slow IV administration avoids the need for painfulintramuscular injections, but the child should beclosely observed whilst this is given.

Codeine is also a useful drug and may be givenorally or intramuscularly in a dose of 0.5-1mg/kg6 hourly. Codeine should not be given intravenously.

Local anaesthetic techniquesLocal wound infiltration with bupivacaine 0.25%at the conclusion of surgery is very effective and isextremely simple and safe. It reduces the need foradditional measures. Other regional blocks areused in specific situations eg intercostal blocksfollowing thoracotomy, ilio-inguinal and ilio-hypogastric nerve blocks following hernia repairand orchiopexy, dorsal nerve blocks of the penis orcaudal blocks following circumcision. Caudalanaesthesia is described on page 14.

Unusual diseases in paediatricsPyloric stenosis. Hypertrophy of the muscle of thepyloric sphincter causes obstruction leading topersistent vomiting. It occurs in about one in every500 live births and usually manifests itself around2-6 weeks of age. Persistent vomiting results in loss


of hydrogen ions with compensatory attempts thekidney to maintain a normal pH by exchangingpotassium for hydrogen. It is the “hypo” diseasewith the result being a dehydrated infant withhypokalaemia, hyponatraemia, hypochloraemia andmetabolic alkalosis. It is not a surgical emergencyand the infant should first be rehydrated withintravenous fluid therapy including sodium chloridewith potassium supplements for 24-48 hours.

When the infant presents for surgery with normalelectrolyte values, the likelihood for aspiration isstill high and the stomach should be emptied witha nasogastric tube before induction. Anaesthesiashould be induced using a rapid sequence patternwith atropine, thiopentone, suxamethonium andcricoid pressure until the position of the endotrachealtube is confirmed. Postoperative respiratorydepression is common in these patients, possibly asa result of CSF alkalosis and the use of opioidsshould be avoided. The postoperative pain is easilytreated with paracetamol and infiltration of localanaesthetic at the time of surgery. The infants areusually happy to feed 3 - 6 hours after the surgicalprocedure.

Epiglottitis. Symptoms of epiglottitis include anacute onset of difficulty in swallowing, high feverand inspiratory stridor in 2-6 year old children.Children suffering from epiglottitis typically remainupright and dribble saliva. It is an emergency andtreatment includes antibiotics and intubation of thetrachea until the swelling has subsided with medicaltherapy. Any attempt to visualise the epiglottisshould not be undertaken until the child is in theoperating room with appropriate airway equipmentfor endotracheal intubation and instrumentationfor tracheostomy. (It goes without saying thatpersonnel capable of using these instruments needto be present!) Induction and maintenance ofanaesthesia for intubation of the trachea is withhalothane in oxygen. Muscle relaxants are avoidedas skeletal muscle relaxation may result in totalupper airway obstruction. Use an endotrachealtube half a size smaller than calculated and have avariety of sizes available, including a stylet. Theswelling usually improves in one to two days afterappropriate antibiotic therapy. Extubation of thetrachea is performed in the operating room afterdirect laryngoscopy confirms reduction of swellingof the epiglottis. The presence of a leak around the

endotracheal tube is used as a sign that swelling hasresolved enough for the child to breathe on theirown without the presence of an endotracheal tube.

Down’s Syndrome (trisomy 21) occurs in about0.15 % of live births. The condition is associatedwith mental retardation, congenital cardiacanomalies (atrial and ventricular septal defects),duodenal atresia, hypotonia, small mouth, subglotticstenosis, hypoplastic mandible and protrudingtongue. Patency of the upper airway may be difficultto maintain after onset of unconsciousness for theabove reasons but intubation is usually not difficult.Manipulation of the neck during intubation shouldbe done cautiously as 10% of these patients haveassociated asymptomatic atlanto-axial instability.

Prematurity. Six percent of infants in the UnitedStates of America are born prematurely, before 37weeks gestational age. During the last 3 months ofgestation, organs are still developing, bothstructurally and developmentally. When an infantis born prior to term, these organs are asked tofunction fully when they may not be ready. Preterminfants are less able to maintain body temperature,suck, swallow, eat and even maintain ventilationadequately. As a result, birth asphyxia predisposesthem to central nervous system damage, retinopathyof prematurity, intraventricular haemorrhage,respiratory distress syndrome, bronchopulmonarydysplasia, anaemia, apnoea, patent ductus arteriosisand necrotizing enterocolitis.

Anaesthesia for premature infants is often difficultbecause they may have multisystem disease andrespond poorly to anaesthesia. It is important togather as much information as possible prior toanaesthesia; birth history, ICU problems, laboratorydata, radiological findings, state of hydration andnutrition and clotting status. It is advisable to havea second anaesthetist in the operating room to help.The operating room needs to be warm, 35-37 degreescentigrade and an infrared heater, if available,should be placed over the operating room table.Fluids are warmed and heating blankets may alsobe used. Oxygen requirements should be dictatedby the neonate’s needs. Using 100 percent oxygento a neonate who does not need it only predisposesthat baby to development of retinopathy ofprematurity.


ConclusionIt has not been possible to cover all aspects ofpaediatric anaesthesia in a single article but it ishoped that this overview of the main principles willprove useful for those called upon to anaesthetisepaediatric patients. More detailed accounts ofparticular techniques and the management ofspecific paediatric problems will appear in futureeditions.

References1. Ryan, J.F., Cote, C.J., Todres, I.D.,

Goudsouzian, N. A Practice of Anaesthesiafor Infants and Children. 1st ed. Grune andStratton Inc. Orlando,Fla., 1986.

2. Stoelting, R.K., Miller, R.D. Basics ofAnaesthesia. 2nd edition. ChurchillLivingston Inc. New York., 1989.

3. Gregory, G.A. Paediatric Anaesthesia. 3rdedition. Churchill Livingston Inc. New York,1994.

4. Barash, P.G., Cullen, B.F., Stoelting, R.K.Clinical Anaesthesia. 2nd edition. J.P.Lippincott Co. Philadelphia, 1989.

5. Procter, L.T., Gregory, G.A. Paediatric

Anaesthesia. Current Opinion inAnaesthesiology 1995;8:3, 221-3.

6. Steward, D.J. Paediatric Anaesthesia. CurrentOpinion in Anesthesia 1993; 6:507-8.

7. Litman, R.S. Gastric volume and pH inchildren. Anaesth Analg 1994;79:482-85.

8. Skues, M.A., Prys-Roberts, C. Thepharmacology of Propofol. J. Clin.Anaesth.1989;1:5.

9. Meakin, G. Drugs in Paediatric Anaesthesia.Current Opinion in Anesthesiology1994;7:3,251-6.

10. Houck CS., Wilder RT, McDermott J, et al.Intravenous ketorolac in children followingsurgery: Safety and cost savings with a unitdosing system. Anaesthesiology1993;79:1139A.

11. Murat I. New inhalational agents in PaediatricAnaesthesia: desflurane and sevoflurane.Current Opinion in Anesthesiology1996;9:3,225-8.

The authors would like to thank Mia S L Wyatt forher secretarial assistance during the preparation ofthis review.

CAUDAL EPIDURAL ANAESTHESIA

Dr Bela Vadodaria and Dr David ConnDepartment of Anaesthetics,Royal Devon and Exeter Hospital, Exeter

IntroductionCaudal anaesthesia has been used for many yearsand is the easiest and safest approach to theepidural space. When correctly performed there islittle danger of either the spinal cord or dura beingdamaged.

It is used to provide peri and post operative analgesiain adults and children. It may be the sole anaestheticfor some procedures, or it may be combined withgeneral anaesthesia.

IndicationsAnaesthesia and analgesia below the umbilicus.Paediatric patients do not generally tolerate surgeryunder regional anaesthesia alone. However in thevery young a caudal block may be adequate to carryout urgent procedures such as reduction ofincarcerated hernias, allowing return of normalbowel function prior to surgical repair. Anaesthesia

can be provided for superficial operations such asskin grafting, perineal procedures, and lower limbsurgery. A general anaesthetic will often be requiredin addition. Pain relief will extend into the postoperative period. The duration of the block canbeen prolonged by the addition of an opiate(pethidine 0.5mg/kg) to the local anaesthetic. Thepossibility of delayed respiratory depression fromepidural opiates needs taken into account, andpatients should monitored in an intensive care orhigh dependency unit for 24 hours following theiradministration.

Obstetric analgesia for the 2nd stage or instrumentaldeliveries. Care should be taken as the foetal headlies close to the site of injection and there is real riskof injecting local anaesthetic into the foetus.

Chronic pain problems such as leg pain afterprolapsed intervertebral disc, or post shingles painbelow the umbilicus.

ContraindicationsInfection near the site of the needle insertion.

Coagulopathy or anti coagulation.


Pilonidal cyst

Congenital abnormalities of the lower spine ormeninges, because of the unclear or impalpableanatomy.

AnatomyThe caudal epidural space is the lowest portion ofthe epidural system and is entered through thesacral hiatus. The sacrum is a triangular bone thatconsists of the five fused sacral vertebrae (S1- S5).It articulates with the fifth lumber vertebra and thecoccyx.

The sacral hiatus is a defect in the lower part of theposterior wall of the sacrum formed by the failureof the laminae of S5 and/or S4 to meet and fuse inthe midline. There is a considerable variation in theanatomy of the tissues near the sacral hiatus, inparticular, the bony sacrum. The sacral canal is acontinuation of the lumbar spinal canal whichterminates at the sacral hiatus. The volume of thesacral canal can vary greatly between adults.

The sacral canal contains:

1. The terminal part of the dural sac, endingbetween S1 and S3.

2. The five sacral nerves and coccygeal nervesmaking up the cauda equina. The sacral epiduralveins generally end at S4, but may extend throughoutthe canal. They are at risk from catheter or needlepuncture.

3. The filum terminale - the final part of thespinal cord which does not contain nerves. Thisexits through the sacral hiatus and is attached to theback of the coccyx.

4. Epidural fat, the character of which changesfrom a loose texture in children to a more fibrousclose-meshed texture in adults. It is this differencethat gives rise to the predictability of caudal localanaesthetic spread in children and itsunpredictability in adults.

Choice of drug and dosage.

Choose the drug with the longest duration of actionand the fewest side effects. Drugs that are commonlyused include Lignocaine 1% and Bupivacaine0.25%, although higher concentrations may beneeded for muscle relaxation. Drugs used forepidural injections should come from single useampoules and be preservative free.

Various regimes have been produced to calculatethe appropriate dose of local anaesthetic, the dosesvary widely:

1. Armitage recommends bupivacaine 0.5ml/kg for a lumbosacral block, 1ml/kg for a thoraco-lumber block, and 1.25ml/kg for a mid thoracicblock. He recommended the use of 0.25%bupivacaine for the block up to a maximum of20ml. For larger volumes he recommended addingone part of 0.9% NaCl to three parts local anaestheticto produce a 0.19% mixture.

2. Scott calculates the dose from the child’s ageor weight. If the child is of average weight for itsheight both figures will be the same. If the child isoverweight use the figure based on age to avoid thepossibility of overdose.

Coccyx

Sacral hiatusTranssacral

foramina

Sacrum

Fig. 1. Anatomy of the sacrum and coccyx

Weight Age Dose(ml) 0.25% Dose(ml) 0.25%in Kg. (in bupivacaine for bupivacaine for

years) a block to T12 for a block to T7

12.5 2 4 6

15 3 5 7.5

16 4 5.5 8

17.5 5 6 9

20 6 7 10.5

22.5 7 8 12

25 8 9 13.5

27.5 9 10 15

30 10 11 16.5


Scott’s lower doses are more likely to produceanalgesia to the expected height, whereas Armitagewill get anaesthesia. Dosages for adults are 20-30ml for a block of the lower abdomen and 15-20mlfor a block of the lower limb and perineum.

Care is needed to avoid the use of toxic doses ofdrugs for high blocks. The recommended maximumdose of Bupivicaine is 2mg/kg or Lignocaine 4mg/kg. These dosages are the maximum for a correctlyinjected dose. If the drug is mistakenly injectedintravenously very small dosages may cause serioustoxicity.

TechniqueThe patient is prepared as for general anaesthesia,

1. He/she should be fasted

2. All appropriate equipment for resuscitationmust be available. Equipment for intubation,airway suction and drugs to stop fitting iethiopentone 2-5mg/kg or Diazepam 0.2-0.4mg/kg.

3. An intravenous cannula should always beinserted in an upper limb, in case of accidentalintravenous injection, or profoundsympathetic blockade from a high epiduralblock.

4. The procedure must be carried out with astrict aseptic technique. The skin should bethoroughly prepared and sterile gloves worn.Any infection in the caudal space isextremely serious.

5. There are three main approaches: the prone,the semi-prone, and the lateral. The choicedepends on the preference of the anaesthetistand the degree of sedation of the patient.

The prone position is often easiest in the adult, as fattends to move away from the mid-line and landmarksare easier to find. However, there could be difficultyif urgent access to the airway is required. Thecaudal space is made more prominent by asking thepatient to internally rotate their ankles (fig. 2).

The semi-prone position is preferred for theanaesthetised or heavily sedated patient as theairway is easier to control in this position, whilestill allowing reasonably easy access to the sacralhiatus.

The lateral position is often used in children, as the

landmarks are easier to find than in adults. Careshould be taken to avoid over flexing the hips (asfor lumber epidurals) as this can make the landmarksmore difficult to palpate.

6. The landmarks are palpated. The sacral hiatusand the posterior superior iliac spines form anequilateral triangle pointing inferiorly. Thesacral hiatus can be located by first palpatingthe coccyx, and then sliding the palpatingfinger in a cephalad direction (towards thehead) until a depression in the skin is felt. (Inan adult the distance from the tip of thecoccyx to the sacral hiatus is approximatelythe same as the distance from the tip of theirindex finger to their proximal inter phalangealjoint)!

As there can be a considerable degree of anatomicalvariation in this region confirmation of bonylandmarks is the key to success. The needle can

Fig. 2. Position (a) causes contraction of the glutecalmuscles. Position (b) allows relaxation of glutecal muscles.


penetrate a number of different structures mimickingthe feel of entering the sacral hiatus. It is importantto establish the midline of the sacrum as considerablevariability occurs in the prominence of the cornua,causing problems unless care is taken.

7. Once the sacral hiatus is identified the areaabove is carefully cleaned with antisepticsolution, and a 22 gauge short bevelledcannula or needle is directed at about 450 toskin and inserted till a “click” is felt as thesacro-coccygeal ligament is pierced. Theneedle is then carefully directed in a cephaladdirection at an angle approaching the longaxis of the spinal canal.

Care should be taken not to insert the needle too faras the dura lies at or below the S2 level in the child.

8. The needle should be aspirated looking foreither CSF or blood. A negative aspirationtest does not exclude intravascular orintrathecal placement. Care should always betaken to look for signs of acute toxicity duringthe injection. The injection should never bemore than 10 ml/30 seconds.

Further tests to confirm the correct position includegently moving the tip of the needle from side toside. The needle will feel firmly held. Introductionof a small amount of air will not producesubcutaneous emphysema, and will be heard as a“woosh” sound if a stethoscope is place further upthe lumbar spine. Light blood staining is notuncommon and indicates entry into the sacral canal.There should be no local pain during injection.Tingling or a feeling of fullness that extends fromthe sacrum to the soles of the feet is common duringinjection.

9. A small amount of local anaesthetic shouldbe injected as a test dose (2 – 4mls). It should

not produce either a lump in the subcutaneoustissues, or a feeling of resistance to theinjection, nor any systemic effects such asarrhythmias, peri-oral tingling, numbness orhypotension. If the test dose does not produceany side effects then the rest of the drug isinjected, the needle removed and the patientpositioned for surgery.

In the post-operative period, motor function mustbe checked and the patient should not be allowed totry and walk until complete return of motor functionis assured. The patient should not be dischargedfrom hospital until he/she has passed urine, asurinary retention is a recognised complication.

Complications

Intravascular or intraosseous injection. This maylead to grand mal seizures and/or cardio-respiratoryarrest.

Dural puncture. Extreme care must be taken toavoid this as a total spinal block will occur if thedose for a caudal block is injected into thesubarachnoid space. If this occurs then the patientwill become rapidly apnoeic and profoundlyhypotensive. Management includes control of theairway and breathing, and treatment of the bloodpressure with intravenous fluids and vasopressorssuch as ephedrine.

Perforation of the rectum. While simple needlepuncture is not important, contamination of theneedle is extremely dangerous if it is then insertedinto the epidural space

Sepsis. This should be a very rare occurrence ifstrict aseptic procedures are followed.

Urinary retention. This is not uncommon andtemporary catheterisation may be required.

Subcutaneous injection. This should be obviousas the drug is injected.

Haematoma

Absent or patchy block.

ConclusionCaudal block is an easy and safe technique whichcan be used provide anaesthesia and postoperativeanalgesia for a wide range of surgical procedures.

When performed carefully complications are rare.


would enlarge because of the increase in cerebralarterial blood volume.

A number of terms will be used in this article andare defined:-

ICP intracranial pressure is the pressure withinthe rigid skull.

CBF cerebral blood flow is the flow of bloodthrough the brain, important for delivery of oxygenand removal of “waste” products

CPP cerebral perfusion pressure is the effectivepressure driving blood through the brain. It isdiscussed in detail later

INTRACRANIAL PRESSURE

The principle constituents within the skull are brain(80%), blood (12%) and CSF (8%). The total volumeis 1600ml. The skull is thus a rigid fluid filled box.If the volume of the contents of a rigid fluid-filledcontainer increase, the pressure inside will riseconsiderably unless some fluid is able to escape. Soit is with the skull and brain within it. If the brainenlarges, some blood or CSF must escape to avoida rise in pressure. If this should fail, or be unable tooccur there will be a rapid increase in ICP from thenormal range (5-13 mmHg). If there is an increasein the volume of either the brain or blood the normalinitial response is a reduction in CSF volume withinthe skull. CSF is forced out into the spinal sac. Thusthe pressure within the skull, ICP, is initiallymaintained. If the pathological process progresseswith further increase in volume, venous blood andmore CSF is forced out of the skull. Ultimately thisprocess becomes exhausted, when the venoussinuses are flattened and there is little or no CSFremaining in the head. Any further increase in brainvolume then causes a rapid increase in ICP. Thischain of events is represented by the sequence in

INTRACRANIAL PRESSURE ANDCEREBRAL BLOOD FLOW

Dr. F.J.M.WaltersConsultant AnaesthetistFrenchay Hospital, Bristol UK

INTRODUCTIONThe physiological changes that maintain cerebralblood flow (CBF) and accommodate alterations inbrain volume are relatively simple to understand.Following trauma or in the presence of majorintracranial disease additional changes occur. Majoradvances in the care of patients with majorneurosurgical problems have been developed overthe last 10 years. These advances have evolvedfrom a sound understanding of basic physiologicalrules and the pathological process of differentdisease situations as well as the pharmacology ofanaesthetic drugs. Successful management of thesepatients relies on a clear understanding of thesephysiological mechanisms and of the added effectof anaesthesia and the manipulation of arterialpressure, CO

2 and O

2 tensions. Poor anaesthetic

technique which allows coughing, straining,hypotension, exaggerated hypertension, hypoxiaand hypercarbia will seriously damage the brain.Better results can be obtained by careful monitoringof the patient and attention to simple details than bycomplex pharmacological interventions. It is thepurpose of this article to explain these factors andhow an understanding of them can be applied topatients following head trauma or intracranialdisease.

The brain is only able to withstand very shortperiods of ischaemia, unlike the kidney, liver ormuscle. Thus cerebral blood flow must bemaintained to ensure a constant delivery of oxygenand glucose as well as the removal of “waste”products. Maintenance of cerebral blood flowdepends on a balance between the pressure withinthe skull, intracranial pressure (ICP) and the arterialpressure of the blood, mean arterial pressure (MAP).It is important to maintain a constant blood flow.Thus when blood pressure falls, physiologicalmechanisms attempt to maintain flow to preventischaemia. This process is autoregulation and isexplained in detail later. Similarly, when bloodpressure rises, the same mechanism stops the bloodflow from increasing to excessive levels. If this didoccur, cerebral oedema could develop and the brain

Teaching pointHigh intracranial pressure (ICP) will causeinternal or external herniation of the brain,distortion and pressure on cranial nerves andvital neurological centres. Cerebral perfusionwill be impeded and operating conditions difficultor impossible. Loss of CSF and reduction ofvenous blood volume act to compensate forincreases in brain volume. Once thesemechanisms are exhausted, any further increase,however small, will cause a large increase ICP.

Fig 1a and 1b.

The pressure changes within the skull are drawn inthe classical curve Fig. 2 which indicates an increasein volume with little change in pressure until acertain point is reached when a further small changein volume results in a large increase in pressure: 1-2 compensation phase; 3-4 decompensation phase.

It is interesting to note that this classic curverepresents the alterations in pressure when the

volume of a single compartment within the skull, inthis case CSF, changes. Therefore it is a CSF-pressure volume curve. In practice when theenlargement of the brain is due to a tumour orhaematoma the curve is less steep. Pressure gradientsdevelop within the brain substance and thecompliance or “squashiness” of the tumour isdifferent from that of brain leading to this alteredcurve.

Cerebral swelling leads to herniation of the braineither internally, when the temporal lobe is pusheddown onto the mid-brain through the tentoriumincisura or externally, with the cerebellar pedunclesbeing forced down through the foramen magnum.This causes torsion of the brain stem and a reductionof local cerebral blood flow as the unrelenting risein ICP opposes arterial pressure. Ultimately cerebralperfusion pressure falls to a point when there is nocerebral blood flow, no cerebral perfusion anddeath. The rise in ICP may be accelerated becauseof acute hydrocephalus. This is caused by brain-stem torsion leading to sudden obstruction of CSFflow.

The volume of blood contained within the venoussinuses is reduced to a minimum as part of thecompensatory process. However, should free flowof venous blood be impeded by a number of simplecauses (Table 1) then this increase in volume of thevenous system in a critically swollen brain will leadto a rapid rise in ICP. In practice, it is imperative toensure that when the patient is in the supine orlateral position that a head up tilt to a maximum of30o is obtained. This improves venous drainagewith minimal effect on arterial pressure (1).

Fig. 1a. Schematic representation of normalintracranial contents SSAS = spinal subarachnoid space, FM= foramen magnum, AV = arachnoid villi, CP = choroidplexus. Arrows indicate direction of CSF flow, heavy lines theskull

Fig. 1b. Schematic representation of contents of skullduring raised intracranial pressure

Fig. 2. Brain volume-intracranial pressure relationships: 1-2 compensation phase; 3-4 decompensation phase

Table 1. Non-Pathological causes of raised ICP

Increased Venous VolumeCoughingObstructed airwayHead-down positionObstructed neck veins

Cerebral oedemaAVOID Hypotonic IV solutions

5% Dextrose, Dextrose-Saline,Hartmann's Solution

USE 0.9% Normal Saline

Increased CBFAnaesthetic drugs - see next article


100

80

60

40

20

0

4

Intracranial volume ->

ICP

(m

mH

g)

3

21


CPP = MAP - ICP

Normal cerebral perfusion pressure is 80 mmHg,but when reduced to less than 50 mmHg there ismetabolic evidence of ischaemia and reducedelectrical activity. There have been a number ofstudies on patients with severe head injuries whichhave shown an increase in mortality and pooroutcome when CPP falls to less than 70 mmHg fora sustained period (2,3). Continuous monitoring ofjugular venous bulb saturation is another tool usedto monitor the adequacy of the cerebral circulationwhen it is at risk. Jugular venous bulb saturation isthe oxygen saturation of venous blood in the jugularbulb which is at the base of the skull. The normalrange is 65%-75%. If blood flow to the brain isreduced below a critical point there is a fall invenous saturation. As the flow of blood and deliveryof oxygen is reduced, the brain, in order to maintainits oxygen supply, extracts more oxygen from theblood, leading to a fall in venous oxygen saturation.

More specifically, when CPP is inadequate theoxygen saturation of jugular venous blood falls(normal range 65%-75%) because of increasedoxygen extraction. Does the jugular venous bulbmeasurement give an indication of the minimumlevel for CPP? Chan (4) in another study of head-injured patients showed that when CPP was below70 mmHg, there was a rapid decrease in jugularvenous bulb saturation. It was concluded that whenCPP was less than 70 mmHg cerebral perfusionwas insufficient.

In the head injured patient, CPP should not fallbelow 70 mmHg.

Venous drainage is passive and thus maximised byensuring there is no pressure on, or kinking, of theneck veins. In addition the higher the head, thegreater the effect of gravity on the flow of venousblood. However, as the head is raised, thegravitational effect on the arterial pressure at thebrain is also increased. This is a disadvantage as itreduces the pressure of blood perfusing the brain.The best compromise is the position describedabove of 30o.

The extent of the change in ICP caused by analteration in the volume of intracranial contents isdetermined by the compliance or “squashiness” ofthe brain. In other words if compliance is low, thebrain is stiffer or less “squashable”. Therefore, anincrease in brain volume will result in a higher risein intracranial pressure than if the compliance werehigh. Compliance affects the elastance or“stretchiness” of the walls of the ventricles. Whenthe elastance is reduced the walls are stiffer.Therefore there is a greater change in pressure fora given alteration in brain volume. If a catheter isinserted into a lateral ventricle via a burr hole, thiscan be assessed by injecting 1ml of saline andobserving the change in intracranial pressure. Afterthe injection, if the rise in pressure is more than 5mmHg then the patient has become has becomedecompensated and is at the right hand end of thepressure-volume curve (Fig 2).

CEREBRAL PERFUSION PRESSURECerebral perfusion pressure (CPP) is defined as thedifference between mean arterial and intracranialpressures. Mean arterial pressure is the diastolicpressure plus one third of the pulse pressure(difference between the systolic and diastolic).MAP is thus between systolic and diastolicpressures, nearer diastolic. It is used as it is the bestvalue to estimate the “head of pressure” perfusingin the brain:

Teaching pointIf the patient is lying in the supine position, andit is necessary to turn the head laterally, a sandbag should be placed under the shoulder toreduce the pressure of the sternomastoid on thejugular vein. When patients with severe headinjuries are nursed or transported it must bewith a 30o head up tilt, and the blood pressuremaintained.

Teaching pointCerebral perfusion pressure (CPP) = MAP - ICP

Inadequate CPP (less than 70 mmHg) has beenshown to be a major factor in the poor outcomeof patients with raised ICP. Assessment of CPPis vital and possible either by measurement ofboth ICP and MAP (mean arterial pressure -see text) or by measuring MAP and making areasonable estimate of ICP. During anaesthesiatherefore, if ICP is raised a fall in blood pressuremust be avoided or treated quickly by volumereplacement or catecholamines whichever isrelevant.

pressure by the process of autoregulation. It is apoorly understood local vascular mechanism.Normally autoregulation maintains a constant bloodflow between MAP 50 mmHg and 150 mmHg.However in traumatised or ischaemic brain, orfollowing vasodilator agents (volatile agents andsodium nitroprusside) CBF may become bloodpressure dependent. Thus as arterial pressure risesso CBF will rise causing an increase in cerebralvolume. Similarly as pressure falls so CBF will alsofall, reducing ICP, but also inducing an uncontrolledreduction in CBF.

More recent work has shown that following traumaautoregulation may still be functioning. Boumareported that it was present in up to 69% patientswith head injuries(5). In this situation if CPP fallsbelow the critical value of 70 mmHg, the patientwill have inadequate cerebral perfusion.Autoregulation will cause cerebral vasodilatationleading to a rise in brain volume. This in turn willlead to a further rise in ICP and induce the viciouscircle described by the vasodilatation cascade (fig3a) which results in cerebral ischaemia. This processcan only be broken by increasing the blood pressureto raise CPP, inducing the vasoconstriction cascade(fig 3b). This explains why the maintenance ofarterial blood pressure at adequate level by careful

Therefore continuous consideration of changes inCPP are vital when anaesthetising patients whomay have raised ICP and a fall in arterial pressureoccurs as a result of anaesthetic agents or bloodloss. Ideally ICP should be monitored, but oftenthis is impossible or impractical. However areasonable estimate can be made in head injuredpatients who are not sedated: (Drowsy and confused(GCS 13-15)ICP=20 mmHg, Severe brain swelling(GCS <8) ICP=30 mmHg).

CEREBRAL BLOOD FLOW

The normal cerebral blood flow is 45-50ml 100g-1

min-1, ranging from 20ml 100g-1 min-1 in whitematter to 70ml 100g-1 min-1 in grey matter. Thereare two essential facts to understand about cerebralblood flow. Firstly, in normal circumstances whenthe flow falls to less than 18-20ml 100g-1 min-1,physiological electrical function of the cell beginsto fail. Secondly, an increase or decrease in CBFwill cause an increase or decrease in cerebral arterialblood volume because of arterial dilatation orconstriction. Thus in a brain which is decompensatedas a result of major intracranial pathology, increasesor decreases in CBF will in turn lead to a significantrise or fall in ICP. The physiological factors whichcan alter CBF and hence ICP are listed in Table 2.There are also a number of drugs which can inducearterial dilatation, the most well known being highconcentrations of volatile agents. These will bediscussed in detail in a subsequent article.

AutoregulationCBF is maintained at a constant level in normalbrain in the face of the usual fluctuations in blood


Teaching pointThe following example illustrates the point. A28-year old patient who has had a recent headinjury where he was unconscious briefly,requires urgent abdominal surgery. He isconfused, restless and drowsy. It would bereasonable to estimate his ICP to be 20 mmHg.Following induction of anaesthesia his systolicarterial pressure (SAP) falls to 80 mmHg. Inthis situation MAP will have fallen to 65 mmHgand therefore CPP will have fallen to less than45 mmHg, significantly below the critical valueof 70 mmHg with a significant risk of causingcerebral ischaemia and a poor cerebral outcome.

Teaching pointThere are a number of physiological factorswhich affect or change cerebral blood flow(CBF). Rises in CBF due to hypoxia, hypercapnia(raised blood CO2) and high concentrations ofvolatile agents will cause a rise in ICP once thenormal compensating mechanisms have beenexhausted. Poor anaesthetic technique duringwhich hypoxia, hypercapnia and hypotensionoccur will seriously damage the critically illbrain further.

Table 2. Physiological causes of raised ICP

Hypoxia

Hypercapnia

Pain

Low Cerebral Perfusion Pressure

Exaggerated Hypertension


monitoring and rapid correction if it falls is soimportant.

Carbon dioxide causes cerebral vasodilation. Asthe arterial tension of CO

2 (fig 4) rises, CBF increases

and when it is reduced vasoconstriction is induced.Thus hyperventilation can lead to a mean reductionin intracranial pressure of about 50% within 2-30minutes (6). When PaCO

2 is less than 25 mmHg

(3.3kPa) there is no further reduction in CBF.Therefore there is no advantage in inducing furtherhypocapnia as this will only shift the oxygendissociation curve further to the left, making oxygenless available to the tissues. Acute hypocapnicvasoconstriction will only last for a relatively shorttime (5 hours). While hypocapnia is maintained,there is a gradual increase in CBF towards controlvalues leading which will lead to cerebralhyperaemia (over-perfusion) if the PaCO

2 is returned

rapidly to normal levels (7). When long termventilation is required, only mild hypocapnia (34-38 mmHg: 4.5-5.1 kPa) should be induced. Worseoutcome was reported in patients after head injuriesat 3 and 6 months in those who had beenhyperventilated to low PaCO

2 levels for long periods

(8).

Fig 3b Vasoconstriction cascadeFig 5 Schematic representation between cerebral blood flowand arterial oxygen tension

Fig 3a Vasodilatory cascade

100

80

60

40

20

00 4 8 12 16 20 24

Arterial Po2 (kPa)

Cer

ebra

l blo

od fl

ow (

ml 1

00g

-1

min

-1 )

100

80

60

40

20

00 2 4 6 8 10 12

Arterial Pco2 (kPa)

Cer

ebra

l blo

od fl

ow (

ml 1

00g

-1

min

-1 )

Fig 4 Schematic representation between cerebral blood flowand arterial carbon dioxide tension

Oxygen. Low arterial oxygen tension also hasprofound effects on cerebral blood flow (Fig 5).When it falls below 50 mmHg (6.7 kPa), there is arapid increase in CBF and arterial blood volume.

APPLIED PHYSIOLOGY - HEAD INJURYFollowing acute head injury, the term “secondaryinjury” has been described. The primary injury isdue to the actual trauma. The secondary braininjury is caused by ischaemia due to the combinationof rapid brain swelling and hypotension. Any patientwho is unconscious can easily develop an obstructedairway and become hypoxic, hypercapnic, possiblyhypotensive and have a rise in intrathoracic pressure.Considering the physiological changes describedalready, the process that results in cerebral swellingand raised ICP is clear. In addition, pain from otherinjuries, despite the patient being unconscious, willcause an increase in CBF as a result of both thehypertensive response and local dilatation in therelevant sensory area of the brain. Thus in the initialmanagement of the acutely head injured patientwho is unable to maintain his airway, intubationand hyperventilation should be instituted followingan intravenous anaesthetic agent, and an opiate, toattenuate the response to intubation. The dose mustbe carefully chosen to avoid hypotension in apatient who may also be hypovolaemic.


Teaching pointWhen there is an acute rise in ICP, for exampleafter an acute head injury ICP can be reduced byhyperventilation to lower arterial CO

2 tension.

This technique is used during neurosurgery toreduce brain size to improve access for thesurgeon. In CONTRAST only mildhyperventilation should be used for long termventilation of patients as described above.

Teaching pointIn an article on the management and resuscitationof patients with serious head injuries Gentlemanet al (9) noted that over an 11 year period therewas significant reduction in mortality, (45% to32%) and an increase in patients making a goodrecovery, (42%-58%) associated with areduction in hypoxaemia and hypotension duringtreatment.

Hypotension must be treated aggressively with arapid infusion of colloid or blood and if, necessary,intravenous (ephedrine 3-6 mg, methoxamine 1-3mg).

REFERENCES1. Durward Q J et al. Cerebral and

cardiovascular responses to changes in headelevation in patients with intracranialhypertension. J.Neurosurgery 1983; 59: 938-944.

2. McGraw C P. A cerebral perfusion pressuregreater than 80 mmHg is more beneficial.Intracranial Pressure VII. Edits. Hoff J T &Betz A L. 839-841. Springer-Verlag, Berlin.1989

3. Rosner M J, Rosner S D & Johnson A H.Cerebral perfusion: management protocol andclinical results. J.Neurosurgery 1985; 83:949-962.

4. Chan K H, Miller J D, Dearden N M, AndrewsP J D & Midgley S. The effects of changes incerebral perfusion pressure upon middlecerebral artery blood flow velocity and jugularbulb venous oxygen saturation after severebrain trauma. J.Neurosurgery 1992; 77: 55-61.

5. Bouma G J, Muizelaar J P, Handoh K &Marmarou A. Blood pressure and intracranialpressure - volume dynamics in severe headinjury: relationship with cerebral blood flow.J Neurosurgery 1992; 77: 15-19.

6. Ruben B H. Intracranial hypertension inAdvances in Anaesthesia. Edit. Gallagher TJ. p.1, London Year Book Medical PublishersInc. 1984.

7. Jones P W. Hyperventilation in themanagement of cerebral oedema. IntensiveCare Medicine. 1981; 7: 205-207.

8. Muizelaar J P et al. Adverse effects ofprolonged hyperventilation in patients withsevere head injury: a randomised clinicaltrial. J.Neurosurgery 1991; 75: 731-739.

9 Gentleman D., Dearden M., Midgeley S. &Maclearn D. Guidelines for the transfer ofpatients with serious head injury. BritishMedical Journal 1993; 307: 547-552


ANAESTHESIA FOR EYE SURGERY

Andrei Varvinski, Archangelsk Medical Academy,Troytski, 51 Archangelsk, 163061 Russia

Roger Eltringham, Gloucestershire Royal Hospital,Gloucester, United Kingdom

Surgery on the eye can be performed under eitherlocal or general anaesthesia. In the previous issueof Update techniques for local anaesthesia weredescribed. In this article the principles of generalanaesthesia for eye surgery are outlined.

General anaesthesia for eye surgery presents anumber of special considerations for the anaesthetist.Patients are frequently at the extremes of age and inthe case of the elderly concomitant medicalconditions are not uncommon, particularly diabetesand hypertension. Drugs used in ophthalmologymay influence the course of the anaesthetic. Forexample agents used in the treatment of glaucomamay include timolol, a beta blocking agent, orphospholine iodide which has anticholinesteraseproperties and may prolong the action ofsuxamethonium.

The anaesthetist must be familiar with the factorswhich influence intra-ocular pressure (IOP). Thisis the pressure within the eyeball and is normally inthe region of 10-20mm Hg. When the surgeon isoperating within the globe (eg cataract surgery) it isimportant that the anaesthetist controls the IOP. Arise in the IOP will impair the operating conditionsand may cause an expulsion of intraocular contentswith permanent damage to the eye. On the otherhand a mild reduction in IOP will improve operatingconditions for the surgeon.

A rise in IOP can generally be attributed to one ormore of the following: pressure from outside, anincrease in the volume of blood in the vesselswithin the eye or an increase in the volume ofaqueous or vitreous humor.

Factors increasing IOP include:1. External pressure eg face mask2. Raised venous pressure, eg by coughing,

straining, vomiting3. Raised arterial pressure4. Hypoxia and hypercarbia which cause

vasodilation of intraocular blood vessels5. Suxamethonium - the precise mechanism is

unknown but may be due to contraction of

extraocular muscles during fasiculation ordilation of blood vessels. The effect ismaximal at 2-4 minutes returning to normalwithin 7 minutes.

6. Ketamine

Factors lowering IOP include:1. Reduced venous pressure, eg. head up tilt.

2. Lowered arterial pressure - at systolicpressures <90mm Hg IOP is proportional tothe blood pressure.

3. Hypocarbia by constricting choroidal vessels.

4. Intravenous induction agents (exceptketamine).

5. Inhalational agents (the fall in IOP isproportional to the inspired concentration).

6. Non-depolarising muscle relaxants.

7. Reduction in aqueous volume, eg byacetazolamide which inhibits production.

8. Reduction in vitreous volume, eg by mannitolwhich exerts an osmotic effect.

A suitable technique for intraocular surgery inadults is as follows:

Premedication. Oral diazepam 0.1 - 0.2mg/kg.Heavy sedation with opiates is best avoided becauseof the dangers of respiratory depression andhypercarbia.

Induction: Thiopentone 4mg/kg

Suxamethonium 1mg/kg

Laryngoscopy. This should not be performed untilthe patient is fully paralysed in order to avoidgagging or coughing. Topical anaesthesia to thelarynx and trachea with 4% lignocaine will reducethe incidence of coughing especially if the head ismoved.

Maintenance. N20:02:halothane 0.5 - 1% (orequivalent concentration of other volatile agent).Vecuronium 0.1mg/kg administered before theeffects of suxamethonium have worn off. IPPV toproduce moderate hypocarbia.

Position. Head up tilt to reduce venous pressure

Monitoring. ECG, oximeter, capnograph andperipheral nerve stimulator should be used ifavailable. In situations where full monitoring isnot available it is probably safer to administeratropine or glycopyrrolate routinely with the


induction of anaesthesia to prevent the bradycardiawhich may occur during manipulation of the eyedue to the oculocardiac reflex.

Reversal. Continue volatile agent until reversal iscomplete and spontaneous respiration is resumedusing atropine or glycopyrrolate and neostigmineas required.

Extubation. This should be accomplished with thepatient on their side. An anti-emetic may beadministered to minimise the incidence of postoperative vomiting.

Post Operative Analgesia. Morphine 0.1mg/kg ifrequired. No food or drink should be administeredfor 3 hours to reduce the possibility of aspiration ofgastric contents.

If muscle relaxants are unavailable and the patientbreathes spontaneously the depth of anaesthesiamust be increased to prevent coughing or strainingagainst the tube. This technique however carriesthe additional disadvantages of subsequenthypercarbia, hypotension and a prolonged recoveryperiod. Some anaesthetists use a reinforced laryngealmask with spontaneous respiration for someophthalmic operations.

Penetrating Eye InjuryWhen the globe has been penetrated the IOP isreduced to atmospheric pressure. An increase inIOP during induction may cause expulsion ofintraocular contents and permanent damage to theeye.

If the repair is carried out as an emergency procedurethe patient must be assumed to have a full stomachand requires a rapid sequence induction. Duringpre-oxygenation care must be taken not to exertpressure on the eye by the face mask.Suxamethonium is theoretically contra-indicatedas it causes a rise in IOP. The anaesthetist musthowever weigh the risk to the eye against the risk ofaspiration of gastric contents.

If intubation is anticipated as being uneventful alarge dose of a non-depolarising relaxant (egvecuronium 0.15mg/kg) may be substituted forsuxamethonium and a modified rapid sequenceinduction performed. Care must be taken to allowtime for full muscle paralysis to occur beforelaryngoscopy is attempted meanwhile, cricoid

pressure is maintained.If, however, difficulties are anticipated withintubation suxamethonium should be used toprovide the best intubating conditions as rapidly aspossible despite the theoretical risk to the eye. Inpractice the risk is minimised by the prioradministration of an induction agent which reducesIOP.

Once intubation has been achieved anaesthesia isconducted using the general principles describedabove.

Strabismus SurgeryDuring surgery for the correction of strabismustraction on the extra ocular muscles may causesudden and profound bradycardia via the oculo-cardiac reflex mediated by the vagus nerve. Thiseffect is also occasionally seen during other formsof eye surgery eg retinal detachment.

When this occurs the surgeon must be immediatelyalerted as the normal heart rate is generally restoredwhen traction is released. If this does not occur anintravenous bolus of atropine 0.02 mg/kg may berequired. It is important that the anaesthetistcarefully monitors the heart rate throughout theoperation, preferably using an audible warningdevice so that the surgeon is aware of changes inheart rate. Intravenous access must be assured andatropine drawn up and ready for immediate use. Inpaediatric patients with their increased vagal tonethe prophylactic administration of atropine beforethe commencement of surgery is advisable.

Examination Under AnaesthesiaAlthough endotracheal intubation is required formost patients requiring general anaesthesia for eyesurgery, examination of the eye in children canoften be provided satisfactorily via a face mask. Ifthe naso-lacrinal duct is to be irrigated steps shouldbe taken to avoid respiratory obstruction due tolaryngospasm. This can be achieved either byintubation or positioning the patient with a pillowunder the shoulders to divert irrigation fluid awayfrom the larynx.

Ketamine can also be used for examination of theeye but pre-medication with atropine is essential toprevent laryngospasm caused by excessivesecretions.


ANAESTHESIA IN CHILDREN USINGTHE EMO SYSTEM

Mr Peter Bewes, Continuing Medical Education,c/o Department of Surgery, Makerere UniversityMedical School, PO Box 4127, Kampala,Uganda

In some places, by necessity, children undergoanaesthesia with inadequate facilities. Transport toanother unit is frequently not an option and thefollowing article describes a method to adapt theEMO system for use in children under 15kg. Thetechnique requires anaesthesia training and shouldnot be attempted by someone without the ability tointubate.

The concept is to use the EMO with a T piece andcontinuous flow. Two people are required; theanaesthetist who anaesthetises the child using astandard T piece and an assistant who pumps theOxford inflating bellows continuously so that thereis always a flow of ether in air +/- oxygen throughthe T-piece. This minimises the work of breathingfor the child and ensures adequate amounts of etherare produced by the EMO.

The Oxford inflating bellows should have themagnet removed from the flap valve and the T piececonnected to the bellows outlet. The T piece can beused with a mask or endotracheal tube (fig. 1).

Induction of anaesthesia using ether. With alarger child you may be able to get good co-operation by “talking the patient to sleep” as youadminister the anaesthetic, but in babies it is ofteneasier to wrap them in a blanket to keep the armsand legs still while the baby cries and inhales theanaesthetic ether.

Ether is a very strong smelling vapour that stimulatesa lot of secretions. In order to prevent problems

give atropine in appropriate doses (around 0.02mg/kg) intravenously or intramuscularly beforeinduction of anaesthesia.

The strong smell of ether frightens many patients,so introduce it gradually. I like to let them breathethrough the mask for a few breaths before attachingit to the T piece. This allows time to check that themask fits the face properly and reassures the patientthat they are not being suffocated. Then tell thepatient that they will smell a strange smell (notunpleasant) and, with the ether concentration leveron the EMO set to transit, connect up the face maskto the T-piece. At this point start your assistantpumping the Oxford inflating bellows 8 times perminute to produce a near continuous flow of gasuntil the end of the operation when anaesthesia isfinished.

Initially the child will detect the residual vapourfrom the rubber tubing, and will get used to thesmell without the feeling of being poisoned! Aftera minute or two, nudge the ether concentrationlever from the transit position to give a weakconcentration of ether. Reassure the child that the“nice smelly stuff” will make him feel sleepy.Keep the face mask snugly fitted to the patient’sface, so that there is no leak. Slowly nudge theconcentration up to 2%, always allowing at leastfour cough-clear breaths between nudges, and neverincrease the concentration by more than one halfper cent. If the patient coughs or objects, nudge itback one step and wait for six clear breaths (withoutswallowing or breath-holding) and talk reassuringlyto the patient saying all is well - then increase theether concentration slowly. All the time keeptalking gently, quietly and confidently until youhave reached an ether concentration of around10%.

< air

<

O2

Fig.1. A slow steady pumping action will provide a near continuous flow of ether vapour.

Keep your finger on the patient’s pulse during theentire induction, or better still have a paediatricstethoscope attached to his chest. Keep listeningand watching the chest to make sure that air is goingin and out freely. In stage 1 of anaesthesia, theeyelash reflex goes. In stage 2 there may be somestruggling, and the patient will need reassuredwhile an assistant holds their limbs. The patientmay vomit at this stage and need to be turned ontheir side and have their pharynx cleared withsuction. During this stage the pupils may dilate,and breathing begins to become irregular. In stage3 (the stage of surgical anaesthesia) there are 4described planes. The first is plane 1 during whichthe respiration becomes more regular but the pupilsare not central. The second is plane 2 when thepupils are central and it is safe to insert a Guedelairway. With deeper anaesthesia the pupils maybegin to dilate (although the atropine may maskthis).

Minor surgery can be done in plane 1 (incision ofabscesses etc.). Most general surgery can beperformed in plane 2. In plane 3 there is progressiveparalysis of the intercostal muscles, which can bedetected by careful observation of the pattern ofbreathing. If it becomes “see -saw” in character,with paradoxical movement of the chest (fallinginstead of rising on inspiration) anaesthesia isbecoming too deep and the face mask should beremoved for a few breaths whilst reducing the etherconcentration to a more satisfactory maintenancelevel. In general this is 6 to 8% for surgicalprocedures that do not require any muscularrelaxation, or nearer 8-10% for intra-abdominalprocedures requiring relaxation. Be careful not tooverdose the patient.

Stage 4 of ether anaesthesia is marked by shallowrespiration and if it occurs should be treatedimmediately by removing the mask and reducingthe ether concentration. Be prepared to assistventilation and if respiratory arrest occurs switchthe ether setting to “Transit” and ventilate thepatient via the T-piece.

During the operation continue to monitor the childclosely paying particular attention to his colour,airway, respiration and cardiovascular signs.Towards the end of the operation allow the patientto lighten by adjusting the ether setting towards 2%or less. With abdominal surgery do not do this too

early as closure may prove difficult. At the end ofthe operation the patient should be breathing air andthe face mask may be removed. Ensure that theairway is completely clear before handing the patientover to the nurse in the recovery position.

Practical points: Aim at a steady level ofanaesthesia and do not allow the patient to get toodeep. Never let the surgeon start until you are ready.If laryngeal stridor develops, allow a few breathsof air and then continue more slowly. However, ifspasm develops during surgery, it means the patientis too light for the procedure. Ask the surgeon tostop and deepen anaesthesia until the stridor stops.Add some oxygen to the circuit if possible.

The safety of this technique is considerablyincreased by adding oxygen to the inspired mixture.It should be put into the circuit upstream (before) ofthe EMO vaporiser using some sort of reservoir.Around 1 litre/minute is adequate duringmaintenance. During induction this should beincreased to around 3 to 4 litres/minute.

The technique may also be used with intubation andcontrolled ventilation. This is the preferredtechnique for longer procedures and in smallerchildren. If muscle relaxants are used then anintravenous induction may be performed, less etherwill be required for maintenance and recovery willbe faster.

Editor’s note: The EMO can also be used with a Tpiece by connecting the vaporiser inlet to a sourceof continuous gas flow (eg Boyles machine, oxygencylinder etc). Connect the T piece to the outlet ofthe EMO. The EMO does not work so efficientlywhen used as a plenum vaporiser and needs acontinuous fresh gas flow of 10 litres/minute toproduce adequate concentrations of ether.

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2

Fig.2.



UPDATE ON THE INTERNET

Dr Michael DobsonConsultant Anaesthetist.

You can now receive an electronic version ofUpdate in Anaesthesia - you can read it on yourcomputer screen (using free software which weprovide). You can use the electronic version whetheror not your computer is connected to the internet.

The electronic version of Update in Anaesthesiacontains almost all the articles ever published inUpdate, together with illustrations. The softwareallows you to search, read and print out selectedmaterial, or to print whole issues if you wish. Youcan make as many reprints as you want wheneveryou need them. This should be of considerable helpto teaching centres.

You do not need the latest and most expensive sortof computer to make use of Electronic Update. A286 PC should be adequate. If you need technicaladvice please write to Dr. Mike Dobson, NuffieldDept of Anaesthetics, John Radcliffe Hospital,Oxford OX3 9DU, UK or send an email request [email protected]

We will need to know a few details about yourcomputer model and operating system [e.g. DOS,Windows 3.x, Windows 95] to ensure that we sendthe correct software for you to use. If you don’thave internet access but do have a computer we canpost you the same materials on floppy disk withinstructions for use (this offer applies only toaddresses in developing countries).

If you have an internet connection you can accessUpdate at

http://www.nda.ox.ac.uk/wfsa/

This site also has links through which you candownload the necessary free software to use Updateoff-line, as well as downloading the issuesthemselves. (To download a complete issue -about300k - via a telephone link will take 2-3 minutes)

If you have a local contact or (for example) BritishCouncil library, with internet access, you can askthem to do the downloading and printing for you.Update is supported by the UK Department forInternational Development (formerly ODA)

Electronic Update has been available for only a fewmonths, but has already been used by anaesthetistsin 56 different countries.

Sponsored by: World Federation of Socieities of Anaesthetists

Typset by: Clinical Graphics, Royal Devon & Exeter Healthcare NHS Trust, Exeter, UK.

Printed in Great Britain by: Media Publishing

Correspondence to: Dr I H Wilson, Anaesthetics Dept., Royal Devon & Exeter Healthcare NHS Trust, Barrack RoadExeter, EX2 5DW, UK.

Subscriptions to: Dr Ray Sinclair, Department of Anaesthesia, Royal Truro Hospital(Treliske) Truro, Cornwall, UK.

PRACTICAL PROCEDURE FOR DEALINGWITH STICKING OMV’S

Mike Yeats, Equipment Maintenance, DerrifordHospital, Plymouth

The Oxford Miniature Vaporiser is designed fordrawover anaesthesia and rarely give problems.Occasionally the pointer becomes stiff to rotate dueto deposits of thymol left behind by halothane. Thefollowing simple procedure should be carried outonce a month or whenever the control lever becomestiff to operate.

Place a bung in the inlet side of the OMV, turn thevaporiser on to its side and pour in some some etheror methylated spirits or halothane whilst movingthe pointer to and fro. The vaporiser should becompletely filled and allowed to stand for 5 minutesbefore emptying. If you are using ether or halothaneperform this procedure outside to avoid inhalingthe fumes. Empty the fluid out of the vaporiser andblow it through with air for 10 - 15 minutes. If thisprocedure does not free the lever the next issue ofUpdate will describe how to deal with a completelyjammed vaporiser.

w a update in anaesthesia - smile train · paediatric anaesthesia covering the basics of anatomy,...

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