Personal Practice

Archives of Disease in Childhood, 1972, 47, 661.

The Management of Acute Croup*R. S. JONES

From the Institute of Child Health, Alder Hey Children's Hospital, Liverpool

Croup is an inflammatory condition of the larynxor trachea accompanied by stridor, which is theharsh noise characterizing upper airway obstruction,as opposed to wheezing which characterizes lowerairway obstruction. The sound may be of highor low pitch and is due to sound waves set up bythe fast flow of air past a narrow point in the airway.This causes stridor of medium or high pitch,chiefly during inspiration. Stridor may however,be of low pitch and rattling in quality when sur-rounding tissue structures are set into oscillatorymotion. This applies particularly to the epiglottisand aryepiglottic folds. Stridor arises primarilyfrom the larynx but may be caused at any pointbetween the pharynx and upper trachea (Fig. 1).The anatomy of this region is crucial to the positionand nature of the obstruction, which varies accord-ing to the main site of impact of the inflammatorylesion. Anatomy is also important in that theremay be underlying structural abnormality, which isdiscovered by superimposed inflammation andmodifies the subsequent course of the disease andits management.

Anatomy and Pathology of the LarynxThere are four levels at which obstruction may

occur: at the introitus, the vestibular fold, the vocalfold, and the subglottis. The first three are mobilestructures and act as sphincters to close off theairway when the controlling muscles contract.The fourth is a rigid structure with walls formedby the cricoid cartilage.The first laryngeal sphincter is formed by the

aryepiglottic folds with the epiglottis anterior andthe arytenoid cartilages posterior (Fig. 1). Thearyepiglottic folds are thick, fibromuscular, andrelatively mobile structures, especially in earlyinfancy. Closure of the orifice is brought about bycontraction of the muscles lying in the lateral wallof the fold (aryepiglottic, thyroarytenoid, and

*In the Personal Practice series of articles an author is invited togive his own views on some current practical problem.

cricoarytenoid) and posteriorly between the twoarytenoid cartilages, the transverse or interary-tenoid muscle. Any inflammation may narrow theintroitus to a critical degree, especially during thefirst few years of life when the structures are smallbut essentially normal, e.g. epiglottitis. Whenthere is an anatomical abnormality, inflammationmay readily precipitate obstruction: for example,small, mobile, or backwardly displaced epiglottis;cyst on the aryepiglottic fold; pharyngeal mass(Table).

TABLELocal Conditions Which May Predispose to Acute

CroupCongenital small larynx (laryngomalacia)Congenital laryngeal webAbductor paralysisTumour or cyst of pharynx, larynx, or tracheaCompression of pharynx, larynx, or trachea from without

The second pharyngeal sphincter is formed by thevestibular folds (or false cords) of fibroelasticstructure. They lie above the vocal cords and areseparated from them by the vestibule (Fig. 1).Closure of the airway by approximation of thesestructures is achieved by contraction of musclespassing around the lateral wall of the larynx in thesefolds to the arytenoid cartilages (thyroarytenoid andcricoarytenoid muscles). This sphincter is fullyeffective without the aid of the vocal cords. Inflam-mation is less critical here but acute oedema dueto allergy, or the inhalation of chemical agents, orhot gases evolved during a fire may narrow theorifice and frequently involves both the vestibularand aryepiglottic folds. A foreign body may wedgeabove the fold or in the vestibule and set upsecondary inflammation.The third sphincter is formed by the true vocal

cords which are fibroelastic structures attached tothe thyroid cartilage anteriorly and to the vocalprocess of the arytenoid cartilages posteriorly.Adduction is brought about by contraction of thelower fibres of the thyroarytenoid muscles which

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R. S. Jones

Epiglottis

-- ~~~Ary-epiglottic fold

Thyroid cartilage

Vestibular fold

- \t.1/ Vocal fold (glottis)

Cricoid cartilage

FIG. 1-Anatomy of larynx at 1 year of age. Levels at which obstruction may occur: 1, supraglottic obstruction at theintroitus (epiglottis and aryepiglottic folds) which form the first laryngeal sphincter; 2, at the vestibular fold andvestibule, the second laryngeal sphincter; 3, at the glottis, the third laryngeal sphincter; and 4, subglottic, at the level

of the cricoid cartilage.

lie in the vocal folds (vocalis muscle). Apart fromvoluntary movement, adduction may be inducedreflexly by the presence of irritant or foreignmaterial in the larynx, causing stridor especiallyon inspiration. Loss of phonation or hoarsenesscharacterizes inflammation of the cords.

All the muscles mentioned are innervated by therecurrent laryngeal branches of the vagus nerve,the centre being in the nucleus ambiguous of themedulla. Unilateral paralysis causes hoarsenessbut no stridor. Bilateral paralysis causes inspira-tory and expiratory stridor with breathlessnessdue to obstruction. Again, superimposed infec-tion may initiate or accentuate symptoms.The fourth level at which obstruction may occur

is the subglottic or cricoid region. Unlike theothers, the walls are not mobile and are formed bythe cricoid cartilage. It is shaped like a signetring with a quadrangular lamina posterior and anarrow anterior arch. It forms the narrowestpart of the larynx and determines the largestdiameter of endotracheal tube which can be inserted.Obstruction at this point may be due to inflamma-tion which is part of a laryngotracheobronchitisinfection, or acute oedema following removal of anendotracheal tube which has traumatized the mucosa.Subsequent deposition of debris on an ulceratedmucosal surface may cause obstruction and subse-quent postinflammatory stenosis may follow.

Tracheal narrowing due to a variety of causes(Table) may cause stridor which has to be distin-guished from laryngeal causes.

Physiological Consequences of ObstructionObstruction which is of the vibratory, inspiratory

type, and usually due to a mobile epiglottis partlyobstructing the entrance to the larynx, causesmarked stridor but little or no breathlessness anddoes not materially interfere with ventilation.A pedunculated polyp may cause similar symptomsbut is potentially serious because it may causecomplete obstruction with little warning. Incontrast, other causes of stridor are accompaniedby increase of respiratory effort which maintainsventilation. Tidal volume decreases but alveolarventilation is maintained by increase of respiratoryrate. The exception is the neonate who mayrespond to airway obstruction with decrease ofeffort, presumably because his capacity to respondto airway obstruction is not fully developed.Increase in airway resistance results in slight hypo-ventilation, a small increase of a few millimetres inarterial Pco2 and decrease in Po2. The compen-satory increase in the force of contraction of respira-tory muscles maintains ventilation and blood gaslevels near to normal until a late stage. An airwaypressure of 5 to 10 mmHg is associated with the

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The Management of Acute Croupsubjective sensation of breathlessness and theobjective appearance of increase of respiratoryeffort. Appreciably greater airway pressures canbe achieved but only for short periods of time (afew minutes) without acute discomfort. A muchhigher respiratory muscle work load is thereforepossible for a short time but cannot be sustainedwhen the obstruction is prolonged beyond a fewhours. Indeed there is an approximate inverserelation between the degree of obstruction and theduration for which ventilation can be maintained.

Failure of compensation is produced by decreaseof respiratory effort, causing decrease of tidalvolume, slowing of rate with irregularity of rhythm.These terminal events are associated with grosshypoventilation, arterial Pco2 rising to > 100mmHgand P02 falling to < 50 mmHg. The resultinggeneralized progressive tissue hypoxia causes lacticacidosis. Hypoxia, hypercarbia, and lactic acidosistogether depress cardiac function, the fall in cardiacoutput causing decrease of cerebral blood flow,depression of the respiratory centre, and cardio-respiratory arrest soon follows. This sequenceof events proceeds rapidly once the rate ofwork output (i.e. power output) of respiratorymuscles begins to fall. The exact mechanism ofrespiratory failure in these circumstances is notclear, but it seems likely that fatigue of respiratorymuscles causes critical reduction in their workcapacity. If the limit of their power output(work per unit time) is exceeded because the workload is too high, or continues for too long, thenhypoventilation will develop sooner or later. Thepatient should be observed carefully for decreaseof stridor. It may indicate improvement, but onthe other hand it may signal deterioration. In theformer situation the blood gases are normal but inthe latter they are abnormal and there is lacticacidosis.

Tachycardia, excessive sweating, and peripheralvasodilatation are the consequence of increase inautonomic activity, stress, and a raised metabolicrate. Increase of oxygen consumption and feverare due not only to the infection, but to the increasedwork of respiratory muscle. There is an increaseof circulating catecholamines. At a late stage,decrease of cardiac output is accompanied by peri-pheral vasoconstriction with pallor and/or cyanosis,the latter being a reflex attempt to maintain arterialpressure. Dehydration due to impaired fluidintake causes hypovolaemia, and this, together withthe above factors, contributes to the precipitationof acute low output circulatory failure. Brady-cardia is accompanied by a variable degree of heartblock with ST segment elevation or depression.

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At this stage the Pao2 is <50 mmHg and thePaCo2 > 100 mmHg.

Such late signs as these involve imminent dangerof cerebral injury due to hypoxia. The crux ofmanagement is to relieve the obstruction in time toprevent respiratory and circulatory failure.

In the various lesions to be discussed below,respiratory failure may at any stage be exacer-bated by two additional factors. (1) Desiccatedsecretions accumulating in the lower airway dueto an ineffective cough (especially in the younginfant) or to dehydration. (2) A pneumothoraxproduced by the increased respiratory effort causedby airway obstruction.

DiagnosisIt is essential to establish a diagnosis and in

particular to define whether the partial obstructioncausing symptoms has arisen in an airway whichwas formerly normal or whether there is pre-existing disease (Table). The latter group requiresa radically different approach to treatment.

History. A history of previous attacks suggestslaryngotracheobronchitis, whereas this history isusually absent in epiglottitis. Stridor dating backto birth or present between respiratory infectionssuggests an underlying abnormality. There maybe no suggestive history when a foreign body partlyobstructs the upper airway, but the absence ofassociated infection or persistence of stridor,should arouse suspicion. The history is usuallyclear cut when the cause is thermal or due to chemi-cal burns after inhalation of noxious gas or vapour.Inquiries should be made regarding past infectiousfevers and recent exposure to infectious cases.

Examination. The mouth, nose, and pharynxshould be examined carefully for evidence ofinflammation, trauma, and Koplik spots. Aninflamed epiglottis may be visible over the back ofthe tongue when this is depressed. The pharynxshould be inspected for distortion due to a mass.An enlarged tongue, retrognathos, a short neck, orother external deformity may suggest an underlyingabnormality of the upper airway. The neck shouldbe inspected for the presence of masses or trachealdisplacement.

EpiglottitisThis is an acute inflammation of the epiglottis

and aryepiglottic folds which occurs mainly in the1- to 7-year age group. It is caused by the Haemo-philus influenzae type B in most instances. Thisorganism may be isolated from the pharynx andfrequently also from the blood stream (Rabe, 1948).

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There is an accompanying polymorphonuclearleucocytosis. The septicaemic spread and the factthat H. influenzae type B is the organism whichalso causes meningitis have been stressed by someauthors. However, in my experience of 30 cases,clinical manifestations have been confined to thelarynx, with signs of airway obstruction. Whensteps have been taken to relieve this in good time,the illness has been no more severe than tonsillitis.The disease has been recognized for many years

(Sinclair, 1941; Alexander, Ellis, and Leidy, 1942;Rabe, 1948; Miller, 1949; Jones and Camps,1957; Jones, 1958), but only recently has its clinicalimportance and potentially lethal nature beenappreciated (Johnstone and Lawy, 1967; Gardneret al., 1967; Andrew, Tandon, and Turk, 1968;Jones, 1970). Baxter (1967) estimated that itcomprised 8% of admissions with upper airwayinfection to the Montreal Children's Hospital, andPhelan and Williams (1968) reported 22 cases seenduring a 3-year period in Melbourne.There is usually no history of previous attacks

and the mode of onset is acute, with malaise, fever,dry cough, loss of appetite, and the onset of stridor.Signs of obstruction may occur within a few hours;a rapid onset usually heralding a severe attack.It is this feature that distinguishes supraglotticlaryngitis from the predominantly subglottic laryn-gotracheobronchitis. The disease runs a courseof 4 to 7 days, fever subsiding after 48 to 72 hours.Stridor is predominantly inspiratory. The pharynxmay appear normal, yet enlargement of cervicalglands suggests infection. This should prompt anexamination of the pharynx and on depression ofthe base of the tongue the epiglottis may be seen asa red oedematous structure. A more detailedlaryngoscopic examination may be necessary toestablish the diagnosis with certainty. The charac-teristic appearance of the supraglottic region isshown in the photograph which was taken from afatal case (Fig. 2).

Management. The patient is best nursed wellpropped up with pillows. Reassurance is impor-tant, but sedation should be used with caution.Light sedation is likely to be ineffective whereasheavy sedation will produce stupor (difficult todistinguish from the effects of hypoxia) and depressrespiratory effort. Trimeprazine tartrate (Valler-gan) 2 mg/kg is suitable. Ampicillin is givenintramuscularly. Streptomycin may be added butis usually not required. If stridor occurs early,i.e. within 12 hours, hydrocortisone 100 mgIMis indicated and may well be repeated 6-hourly for24 hours.

The child should be transferred to hospital ifthere is appreciable increase of respiratory effortand restlessness sufficient to cause interference withsleep and feeding. Evidence of cyanosis is ofserious significance. When there is any doubtaboutthe severity or possible course of the disease overthe next few hours, admission to hospital should beadvised.

In hospital, the child is nursed in an oxygen tentinto which humidified oxygen-enriched gas ispassed to give a concentration of 30 to 40% oxygen.It is important that the tent be transparent and thehumidity insufficient to cause a fog. The childmust be clearly visible at all times and be underconstant surveillance so that the nurse can giveearly warning of deterioration. The face shouldbe observed for colour of lips, and the chest forrespiratory rate and effort. Instruments for endo-tracheal intubation or tracheostomy should be athand. Swallowing may be difficult and droolingmay occur. Pharyngeal suction is indicated asoften as required to remove secretion which mayaccumulate in the pharynx.

Indications to relieve obstruction. In mostinstances these measures will result in diminutionof obstructive symptoms within a few hours.Persistence of obstructive signs, namely appreciableincrease of respiratory effort, sufficient to causerestlessness, interference with sleep and feeding,together with any evidence of cyanosis in the oxygentent, are indications to relieve obstruction. A raisedarterial Pco2 (> 50 mmHg) is also an indication torelieve obstruction, but a figure within the normalrange does not contraindicate relief when the clinicalevidence is present.The passage of an endotracheal tube by the oral

FIG. 2.-Acute epiglottitis. Appearance at necropsy ofthe epiglottis and aryepiglottic folds which are grosslycongested and oedematous, larynx unopened A child of6 years who sustained hypoxic brain injury due to acute low-output circulatory failure before admission to hospital.

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The Management of Acute Croupor nasal route, or a tracheostomy, are both effectivemethods of relief. When the appropriate skill isavailable the passage of an endotracheal tube ispreferable. It has the advantage that since thetechnique is simple, it can be implemented earliergiving a greater margin of safetyand thus minimizingthe possibility of collapse with the great likelihoodof disastrous sequelae due to cerebral hypoxia.The presence of the tube does not aggravate theinflammatory lesion. The technique of intubationthrough the inflamed entrance to the larynx has notproved to be a problem in skilled hands. Once thetube is in place the child experiences marked reliefand usually goes straight off to sleep. The swallow-

ing of fluids may be possible but when there isreluctance or any difficulty, a fine plastic tube shouldbe inserted through a nostril into the stomach, andvia this appropriate hydration and nutrition can beensured. The tube should be left in situ for 48hours after which it is removed and the patientcarefully observed for evidence of obstructivesymptoms. If these are present it may be necessaryto reintubate for a further 24 or 48 hours. Oncethe subject has been intubated, the general course

of the disease is very similar to that of tonsillitis.When the skill required to insert an endotracheal

tube is not available, tracheostomy is indicated.It provides effective relief but because it is an

operative procedure with residual scar formation,the tendency is to delay longer with increase ofattendant risks.

LaryngotracheobronchitisThis common respiratory infection in the 1- to 5-

year age range may also be associated with obstruc-tion at laryngeal level. It is a virus infection inmost instances but secondary bacterial involvementoccurs. There is usually a clear history of recur-

rent attacks with malaise, cough, and fever,followed after 24 to 48 hours by stridor. Sometimesstridor occurs early in the attack and there may or

may not be preceding upper respiratory tractinfection. Stridor is inspiratory and expiratoryand of variable degree. A cough is prominentand may be productive. On examination, thesigns of airway obstruction are the same as thosefound in epiglottitis. The obstruction in thisdisease is predominantly subglottic. The walls ofthe trachea are red and oedematous. There maybe a deposit of exudate which tends to dry andencrust. A variety of organisms may be isolatedfrom this exudate, including nonhaemolytic andhaemolytic streptococci, and staphylococci (Davi-son, 1966). There may be rales over the lung fieldsdue to bronchitis.

The general principles of management are similarto those advocated in epiglottitis. Adequatehumidification with an ultrasonic humidifier isparticularly important to liquefy and prevent furtherdrying of secretion.Mucopurulent secretion accumulates in the

lower airway and may also cause obstruction.Intermittent pharyngeal suction removes materialat the entrance to the larynx, and also stimu-lates coughing which causes secretions to beexpectorated from the major airways. This isparticularly important in the child under 2 yearswho is less co-operative and cannot otherwise beencouraged to cough and remove secretion. Whenthe child will tolerate it, the right and left lateralposition with head dependent should be adopted4 times daily with the object of aiding removal ofsputum. During these sessions physiotherapy andcoughing are encouraged.

Despite the fact that virus infection initiates thedisease, bacteria are frequently also present,especially after intubation which increases the riskof contamination of the respiratory tract. Hencewide spectrum antibiotic cover with ampicillin andcloxacillin is required in the first instance.

Corticosteroid therapy is advocated by a numberof authors (Novik, 1960; Pennington, 1964;Davison, 1966). It is probably of help in relievingobstructive symptoms during the 48 hours afteradmission and is advised as for epiglottitis.The indications for relief of obstruction are the

same as in epiglottitis. An endotracheal tube isagain preferable to tracheostomy. The exceptionis the subject in whom the larynx as a whole isstructurally smaller than normal due to a localizednarrowing in the subglottic region which will notadmit an endotracheal tube of adequate size.

Measles

Upper airway obstruction causing stridor mayoccur prior to the exanthem of measles. There ismalaise, fever, conjunctival and nasal congestion:Koplik spots are usually evident. Obstructivesymptoms occur chiefly in the 3- to 6-year agegroup. In most instances stridor is not severe,but, in a few, relief of obstruction is necessary.Management is along similar lines to that already

described except that antibiotics and steroids are notindicated. Feeding via a nasogastric tube may benecessary. The indications for relief of obstructionare as described for epiglottitis and the method ofchoice is a nasoendotracheal tube. This is leftin situ for 1 to 3 days after which it may be removed,the subsequent course being uneventful.

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Laryngeal DiphtheriaLaryngeal diphtheria, though rare in this country,

should still be mentioned. There may be nomembrane visible in the pharynx. Hoarseness isa feature since the cords are involved. Two tothree days may elapse before obstructive symptomsoccur (Davison, 1966). Antitoxic serum 20,000 to100,000 units, one half IV, is given after testing forserum sensitivity. Penicillin and erythromycinare effective antibiotics. Tracheostomy for reliefof obstruction is advocated (Lang, 1965). A naso-gastric feeding tube is required if there is palato-pharyngeal paralysis.

Foreign BodyA foreign body may wedge in the larynx imme-

diately above or below the glottis. A less commonposition, which may easily be missed on laryngo-scopy, is in the upper oesophagus where it mayobstruct the entrance to the larynx. The danger ofobstruction in these situations is that it maysuddenly become complete thus asphyxiating thesubject. When the previous history is negativeand there is no evidence of an inflammatory diseasethe possibility should always be considered andlaryngoscopy undertaken. No further measuresmay be necessary after removal but when traumato the mucosa has been sustained hydrocortisone100 mgIM 6-hourly and an antibiotic are indicated.Should obstructive symptoms follow, tracheostomyis indicated in order to ensure no further injury tothe larynx and to allow laryngoscopic inspectionfrom time to time.

Primary Disease of Larynx and TracheaThe possibility of an underlying abnormality of

the larynx should always be considered whenevidence of upper airway obstruction (1) presentsin early infancy; (2) recurs frequently or is severeduring upper airway infection; (3) persists in theabsence of infection or after it has cleared up.

Obstruction due to infective causes is aggravatedby the primary disease and frequently renders thecondition potentially serious (Table).

Congenitally small larynx-laryngomalacia.The larynx as a whole is smaller than normal sothat any infection causes a critical degree of narrow-ing. This condition tends to declare itself during aninfection in early infancy. The diagnosis isestablished by laryngoscopy. Relief of obstructionduring an infection by passage of an endotrachealtube is contraindicated since not only is intubationdifficult but a tube which can be passed safely

may be too small to provide an airway andreadily becomes obstructed by secretion. A tubeof adequate size would readily cause pressure necro-sis especially in the subglottic area, with the atten-dant risk of subsequent stenosis on healing. Atracheostomy is therefore required and it is occa-sionally necessary to retain it for a year or twountil the larynx enlarges sufficiently for the dangerfrom recurrent infections to have disappeared.

Other diseases. Tumours and cysts within thelarynx or trachea, or causing compression fromwithout, may be symptomless until infection occursand then cause airway obstruction which demandsrelief. An accurate diagnosis is essential and inmost instances tracheostomy is the method ofchoice since the problem of management is rela-tively long term.

Compression of the trachea may be present in achild with a history of recurrent croup. One ofthe commoner causes is a vascular ring. It isrelatively easy to diagnose with its characteristicappearance in the barium swallow x-ray and pulsatilecompression of the trachea visible on bronchoscopy.

General Principles of ManagementIf the patient has collapsed it is necessary to

perform oral endotracheal intubation without delay.Anaesthesia is unnecessary and the muscle tone isusually insufficient to prevent laryngoscopy andinsertion of a tube. After preliminary removal ofsecretion from the pharynx, the laryngoscope ispassed and an endotracheal tube inserted, avoidingall use of force. The diameter of the external naresis a guide to the diameter of tube required. Whenmuscle tone is present, oxygen and halothane shouldbe administered before laryngoscopy. Afterpassage of the tube, the lower airway is clearedusing a thin rubber catheter. The tube is con-nected to a 'T' piece and rubber bag for supply ofan air/oxygen mixture and intermittent pulmonaryinflation. At this point inspection of the pharynxand larynx will have established the diagnosis ifthe obstruction lies above the cords. A decisionthen has to be made whether an airway is necessaryand, if so, whether it should be a nasoendotrachealtube or a tracheostomy.When an endotracheal tube is used, it is essential

that the external diameter should be such that aleak around it can be heard during expiration whenthe tube is obstructed with the finger or afterinflation of the lungs with gas. A tube which istoo large in diameter very rapidly ulcerates themucosa, especially in the cricoid region. When insitu the tube must be adequately supported. A

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The Management of Acute Crouptube with a crosspiece* is convenient, and supportpresents no difficulty. A piece of strapping issufficient to anchor it and there is no danger of itpassing into the trachea. The end of the tube iskept closed with a plastic bung at all times, exceptwhen endotracheal suction is being performed(Jones and Owen-Thomas, 1971).

Obstruction may be due to kinking in the pharynx,or to the fact that it is too long, but by far the com-monest cause is dried secretion due to inadequatehumidification. Humidified gas can be passedthrough one lateral limb of the crosspiece and anextension tube 3 feet in length attached to the otherlimb will ensure that all the inhaled gas is adequatelyhumidified. This procedure is much more efficientin achieving humidification (and high oxygen levels,when required), than feeding gas into an oxygentent and using a simple open-ended endotrachealtube. When the latter procedure is used anultrasonic humidifier is necessary to providesufficient humidification in the tent, but under thesecircumstances the patient is less easily observed.Oxygen 30 to 40% is used in the inspired mixture

and is adequate in all problems of upper airwayobstruction unless there is associated lung diseasesuch as bronchitis, bronchiolitis, or pneumonia.Suction to remove secretion from the tube isnecessary from time to time but should be carriedout at infrequent intervals which will vary dependingupon the amount of secretion present. Three orfour times per day is usually sufficient but occa-sionally 1- or 2-hourly suction is necessary. Thenurse who is to perform it wears a mask and steriledisposable plastic gloves. The sterile catheter ispicked up and the bung removed from the end ofthe tube. The catheter is passed to approximatelythe tip of the nasoendotracheal tube, the nursebeing instructed to suck only to this depth. Thepassage of a catheter into the major bronchishould be carried out only by specially trainednursing or medical staff. This is a more skilledprocedure, carrying the hazard of mechanicaltrauma to the mucosa and greater risk from theintroduction of infection and the production ofhypoxia due to prolonged suction. In general, itshould be performed only once or twice a day andis usually not necessary in pure upper airwayobstruction.The duration of endotracheal intubation should

be not more than one week. This is sufficient tocater for all inflammatory causes of upper airwayobstruction, except when there is a primary laryn-

*Such as the Jackson Rees endotracheal tube made by PortlandPlastics, Hythe, Kent.

geal disease, and in these tracheostomy is indicatedeither initially or as a planned procedure within 24to 48 hours of intubation.

Extubation is attempted after about 48 hours ifthe temperature and general signs of infection aresubsiding, the amount of secretion from the airwayis minimal, the chest x-ray is satisfactory, and theblood gas levels are within normal limits whenbreathing air. After extubation, the patient isobserved closely for evidence of stridor. Shouldthis recur, laryngoscopy is carried out and whennecessary the tube is reinserted. Recurrence ofstridor may occur between 12 and 24 hours afterextubation and in most instances it is not due tothe initial lesion but to deposition of debris oninjured mucosa in the subglottic region. It maybuild up to form a diaphragm with a small hole inthe centre. Accumulated debris should always besuspected when stridor recurs and when presentmay be removed with forceps or by suction atlaryngoscopy. Laryngeal stenosis, especially inthe subglottic region is due to subsequent scarring.It does not occur, however, if a tube of the correctdiameter is used and the duration of intubationdoes not exceed one week.Tracheostomy care follows exactly similar lines

to that described for endotracheal intubation.

Complicating factors. In the great majorityof instances once obstruction has been relieved themaintenance of ventilation presents no difficulty.Should this prove to be inadequate three causesshould be considered.

(1) A pneumothorax may occasionally occur aftera period of considerable increase of respiratoryeffort, and when suspected an x-ray of the chestshould always be taken. When there is evidenceof hypoventilation, the air should be removed.It usually does not recur, but an underwater drainmay be required.

(2) There is associated lower airway or lungdisease. The lower airway may be obstructed bysecretion, or the level oftracheal compression may bebeyond the end of the endotracheal tube. Thismay occasionally occur with a mediastinal tumoursuch as a neuroblastoma or when there is a vascularring. It is essential to maintain a sufficiently longtube in position in order to keep the airway open,but because of the danger of pressure necrosis,relief of obstruction by operative means shouldfollow without delay.

(3) By contrast with the above two causes inwhich there is usually increase of respiratory effort,there may be decrease of effort, and this is usuallydue to hypoxic injury to the brain during a period

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668 R. S. Jonesof low output circulatory failure due to delaypreceding relief of obstruction. Pulmonary ventila-tion should be maintained by a mechanical ventilatoruntil adequate respiratory effort returns or deathoccurs.

REFERENCES

Alexander, H. E., Ellis, C., and Leidy, G. (1942). Treatment oftype-specific Haemophilus influenzae infections in infancy andchildhood. journal of Pediatrics, 20, 673.

Andrew, J. D., Tandon, 0. P., and Turk, D. C. (1968). Acuteepiglottitis: challenge of a rarely recognized emergency.British Medical Journal, 3, 524.

Baxter, J. D. (1967). Acute epiglottitis in children. Laryngoscope,77, 1358.

Davison, F. W. (1966). The antibody deficiency syndrome.Laryngoscope, 76, 1254.

Gardner, P. S., Turk, D. C., Aherne, W. A., Bird, T., Holdaway,M. D., and Court, S. D. M. (1967). Deaths associated withrespiratory tract infection in childhood. British MedicalJournal, 4, 316.

Johnstone, J. M., and Lawy, H. S. (1967). Acute epiglottitis inadults due to infection with Haemophilus influenzae type b.Lancet, 2, 134.

Jones, H. M. (1958). Acute epiglottitis and supraglottitis. Journalof Laryngology and Otology, 72, 932.

Jones, H. M. (1970). Acute epiglottitis: a personal study overtwenty years. Proceedings of the Royal Society of Medicine, 63,706.

Jones, H. M., and Camps, F. E. (1957). Acute epiglottitis: supra-glottitis. Practitioner, 178, 223.

Jones, R. S., and Owen-Thomas, J. B. (1971). Care of the CriticallyIII Child, p. 234. Arnold, London.

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Correspondence to Dr. R. S. Jones, Institute ofChild Health, Alder Hey Children's Hospital, EatonRoad, Liverpool L12 2AP.

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