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Brit. J. Anaesth. (1963), 35, 237

ANAESTHESIA IN UPPER RESPIRATORY OBSTRUCTION

BY

P. J. VERRILL

Department of Anaesthesia, University College Hospital, London

SUMMARY

The causes of upper respiratory obstruction are reviewed. The symptoms and signs aregraded according to severity. It is stressed that cyanosis indicates very severe obstruction,and that stridor at rest is a very informative local sign of severe obstruction. In severeobstruction respiratory depressant drugs and atropine are contraindicated while heliummay be helpful. When general anaesthesia is necessary in severely obstructed patients,the obstruction may first be bypassed by nasotracheal or orotracheal intubation, trache-ostomy or bronchoscopy. Each of these can be performed with local anaesthesia. Thevalue of blind nasal intubation in the conscious patient cannot be over-stressed. Whentracheostomy is indicated it should be done early, as an elective procedure.

Maintenance of a clear airway is a fundamentalprinciple of anaesthesia. Obstruction of the upperrespiratory tract, occurring anywhere from the lipsor nostrils to the carina, is a danger to life. Thedegree of obstruction is likely to be increased byanaesthesia. This problem has engaged the atten-tion of anaesthetists since the early days of anaes-thesia, as shown by the following references.

Sansom (1866) was one of the first to emphasizethe dangers of chloroform in cases requiringtracheostomy or laryngotomy, and in 1912 SirFrederick Hewitt wrote: "There are perhaps nocases demanding greater care and experience onthe part of the anaesthetist than those in whichextensive cellulitis of the submaxillary or cervicalregions is present." The dangers of general anaes-thesia in abscesses related to the upper respiratorytract were stressed by Layton (1913). Thirty-onecases of Ludwig's angina were reviewed byWilliams (1940). Five of these required emer-gency tracheostomy during anaesthesia, and onepatient died while this was being performed.Bennett (1943) reported on anaesthesia in sixcases of submandibular abscess. Death occurredin one patient during the induction of anaesthesiaand another required emergency tracheostomybecause of failure to intubate.

In a series of 1,000 deaths associated with anaes-thesia, Edwards et al. (1956), reported that 463were reasonably certainly due to anaesthesia and,of these, six were associated with pre-operative

237

respiratory obstruction. Of the latter, three caseshad inflammatory oedema of the glottis, one hadcarcinoma of the tongue, one had an obstructivelesion of the larynx and the other thyrotoxicosiswith deviation of the trachea. Boyan and How-land (1959) reviewed 839 patients who underwenttotal laryngectomy and 190 who underwent partiallaryngectomy. Of this total, twenty-seven patientsrequired emergency tracheostomy because of in-tubation difficulties.

In this paper, the causes and effects of upperrespiratory obstruction are reviewed, the assess-ment and anaesthetic management discussed andsome illustrative cases described.

THE CAUSES OF UPPER RESPIRATORY

OBSTRUCTION

For the purpose of this paper the upper respira-tory tract is divided into five regions: the mouth,nose, pharynx, larynx, and trachea.

Any lesion of the upper respiratory tract, abovethe level of the posterior part of the tongue, mayobstruct the oral or nasal airway, but rarely both.The pre-anaesthetic obstruction of the alter-native airway increases the likelihood of seriousobstruction during anaesthesia.

Oral Obstruction.Congenital abnormalities limiting the oral airwayinclude microstomia, macroglossia and hypoplasiaof the mandible with prolapse of the tongue.Tumours of the tongue and jaws encroach upon

238 BRITISH JOURNAL OF ANAESTHESIA

TABLE ICauses of oral obstruction.

TABLE IICauses of nasal obstruction.

CongenitalMicrostomia; macroglossia; hypoplasia of themandible with prolapse of the tongue.

NeoplasticTumours of tongue, jaws, palate and floor of themouth.

InflammatoryDental infections causing trismus; jaw infections,e.g. osteomyelitis, actinomycosis, Ludwig's angina;temporo-mandibular arthritis.

TraumaticInjuries to jaws and tongue; scarring of lips;haemophilia; burns and scalds.

NeurologicalBilateral hypoglossal nerve palsy; tetanus.

Allergies and hypersensitivitiesAngioneurotic oedema; insect stings.

Other causesWiring of jaws for fractured mandible; plasticprocedures on lips.

the oral cavity. Inflammatory conditions of the jawsand teeth obstruct by virtue of the bulk of theinflammatory reaction and may also cause trismus.

Ludwig's angina is an inflammatory conditionof the submaxillary space, which obstructs theairway, by pushing up the tongue, by trismus andby oedema of the tissues around the glottis.Trauma in the mouth leads to swelling and theoccurrence of bleeding further threatens the air-way. Burns and scalds inevitably cause oedema andlater scarring. Hypersensitivity phenomena such asangioneurotic oedema and insect stings may causegross swelling of the tongue or lips.

Neurological disorders which may give rise tooral obstruction include bilateral hypoglossalnerve palsy causing prolapse of the tongue andtetanus with trismus. The opening into the mouthmay be scarred into a small aperture or obstructedby a plastic procedure such as the creation of anAbbe flap. Conditions which affect the oral airway,by limiting the movement of the jaw, includetemporo-mandibular arthritis and the wiringtogether of the jaws which is often practised inthe treatment of the fractured mandible.

Nasal Obstruction.Congenital absence of the nose has been recordedand the nasal airway may be obstructed from birthby post-choanal atresia or by marked deviation ofthe septum. Neonatal nasal obstruction is relativelyserious as it interferes with feeding and the neo-nate does not readily adopt the oral airway. Polypsand other neoplasms, such as haemangiomata,

CongenitalAbsence of the nose; post-choanal atresia; deviatedseptum.

NeoplasticPolyps; fibromata; haemangiomata; dentigerouscysts.

InflammatoryCoryza; abscess; adenoids.

TraumaticBroken nose, haemophilia.

A llergyHay fever.

Foreign bodiesBeads, beans, etc.

fibromata and dentigerous cysts, may limit thenasal airway. The common cold is a familiarcause of blocked nose and the nostrils may beobstructed by other infections. Hypertrophy of theadenoids is the commonest cause of chronic nasalobstruction in childhood.

Fracture of the nasal bones leads to muchswelling and narrowing of the nasal passages. Hayfever and other forms of allergic rhinitis lead todifficulty in nasal breathing. Children commonlyinsert foreign bodies such as beads and beans intothe nostrils.

Pharyngeal Obstruction.The pharynx may be congenitally obstructed bycystic hygroma, branchial cysts, or by aberrantthyroid tissue and cysts at the base of the tongue.Carcinoma of the pharynx is not uncommon.Abscesses may arise in the peritonsillar and retro-

TABLE III

Causes of pharyngeal obstruction.

CongenitalCystic hygroma; branchial cysts; abeirant thyroidtissue.

NeoplasticCarcinoma; sarcoma.

InflammatoryHypertrophied tonsils; retropharyngeal abscess;peritonsillar abscess.

TraumaticHaemophilia; burns; scalds; acid or alkalinefluids; post-surgical scarring.

NeurologicalBulbar palsy; pseudobulbar palsy; vagal palsy.

Foreign bodiesFish and meat bones.

AllergiesStings; angioneurotic oedema.

Other causesCervical fusion; plaster cast; kyphoscoliosis;rheumatoid spondylitis.

ANAESTHESIA IN UPPER RESPIRATORY OBSTRUCTION 239

pharyngeal regions and the resulting oedema mayinvolve the glottis. These infections are much lesscommon since the introduction of antibiotics.

Children may swallow corrosive fluids whichcause acute oedema and later scarring. Occasionallyafter thyroidectomy or parathyroidectomy exten-'sive scarring develops in the tissues around theglottis, causing intubation difficulties during anaes-thesia.

Paralysis of the pharyngeal musculature is seenin myasthenia gravis, pseudobulbar palsy, inlesions of the vagi and in progressive bulbarparalysis. The last-named may result from motorneurone disease, poliomyelitis, arteriosclerosis,tumours, disseminated sclerosis or syringomyelia.Reduction in the efficiency of swallowing andlaryngeal reflexes makes likely the aspiration offoreign material into the tracheobronchial tree.

Angioneurotic oedema may cause massive swel-ling of the uvula and posterior pharyngeal wall.Fish and meat bones commonly lodge in themucosa of the pharynx and may result in muchswelling. Leatherdale (1960) has drawn attentionto the massive extravasations of blood which maydevelop in the tongue, floor of the mouth, andaround the pharynx and larynx in haemophiliaand other haemorrhagic diatheses. The maximumoropharyngeal airway is obtained by extension ofthe head in the midline. Conditions which preventthis are potential causes of respiratory obstruction.They include rigid fixation of the neck as a resultof osteoarthritis, rheumatoid spondylitis, kypho-scoliosis and torticollis. Causes resulting frommedical treatment include surgical fusion of thecervical vertebrae and the encasing of the headand neck in plaster of Paris.

Lipoid storage disorders such as Niemann-Pickdisease, Gaucher's disease and lipochondro-dystrophy may lead to gross lymphoid hyperplasiain the pharynx (Bougas and Smith, 1958).

Laryngeal Obstruction.Eckenhoff (1951) has described the features of theinfant larynx which are of interest to the anaes-thetist. The organ is funnel-shaped with itsnarrowest diameter at the cricoid ring. In con-genital stenosis the cricoid cartilage is the site ofobstruction. The infant larynx may be the siteof congenital webs which bridge the anterior partsof the vocal cords. Laryngoceles and laryngealcysts may also be present from birth.

Congenital laryngeal stridor, or laryngomalacia,is a transient form of stridor occurring in infantsand associated with an abnormal flaccidity of thetissues of the larynx. With each inspiration theepiglottis is, folded and drawn into the glottis.There may be, in addition, laxity of the mucosaof the aryepiglottic folds. This condition may beencountered by the anaesthetist attempting intu-bation in the infant. The abnormality improveswith growth and increasing rigidity of the laryn-geal cartilages and usually disappears in thesecond year of life.

Carcinoma of the larynx is one of the com-monest causes of upper respiratory tract obstruc-tion of concern to the anaesthetist. Laryngealpolyps and papillomata occur. The latter may bemultiple and recurrent in juveniles, necessitatingrepeated surgery. Cysts of the epiglottis are usuallysmall but may become grossly enlarged (Norris,1957).

Infections of the larynx may compromise theairway by causing oedema. Acute laryngitis is acommon affliction but usually causes negligiblerespiratory obstruction in the adult. Laryngo-tracheobroncbitis occurring in infants is a seriousdisease and respiratory obstruction results fromoedema and laryngeal spasm. Epiglottitis is adisease characterized by enormous enlargement ofthe epiglottis and septicaemia with Haemophilusinfluenzae as the causal organism in most cases. Itis rapidly progressive and tracheostomy is usuallyrequired.

Laryngeal diphtheria, tuberculosis and syphilis

TABLE IV

Causes of laryngeal obstruction.

CongenitalStenosis; webs; laryngomalacia; laryngocele;cysts.

NeoplasticCarcinoma; polyps; papillomata, cysts of epi-glottis.

InflammatoryLaryngitis; diphtheria; tuberculosis; syphilis;epiglottitis; perichondritis; leprosy.

TraumaticInternal and external violence; post-traumaticstenosis; post-laryngotomy stenosis; flash burns.

NeurologicalVagal and recurrent nerve palsies; laryngealtetany; laryngeal spasm.

AllergyGlottic oedema.

Foreign bodiesVegetable and non-vegetable.


are now uncommon. Unusual inflammatory lesionscausing laryngeal obstruction include crico-arytenoid arthritis, perichondritis, acute thyroiditisand leprosy.

Injuries to the larynx may result from externalor internal violence. In the latter case endotrachealtubes, laryngoscopes and bronchoscopes arepossible agents. Trauma to the laryngeal carti-lages may lead to stenosis and laryngotomy is noexception.

Bilateral midline abductor paralysis of thelarynx, whether due to recurrent laryngeal nervedamage or central causes, leads to respiratoryobstruction in the conscious patient. Other formsof laryngeal paralysis may not cause respiratorydifficulties in the conscious patient but predisposeto laryngeal obstruction in the anaesthetized.Laryngeal spasm is a complication with whichanaesthetists are familiar. Fink (1956) has dis-cussed the aetiology and treatment. Other neuro-logical causes of laryngeal obstruction are laryngis-mus stridulus and laryngeal tetany.

Glottic oedema may result from the inhalationof hot or irritant gases and from insect stings andhypersensitivity phenomena, such as angioneuroticoedema and food and drug allergies. The larynxmay also be the site of foreign body obstruction.

Tracheal Obstruction.The trachea may be the site of congenital stenosisor webs. It may be compressed by anomalies ofthe aortic arch (Kirklin and Clagett, 1950).

Primary malignant disease of the trachea is un-common but secondary invasion may occur fromcarcinoma of the thyroid or upper oesophagus.Papilloma of the trachea is uncommon but maybe associated with multiple papillomata through-out larynx, trachea and bronchi (Stein and Volk,1959).

TABLE VCauses of tracheal obstruction.

CongenitalStenosis; webs; vascular rings.

NeoplasticMediastinal tumours; carcinoma of thyroid oroesophagus.

InflammatoryTracheitis.

TraumaticPost-tracheostomy stenosis.

Foreign bodyRare.

Other causesAneurysm of aortic arch; collapse of trachea.

Injury involving tracheal cartilages may leadto stenosis. High tracheostomy is more likely to befollowed by stenosis than a low tracheal incision.Occasionally, collapse of the tracheal cartilagesfollows the relief of chronic compression of the'trachea. Foreign bodies small enough to passthrough the glottis often lodge in the main bronchirather than the trachea. Smaller foreign bodies maymove up the trachea with expiration and downwith inspiration.

Allergic responses causing bronchospasm ofteninvolve the trachea in a similar process. Many ofthe lesions which have been discussed here requiresurgical intervention in the form of tracheostomy.Any lesion of the upper respiratory tract will,however, complicate anaesthesia for surgery un-related to the respiratory system.

SYMPTOMS AND SIGNS OF UPPER RESPIRATORY

TRACT OBSTRUCTION

The symptoms and signs of obstruction of theupper respiratory tract depend on the site andseverity of the obstruction. Local effects are pro-duced by the lesion and in severe obstruction thegeneral manifestations of asphyxia are present.

The symptoms and signs of respiratory obstruc-tion may be graded according to severity as shownin table VI (modified from Forbes, 1961).

TABLE VISymptoms and signs of respiratory obstruction gradedaccording to severity (modified from Forbes, 1961).

Stage 1 {Mild or potential obstruction)Hoarseness; cough; stridor on moderate exertion;oral obstruction alone; nasal obstruction alone.

Stage II (Moderate obstruction)Stridor on slight exertion; rib retraction on in-spiration; accessory muscles of respiration in use;alae nasi dilating on inspiration; indrawing ofsoft tissues of neck; jaw and trachea tugged downon inspiration; dyspnoea.

Stage III (Severe obstruction)Stridor at rest; apprehension; restlessness; sleep-lessness; sweating; pallor; increase of pulse rateand blood pressure; exaggerated excursion ofneck veins.

Stage IV (Very severe obstruction)Slowed respiration; hypotension; cyanosis; im-pairment of consciousness.

General symptoms and signs.Asphyxia is a combination of hypoxia and

carbon dioxide retention. Its effects on the centralnervous system produce apprehension in the adultand restlessness in the child.

Moderate obstruction necessitates the use of the


accessory muscles of respiration in an effort tomaintain normal ventilation. Only the scalene andsternomastoid muscles show significant activity asaccessory muscles of respiration in man (Camp-bell, 1958). These muscles are under voluntarycontrol so that sleeplessness results from severeobstruction. Observation of the patient and pal-pation of the neck will quickly reveal whether theaccessory muscles are in use. Their action is oftenaccompanied by dilatation of the alae nasi oninspiration.

Dyspnoea has been defined by Meakins (1934)as "consciousness of the necessity for increasedrespiratory effort". It is frequently caused bymechanical difficulties in ventilating the lungs.One measurable facet of dyspnoea is the work ofbreathing. Upper respiratory tract obstructionimplies narrowing of the airway and hence in-creased resistance to airflow; the work of breath-ing is increased and this leads to dyspnoea. Thisincrease in the work of breathing results ingreater oxygen consumption and energy expendi-ture. A vicious circle is set up. The mechanicalefficiency of the respiratory muscles is low (5-10per cent) so that much of this energy is dissipatedas heat; sweating is a common accompaniment ofrespiratory obstruction.

When the airway is inadequate, the exagger-ated actions of the respiratory muscles produce avariety of effects. The muscular efforts to expandthe chest increase the negative intrathoracicpressure normally present during inspiration andthe intrathoracic pressure becomes increasinglypositive during expiration. These pressure changesare reflected in the jugular veins which may beseen exaggeratedly filling and emptying. The softtissues between the ribs, the supraclavicular andsuprasternal areas, may be indrawn during inspira-tion and pushed out during expiration. The chestexpansion remains small in spite of these efforts.

The diaphragm acts very forcibly in thesesituations and may draw in the lower ribs duringinspiration. This may be particularly noticeablein the flexible rib cage of the child. The jerk ofthe diaphragm in its efforts to descend may betransmitted via the fibrous pericardium and thedeep fascia of the neck to the trachea and eventhe lower jaw—the familiar tracheal tug.

In acute and severe obstruction, hypoxiadominates the situation and respiratory failure is

quickly followed by circulatory failure. In chronicobstruction the effects of carbon dioxide retentionmay overshadow those of hypoxia. This results inincreases in pulse rate and blood pressure. Severeand prolonged obstruction will result in circula-tory failure.

Cyanosis is an unreliable index of the oxygensaturation of the blood. The average physician willrecognize it when the arterial oxygen saturationhas fallen to within 75-85 per cent. Well knownare the difficulties of assessing cyanosis in thepresence of anaemia, regional slowing of bloodflowand pigmentation of the skin. In the absence ofother complicating factors, cyanosis is a late signof upper respiratory tract obstruction and indi-cates very severe restriction of the airway.

Local signs.The local signs of respiratory obstruction indi-

cate the site of the lesion and may point to itsseverity. The patient may be able to localizeaccurately the site of his airway obstruction.Palpation and auscultation of the neck may revealthe level of obstruction.

It is a simple matter to test the patency of thenostrils by their alternate occlusion. The oralcavity is easily inspected, as is the oropharynx.This should be done routinely before any anaes-thetic procedure.

Difficulty in swallowing obviously suggests apharyngeal or oesophageal lesion, which maycompromise the airway.

The quality of the voice may provide usefulinformation. Patency of the nasal passages isnecessary for resonance. Lesions in the mouthcause defects in articulation, while pharyngealaffections may cause a moist guttural voice. Hoarse-ness directs attention to the larynx. Lesions belowthe level of the vocal cords may be associated witha weak but clear voice.

The croupy cough of the child with laryngitisis a familiar sound. Other afflictions of the upperrespiratory tract commonly produce a reflex non-productive cough. Bilateral adductor paralysis ofthe larynx is evidenced by a non-explosive typeof cough which has been described as bovine.Tracheal lesions may produce a rough, barkingcough, worse at night. Classically, aneurysm of theaortic arch produces a brassy cough.

Stridor is the most important localizing physicalsign indicating serious obstruction in either larynx,


trachea or bronchus. Stridor is a harsh noise pro-duced by respiratory air passing through anobstructed main air passage. Airflow through thenormal upper respiratory tract is mainly laminarbut severe obstruction causes turbulence andstridor is produced by the vibration of soft tissuesin a turbulent airflow. The vibrating surface maybe the vocal cords or the mucosa of the larynx,trachea or bronchus.

There is a certain critical velocity below whichairflow is laminar. Above this, flow becomesturbulent (Dean and Visscher, 1941). A patientwith mild obstruction may therefore have nostridor at rest, but stridor may result from exercise,dyspnoea, apprehension or pain because of theincreased airflow through the obstruction. It hasteen said that the patient with stridor going up-stairs may need tracheostomy, one with stridorwalking on the flat will need tracheostomy and thepatient with stridor at rest does need tracheostomy(Watkyn-Thomas, 1953).

Stridor is best listened for by having the patientbreathe through the half-opened mouth. It may bemainly inspiratory or expiratory and this gives aclue to the site of its origin (Wilson, 1952).Obstruction at or above the vocal cords producespredominantly inspiratory stridor. This may bedue to the relative lack of support of the softtissues above the glottis and their tendency to bedrawn into the airway by the negative intra-thoracic pressure. Bronchial obstruction commonlygives rise to expiratory stridor; this may be cor-related with the decrease in bronchial diameterduring expiration and an increase in diameterduring inspiration. Severe tracheal obstructionand lesions of the larynx below the cords usuallyproduce inspiratory and expiratory stridor.

Stridor is often the presenting symptom oflaryngeal disease in infants. Early lesions of theadult larynx are more likely to cause hoarseness.

Investigations.Indirect examination of the glottis provides in-

formation of great value to the anaesthetist. Thefactors of particular interest are the site and extentof the lesion, its consistency, and whether it bleedseasily, the degree of obstruction and the move-ment of the vocal cords.

Routine chest films often reveal tracheal devia-tion and compression likely to lead to intubationdifficulties. Radiological examination of the larynx

may be useful. The epiglottis, pharynx, pyriformfossae and aryepiglottic folds can often be seenin a lateral view. Anteroposterior tomograms mayreveal the extent of lesions below the cords(Sheehan et al., 1960, and figure 1).

Upper respiratory obstruction usually results inprolongation of inspiration and expiration, andreduction of tidal volume. Vital capacity usuallyremains within normal limits. Timed vital capacityand maximum breathing capacity are progressivelyreduced with increasing airway obstruction. Resi-dual volume is often increased.

Consideration of the signs, symptoms and in-vestigations dealt with here should enable theanaesthetist to assess the severity of upper respira-tory obstruction in most cases.

PREPARATION FOR ANAESTHESIA

Premedication of patients with upper respiratoryobstruction merits careful attention. Atropinestimulates the cortex, raises oxygen requirementsand increases the viscosity of secretions so thatthey are more likely to clog a diminished airway.The drug is therefore contraindicated in moderateor severe obstruction.

There is disagreement on the place of sedationin these cases. There is no doubt that the use ofpowerful respiratory depressants is dangerous inthe presence of severe obstruction. In mild ormoderate obstruction, however, there are thosewho believe that effective sedation leads to lessen-ing of anxiety and apprehension and reduction inoxygen requirements. The antagonists of thisview regard anxiety and apprehension as signs ofhypoxia and contraindications to sedation. Thewriter believes that the opium alkaloids and thesynthetic narcotic analgesics should not be usedin the presence of respiratory obstruction, butthat the phenothiazine derivatives in carefullyassessed doses will often produce effective sedationwithout serious respiratory depression.

In severe respiratory obstruction when airflowhas become turbulent, the factors determining theresistance to flow are the dimensions of the re-maining airway and the density of the flowinggases. A mixture of 80 per cent helium with 20per cent oxygen has a density of 0.33 comparedwith 1.0 for air. The resistance to flow with thehelium and oxygen mixture is therefore approxi-mately one-third of that for air.

ANAESTHESIA IN UPPER RESPIRAT™v OBSTRUCTION 243

FIG. 1Anteroposterior tomogram of the neck showing gross soft tissue swelling of the right vestibularfolds and vocal cords, with obliteration of the right pyriform fossa. The left cord is thickenedand the laryngeal sinuses are obliterated on both sides. A normal tomogram is shown for

comparison.

In mild respiratory obstruction, where, with thepatient at rest, airflow is predominantly laminar,the viscosity of the flowing gases is the relevantfactor. As a mixture of 80 per cent helium and 20per cent oxygen has a viscosity of 1.11 comparedwith 1.0 for air, helium offers no advantage inmild respiratory obstruction.

Breathing a mixture of helium and oxygen mayimprove oxygenation in patients with severe res-piratory obstruction and the inhalation of such amixture should be a useful preliminary to anaes-thesia.

ANAESTHETIC MANAGEMENT

Oral obstruction.When the opening into the mouth or the oral

cavity is obstructed, the nose can often be utilizedas the alternate pathway. Nasotracheal intubationis indicated and it has to be decided whether tointubate with the patient awake or whether it is

justifiable to induce anaesthesia before intubation.Blind nasal intubation under local anaesthesia

is not a difficult technique to master and this isthe procedure of choice; 5 or 10 per cent cocainesprayed into the nostril provides good local anaes-thesia and shrinks the mucosa, increasing the air-way and reducing the likelihood of epistaxis. Caremust be taken not to exceed a total dosage of3 mg/kg. A selection of tubes should be available;it is often easier to introduce one with a long bevel.

If there are signs of moderate or severe obstruc-tion, the mouth cannot be opened sufficiently touse a laryngoscope and it is not possible to per-form blind nasal intubation under local anaes-thesia, tracheostomy should be performed.

When the oral airway is restricted but there isotherwise no evidence of upper respiratory obstruc-tion, the anaesthetist may be tempted to tryintubation with the patient asleep. It is difficult


to suck out the pharynx if the oral airway isinsufficient to admit the sucker and the treatmentof laryngeal spasm is seriously hindered by theabsence of a good oral airway. For these reasonsblind nasal intubation under local anaesthesia isindicated and if this fails tracheostomy must beseriously considered. General anaesthesia shouldprecede intubation only when the oral airway issufficient to admit the use of laryngoscope andsuction.

CASE 1.An 18-year-old girl was involved in a traffic accident.

She was conscious when seen but had sustained con-cussion and multiple superficial lacerations of the face.There was an extensive laceration of the chin exposingthe mandible. The lips were cut and the mouth andnostrils were full of blood. She had eaten a full mealseveral hours before the accident. Blood pressure was140/80 mm Hg and pulse rate 100/min. The mouthcould be opened about 2 cm only but there were noother signs of respiratory obstruction.

For premedication atropine 0.5 mg was given intra-venously. After sucking out blood, the right nostrilwas sprayed with 4 per cent lignocaine. A No. 6 plainrubber nasotracheal tube was carefully advanced andlignocaine sprayed through the tube as it approachedthe larynx. The pharynx was kept empty by suctionwith a rubber catheter through the mouth. The tracheawas intubated without difficulty and general anaes-thesia induced with a mixture of nitrous oxide, oxygenand halothane 1 per cent. A throat pack was insertedwhen the pharyngeal reflexes were sufficiently subdued.

Toilet and suture of the wounds was carried outand at the end of the procedure the patient was turnedon to her side. The throat pack was removed but thenasotracheal tube remained in place until the patientawoke. It was then removed and there was no evidenceof respiratory obstruction.

Comment. This case was one of potential respiratoryobstruction because of blood in the mouth, nose,pharynx and almost certainly the stomach, with anoral airway inadequate for laryngoscopy. A quicklyeliminated inhalational sequence was chosen so thatprotective reflexes returned quickly. Lignocaine waspreferred to cocaine because of the risk of rapidabsorption of the drug from injured mucous mem-branes.

In the infant it is very difficult to perform blindnasal intubation so that obstruction of the oralairway always indicates tracheostomy before theinduction of anaesthesia.

Ludwig's angina presents a serious problem tothe anaesthetist. Williams (1940) has discussed themortality associated with anaesthesia for this con-dition and points out that intubation is oftendifficult or impossible owing to distortion of theairway. Bennett (1943) described six cases. Onepatient died during induction with nitrous oxide,oxygen and ether. The remainder were success-

fully managed by nasal intubation with localanalgesia using a narrow-bladed laryngoscope. Thenasotracheal tubes were kept in place for 24 hours.

Proctor (1957) has stressed the possible dangersof removing the tube as soon as the patient isawake and the importance of extubation beingperformed by somebody able and equipped toreintubate or perform tracheostomy. Early tracheo-stomy was advised by Kelly, Hodge and Grossman(1957) as the key to correct treatment. Intravenousanaesthesia was quickly recognized to be particu-larly dangerous in this situation. Weese (1939) feltthat the sudden deaths so often resulting fromintravenous anaesthesia in severe obstruction weredue to reflexes mediated through the carotid sinus.Macintosh and Bannister (1943) displaced Weese'stheory by observing that in a patient who hadrespiratory obstruction, necessitating the use ofhis accessory muscles of respiration, any form ofgeneral anaesthesia was dangerous and would leadto anoxia by reducing the efficiency of the acces-sory muscles of respiration.

Emergency tracheostomy may be difficult toperform quickly in these patients. Oedema in theneck and displacement may make it difficult tofind the trachea. If obstruction is obviously severeelective tracheostomy should be done. In lessserious cases nasotracheal intubation should beattempted under local anaesthesia. If this failsafter one or two gentle attempts, tracheostomymust be performed.

When major surgery is performed in the mouth,as for malignant disease of the jaws and tongue,even if the anaesthetist has successfully passed anasotracheal tube, it is wise to perform tracheos-tomy at the end of surgery in order to retaincontrol of the airway.

Where there has been severe trauma to theupper airway as may result from gunshot woundsor motor accidents, tracheostomy should be carriedout before anaesthesia, otherwise oedema andhaemorrhage will almost always compromise theairway and may take several days to subside.

Trismus is commonly seen in association withdental infections. Usually the mouth can be openedonly slightly and this causes potential rather thanactual respiratory obstruction.CASE 2.

A girl of 19 attended the dental surgery of acasualty department, having had a left lower molarextracted 7 days previously. There was considerable


swelling and redness overlying the angle of the leftmandible and the inflammation extended down into theneck on the left side. The mouth could not be openedmore than 1 cm without severe pain. There were noother signs of respiratory obstruction.

The patient was admitted for drainage of the abscess.Premedication consisted of promethazine 25 mg andatropine 0.5 mg. The right nostril was sprayed with10 per cent cocaine and blind nasal intubation wasperformed, using a No. 7 plain rubber tube, on theconscious patient without difficulty. General anaesthesiawas induced with thiopentone 300 mg and continuedwith a mixture of nitrous oxide, oxygen and halothane.The jaw relaxed with the onset of unconsciousness anda throat pack was inserted. The abscess was drainedinto the mouth and a small rubber drain stitched intothe cavity. The larynx was inspected with a Macintoshlaryngoscope and was normal in appearance. Therewas, however, reddening and oedema of the mucosa ofthe left pharyngeal wall. The nasotracheal tube wasreplaced and left in position until consciousnessreturned.

Comment. This patient's trismus disappeared withthe onset of unconsciousness and obviously anaesthesiacould have been induced with thiopentone and a re-laxant without difficulty. Nevertheless the appearanceof the pharynx illustrates how a dental infection canspread downwards towards the glottis.

Macintosh and Bannister (1943) have advisedthe gradual introduction of a boxwood wedge toovercome trismus and Goldman (1959) has sug-gested the infiltration of the masseter musclesthrough the cheek with lignocaine. These methodsmay be used to reduce the hazards of anaesthe-tizing a patient who cannot widely open his mouth,but blind nasal intubation with the patient con-scious is seldom difficult, and completely bypassesthe obstructed mouth.

CASE 3.A man of 21 years was admitted to hospital with a

swelling the size of a walnut under the right angleof the jaw and complete inability to open the mouth.The incisor teeth could be separated only 2 mm. Therewere no other signs of respiratory obstruction.

Premedication consisted of pethidine 100 mg andatropine 0.5 mg; lignocaine, 5 ml of 1 per cent, wasinjected into each masseter muscle through the cheekand this increased the opening of his mouth to 1 cm.The right nostril was sprayed with 10 per cent cocaineand a No. 7 plain rubber nasotracheal tube passedblindly into the trachea. General anaesthesia was in-duced with thiopentone 350 mg and gallamine 80 mgand continued with nitrous oxide, oxygen and trichloro-ethylene. The mouth had to be forced open in order toinsert a throat pack and the dentist had to open themouth further forcibly in order to insert his prop.Four wisdom teeth were extracted and the abscesseffectively drained. The patient was returned to theward with the endotracheal tube in position and thiswas removed by the anaesthetist when consciousnessreturned. At this stage trismus had returned as severelyas before.

Comment. This case illustrates a very severe trismusunresponsive to almost all measures and emphasizesthe value of blind nasal intubation.

Nasal obstruction.In the adult, complete obstruction of the nose

presents few problems if the oral airway is avail-able.

CASE 4.A 47-year-old man required surgery because of

obstruction of the nose and recurrent sore throats. Hehad undergone guillotine tonsillectomy at the age of7. Inspection of the oropharynx revealed bilateraltonsil remnants. The posterior pillars of the fauceswere adherent to the posterior pharyngeal wall andthe only nasopharyngeal airway was a chink behindthe uvula and a hole through the soft palate on theright side. There were no other signs of upper "respira-tory tract obstruction.

After premedication with papaveretum 20 mg andhyoscine 0.4 mg, anaesthesia was induced with thio-pentone 400 mg followed by suxamethonium 40 mg.A No. 10 cuffed armoured latex orotracheal tube wasinserted without difficulty and anaesthesia continuedwith nitrous oxide, oxygen and halothane 1.5 per cent.

The tonsil remnants were removed; both posteriorpillars of the fauces were mobilized and their rawedges sutured. A rubber tube was tied into the naso-oropharyngeal airway to maintain its patency. Afterpharyngeal suction the armoured orotrachael tube wasremoved and the patient breathed freely through hismouth.

Comment. In spite of almost complete nasopharyn-geal obstruction pre-operatively and the presence ofa foreign body in the nasopharynx postoperatively, thispatient had no problems with his airway because ofthe availability of the mouth as an alternative pathway.

Nasal obstruction presents difficulties in theinfant as it has great difficulty in adapting to theoral airway. With complete nasal blockage infantsmay have severe respiratory obstruction with as-piration of feeds and oral secretions; tracheostomymay become necessary even when anaesthesia isnot intended.

When surgery is to be carried out for relief ofpostchoanal atresia in infancy, it is often possibleto intubate the child before the induction of anaes-thesia. In the older child with this condition orwith enlarged tonsils or adenoids, once anaesthesiais deep enough to permit the insertion of anoropharyngeal airway, the problems are resolved.This can usually be achieved with a suitable inha-lational sequence. Occasionally the tonsils andadenoids are so hypertrophied that tracheal intu-bation is the only way of achieving a satisfactoryairway.


Pharyngeal obstruction.Cystic lesions of the pharynx and larynx may

often be aspirated under topical anaesthesia, beforegeneral anaesthesia is induced in the usual way.

Peritonsillar and retropharyngeal abscesses pre-sent the hazards of inhalation of pus and they mayeasily be ruptured by the instrumentation neces-sary to perform intubation. For this reason, theselesions should be dealt with under local anaesthesiawithout regard to the degree of respiratoryobstruction.

It is helpful to rinse out the mouth withbicarbonate solution to dissolve excess mucus.After spraying the mucosa with 10 per cent cocainesolution the site of the proposed incision may berubbed with a 10 per cent cocaine stick untilblanching occurs. Incision is then carried out withthe patient in a "head down" position.Laryngecd obstruction.

Tracheostomy should precede all but the mostminor surgical procedures on the infant larynx. Anairway which is just adequate before surgery islikely to be further impaired by oedema in thepostoperative period. If the accessory muscles ofrespiration are in use, or there are other evidencesof moderate to severe obstruction tracheostomyshould be done under local anaesthesia, prior tosurgery. In the absence of these signs, the surgeonmay be assisted by the passage of an endotrachealtube or bronchoscope before tracheostomy. Aninhalational anaesthetic technique is indicated,and relaxants are best avoided. If there is theslightest difficulty with intubation, the attemptshould be abandoned and tracheostomy performedwithout delay. Infants, up to the age of 4 weeks,may usually be intubated orally without anaes-thesia.

Laryngo-tracheobronchitis in infancy necessi-tates tracheostomy when signs of severe respira-tory obstruction develop. Seward and Fraser(1961) have discussed the merits of general andlocal anaesthesia in this particular situation, andhave expressed a preference for the former,employing an inhalational technique and orotra-cheal intubation with every facility available forperforming emergency tracheostomy. The writerfavours careful sedation with a phenothiazinederivative such as trimeprazine (2 mg/stone; 0.3mg/kg), followed by tracheostomy under localanaesthesia.

Small papillomata and polyps of the larynxusually cause little obstruction to respiration andanaesthesia for laryngoscopy and removal of theselesions can usually be safely conducted by a com-bination of local and general anaesthesia. In thissort of situation, however, sudden difficulties mayarise, necessitating emergency tracheostomy andthe anaesthetist and surgeon must always be pre-pared for this.

CASE 5.A woman of 66 years was admitted for direct laryn-

goscopy. Twelve years previously small nodules hadbeen removed from the interarytenoid region and asmall papilloma from the left cord. She had beenhoarse for 3' years before this time. Other complaintswere shortness of breath and occasional attacks ofparoxysmal nocturnal dyspnoea. She slept proppedup on three pillows. The blood pressure was 160/120mm Hg. There was no stridor and the accessorymuscles of respiration were not in use.

At indirect laryngoscopy it was not possible to geta good view, but both cords appeared to be movingand no gross lesion was seen.

After premedication with pethidine 50 mg and atro-pine 0.5 mg anaesthesia was induced with thiopentone200 mg and gallamine 40 mg followed by inhalationof nitrous oxide, oxygen and halothane. After a fewbreaths of this mixture, complete respiratory obstruc-tion occurred and the patient became very cyanosed.A laryngoscope was easily inserted into the oro-pharynx. The vocal cords could not be seen, beingtotally obscured by voluminous false cords which weredrawn into the glottis leaving a small diamond-shapedchink in their centre. A No. 2 plain tube was thelargest that could be pushed through this opening andthe surgeon was advised to perform immediate trache-ostomy. This was promptly done and the cyanosisrelieved by oxygen inflation through the tracheostomy.Direct laryngoscopy then revealed essentially normalappearances.

Postoperatively the patient was mildly hypotensiveand complained of chest pain. Electrocardiograph^examination 3 days later showed unequivocal evidenceof anterolateral myocardial infarction.

Comment. This case illustrates the onset of severeand unexpected difficulties during the induction ofanaesthesia. The situation was salvaged by the promptintervention of the surgeon. The myocardium, whichhad given pre-operative evidence of its weakness, suf-fered permanent damage from the hypoxic episode.

The rapidly recurring multiple papillomata ofchildhood often necessitate tracheostomy to permitrepeated excisions.

In carcinoma of the larynx or invasion of thelarynx by other carcinomata, tracheostomy isalmost inevitable. Careful assessment of the degreeof obstruction will help to decide the timing ofthis procedure. When laryngectomy is projected,the anaesthetist should acquaint himself with thesite and nature of the lesion, and assess the degree


of obstruction. If there is stridor at rest tracheo-stomy should not be delayed and should be per-formed under local anaesthesia.CASE 6.

A 62-year-old man was admitted with respiratoryobstruction. Several months previously he had receiveddeep X-ray therapy for a carcinomatous ulcer of thepyriform fossa. He was sitting upright in a chair, ina state of great anxiety. He was hoarse, had a bovinecough and was able to swallow fluids only. He com-plained that he had not slept for a week.

Pulse rate was 84/min, respiration rate 30 b.p.m.The skin was pale, dry and slightly cyanosed, withgoose-pimples. The arteriolar capillary refill time wasprolonged. There was inspiratory and expiratorystridor, the former predominating. The accessorymuscles of respiration and the alae nasi were working.The trachea was tugged downwards in inspiration andthere was an exaggerated filling and emptying of theneck veins. The intercostal tissues and supraclavicularareas were indrawn during inspiration.

After premedication with promazine 25 mg therespiration rate fell to 20 b.p.m. Tracheostomy wasthen performed under local anaesthesia. The patientsubsequently underwent total laryngectomy.

Comment. Clearly this patient was suffering fromvery severe respiratory obstruction, which necessitatedtracheostomy without delay. The surgical treatment ofhis disease could then be planned unhurriedly.

Local anaesthesia for tracheostomy should belimited to the incision and a small injection intothe lumen of the trachea, before opening it. Morewidespread infiltration may decrease the efficiencyof the sternomastoid muscles, or occasionallydiffuse into the recurrent laryngeal nerves, therebyincreasing obstruction.

When the laryngeal growth is friable, attemptsat intubation are likely to cause bleeding and thepossible avulsion of pieces of the tumour. Thesemay lodge in the bronchi.

CASE 7.A 67-year-old man was admitted with respiratory

obstruction. He complained of noisy breathing, short-ness of breath, hoarseness and haemoptysis. The nightbefore admission he had been walking about in hisroom trying to get his breath. He had a history ofpost-traumatic epilepsy and was having daily dosesof phenytoin and phenobarbitone. He was irrationaland unco-operative.

The respiration rate was 16 b.p.m. and pulse rate80/min. There was no cyanosis. Stridor was presentat rest in inspiration and expiration. The accessorymuscles of respiration were not in use and the alaenasi were not moving. At indirect laryngoscopy, amass was seen below the left cord.

After premedication with atropine 0.5 mg, the mouthand pharynx were sprayed with 4 per cent cocaine.The patient became violently unco-operative whenattempts were made to use a laryngoscope. The nasalseptum was grossly deviated to the right, so the leftnostril was sprayed with 4 per cent cocaine and blindnasotracheal intubation carried out through this nostril

with a No. 6 rubber tube. As soon as the tube wasin place, general anaesthesia was induced with thio-pentone 500 mg and continued with nitrous oxide,oxygen and halothane. A suction catheter was passeddown the nasotracheal tube and a small quantity ofblood aspirated.

Tracheostomy was performed uneventfully and directlaryngoscopy revealed a growth below the left vocalcord, occupying the left lateral and anterior walls ofthe larynx.

Comment. Tracheostomy under local anaesthesiawas not possible in this violently unco-operativepatient. Neither was orotracheal intubation under localanaesthesia. Nasotracheal intubation can be achievedwith less co-operation but in this case led to somebleeding from the growth.

If stridor is not present and the growth is notfriable endotracheal intubation under generalanaesthesia is usually without difficulties. A selec-tion of tubes and gum elastic catheters shouldalways be available and induction carried out inthe presence of a surgeon, equipped and ready toperform tracheostomy.

If stridor is present, but there are no other signsof severe respiratory obstruction, an attempt maybe made to pass an orotracheal tube under localanaesthesia. If the anaesthetist is not experiencedin this manoeuvre or any difficulty is encountered,tracheostomy must be performed. As soon as eitheran endotracheal tube or tracheostomy tube is inplace, general anaesthesia may be induced.

Elective surgery is contraindicated for a patientwith an acute infection of the larynx. Shouldemergency surgery be necessary, pre-operativetracheostomy must be considered. Orotracheal ornasotracheal intubation in these circumstances iscontraindicated because of the likelihood ofspreading infection and the near certainty ofincreasing oedema following removal of the tube.If minor surgery is intended and there is noevidence of serious respiratory obstruction, aninhalational sequence without intubation is indi-cated. Thiopentone must be used with greatcaution in the presence of lesions affecting thelarynx. It may predispose to laryngeal spasm.

Acute injuries of the larynx result in severeobstruction necessitating emergency tracheostomy.Patients with severe laryngeal stenosis coming tosurgery will usually have a well-establishedtracheostomy and general anaesthesia may be con-ducted through this.

Occasionally a patient will present for generalsurgery with a history of previous laryngostomy ortracheostomy. The anaesthetist should be alert for


the scars of these procedures in the neck andaware of the possibility of stenosis. If stridor orany sign of serious obstruction is present, intuba-tion should be carried out under local anaesthesia.The tube should be left in until the patient is wellawake and then removed by the anaesthetist.

Bilateral midline abductor paralysis of the larynxrequires tracheostomy under local anaesthesia.Other laryngeal palsies may cause obstructionduring general anaesthesia. Patients with theselesions are best dealt with by intubation. Thisusually presents no difficulties under general anaes-thesia. The tube should remain until the patientis awake.

A foreign body in the glottis is likely to producesigns of serious obstruction. In the adult it maybe possible to perform laryngoscopy under topicalanaesthesia and then treat the residual glotticoedema expectantly. In the child, topical anaes-thesia may not be practicable and preliminarytracheostomy with local anaesthesia is the leastdangerous approach to the problem.

Trachea! obstruction.Obstructions in the upper part of the trachea

may be assessed and managed in the same manneras similar lesions of the larynx.

When obstruction occurs in the lower part ofthe trachea, the situation is extremely serious, as itis not then possible to relieve the condition bytracheostomy. It is often possible to pass an endo-tracheal tube past the lesion under local anaes-thesia. The selection of an appropriate endo-tracheal tube is very important. It must be longenough to get below the obstruction. A tube with-out a cuff is easier to pass and enables a largersize to be used. When there is deviation of thetrachea, the direction of the bevel is important.It should be chosen so that the opening will not lieagainst the wall of the deviated trachea.

In cases of low intratracheal obstruction the onlyway to establish an airway may be the passage ofa small bronchoscope past the lesion. It may evenbe necessary to core out a passage through thetumour aspirating the debris through the broncho-scope.

CASE 8.A boy of 16 years was admitted, having been in

great respiratory distress for 12 hours. He had beentreated in the past for carcinoma of the thyroid andthe growth was ulcerating through the skin of theneck. His main complaints were difficulty in breathing,

difficulty in swallowing, sleeplessness and a wheezingcough.

The blood pressure was 170/80 mm Hg, the pulserate 108/min and the respiration rate 12 b.p.m. Therewas marked inspiratory and expiratory stridor at rest.The accessory muscles of respiration were actingstrongly and the alae nasi were moving. Auscultationrevealed slow air entry into the chest. Cyanosis wasnot present.

After premedication with promazine 50 mg thepatient was given a mixture of 79 per cent heliumand 21 per cent oxygen to breathe. The mouth andpharynx were sprayed with 4 per cent lignocaine andwith the aid of a laryngoscope the vocal cords andpyriform fossae were sprayed. Lignocaine, 4 ml of 2per cent, was then sprayed through the cords. Afterfurther inhalation of helium and oxygen a broncho-scope was passed into the trachea. Its wall was seento be infiltrated with growth and the lumen wasnarrowed to a chink at the level of the sixth cervicalvertebra. The bronchoscope was manoeuvred past thisobstruction. General anaesthesia was then induced withthiopentone 150 mg, followed by inhalation of nitrousoxide, oxygen and halothane through the broncho-scope.

A low tracheostomy was performed. There was greatdifficulty in finding the trachea in the neck, even withthe bronchoscope in sjtu, because of the mass ofgrowth present. In making the tracheostomy opening,which involved coring out some of the growth, theright common carotid artery was inadvertently opened,it having become an anterior relation of the trachea.It was successfully sutured.

Comment. This case illustrates severe respiratoryobstruction due to tracheal obstruction, and showsthat general anaesthesia may be safely induced oncethe obstruction is bypassed. The difficulties encounteredduring tracheostomy emphasize the futility of depend-ing on a quick emergency tracheostomy in this sortof situation.

CASE 9.A man of 44 years was admitted in the terminal

stages of bronchial carcinoma. His main complaintswere of a cough with bloody sputum and difficultyin breathing.

He was semiconscious and sitting bolt upright in achair with his head thrown back in the midline. Theblood pressure was 110/75 mm Hg, pulse rate 140/minand respiration rate 3-4 b.p.m. He had been havingincreasing doses of morphine and had had 30 mg byinjection 3 hours previously.

He was cyanosed, the accessory muscles of respira-tion were in use and stridor was present in inspirationand expiration, more marked in the latter. Ausculta-tion revealed diminished breath sounds and very slowair entry into both lungs. Stridor was maximum at thelevel of the manubrium sterni.

It was felt that his condition might be improvedtemporarily by bronchoscopy. The mouth and pharynxwere sprayed with 2 per cent lignocaine and with theaid of a laryngoscope 4 ml of 4 per cent lignocainewere squirted down the trachea. At bronchoscopygrowth was seen blocking both bronchi at the trachealbifurcation. A total of 2 ounces of growth was coredout and aspirated through the bronchoscope. His con-dition was greatly improved as a result; he becamepink and the stridor largely disappeared.


Comment. This was a case of very severeobstruction of the lower trachea and main bronchiwhich could not be bypassed by tracheostomy. Generalanaesthesia has no place in this situation.

ACKNOWLEDGMENT

I am grateful to the members of the consultant staffof University College Hospital for allowing me tomake use of details of cases in their care.

REFERENCES

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Boyan, P. C , and Howland, W. S. (1959). Manage-ment of anesthesia for laryngectomy. Anesth.Analg., Curr. Res., 38, 150.

Campbell, E. J. M. (1958). The Respiratory Musclesand the Mechanics of Breathing, p. 43. Chicago:Year Book.

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of the infant larynx influencing endotrachealanesthesia. Anesthesiology, 12, 401.

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Goldman, V. (1959). General Anaesthesia, (eds. Evans,F. T., and Gray, T. C), vol. 2, p. 276. London:Butterworth.

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Kelly, J. J., Hodge, G. E., and Grossman, A. (1957).Ludwig's angina. Canad. med. Ass. J., 77, 1089.

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SOMMAIRE

L'auteur fait une etude d'ensemble des causes del'obstruction du tractus respiratoire superieur. IIetablit une e'chelle des symptomes et signes selon ledegr6 de la gravite qu'ils indiquent, faisant remarquerque la cyanose est un signe d'obstruction tres graveet que la respiration striduleuse se produisant alorsque le patient repose est un signe tres caracte'ristiqued'obstruction tres grave. Dans ces derniers cas desse'datifs abaissant l'activite' fonctionnelle sont contre-indiques autant que l'atropine. Par contre Thuliumest susceptible d'etre utile. Lorsque chez les patientssouffrant d'obstruction grave une anesthe'sie generateest indispensable, on peut tout d'abord court-circuiterl'obstruction soit par catheterisme naso- ou oro-trache'al, soit par trache'otomie ou bronchoscopie,chacune de ces mesures pouvant etre rtalise'e sousanesthe'sie locale. On ne pourra jamais insistersuffisamment sur l'importance du cathete'risme"aveugle" nasal du patient conscient. Lorsque latracheotomie est indiquee, on devrait la faire totapres un choix conscient et tres reflechi choisi depreference aux autres mesures.

ZUSAMMENFASSUNG

Es wird eine Obersicht iiber die Ursachen fiir eineObstruktion der oberen Atemwege gegeben. Die Symp-tome und Zeichen werden nach ihrer Schwere einge-ordnet. Es wird besonders darauf hingewiesen, dafiZyanose fiir eine schwere Obstruktion spricht undStridor beim ruhenden Patienten ein sehr informativesortliches Zeichen fiir eine schwere Obstruktion ist.Atemdepressorische Drogen und Atropin sind beischwerer Obstruktion kontraindiziert, dagegen kannHelium von Hilfe sein. Falls bei einem Patienten mitschwerer Obstruktion eine Allgemeinnarkose notwendigwird, mufl die Obstruktion zunachst durch eine naso-tracheale oder orotracheale Intubation, eine Trache-otomie oder Bronchoskopie umgangen werden. Jedesdieser Verfahren kann in ortlicher Betaubung durchge-fiihrt werden. Es kann nicht geniigendauf den Wert derblinden nasalen Intubation am wachen Patienten hinge-wiesen werden. Wenn eine Tracheotomie angezeigt ist,sollte sie friihzeitig als ein elektiver Eingriff vorgenom-men werden.

by - semantic scholarin the pharynx (bougas and smith, 1958). laryngeal obstruction. eckenhoff...

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