Airway, the reference

Direct laryngoscopy displaces the tongue into the space beneath the mandible. A small or poorly mobile jaw leaves too little room and the glottis stays hidden, so the upper lip bite test, which checks forward jaw movement, detects the most difficult cases, 67%. Mallampati detects 53%, the best of the remaining signs. Restricted mouth opening rarely gives a false alarm, so it is the most specific sign, 94%, but it misses most difficult airways. Each sign samples one factor, so combined scores predict better than any single test.

Mallampati as best predictor. Mallampati is the best-known sign and is the right pick when jaw protrusion is not offered. When inability to protrude the jaw is among the options, the upper lip bite sign wins: it detects more difficult laryngoscopies and is also more specific.

Pooled data give upper lip bite testing the highest sensitivity, 67%, with Mallampati 53%, thyromental 37%, sternomental 33% and mouth opening 22%; mouth opening is most specific, 94%. Failure to advance the lower incisors past the upper predicts difficulty; combined scores outperform single tests.

Sources: Barash 9eMiller 10e

Thyromental distance measures the submandibular space. During laryngoscopy the blade pushes the tongue into that space. A small mandible shrinks it, so the tongue stays in the line of sight and the glottis is hidden: the so-called anterior larynx. The ASA guideline, quoted in Miller, flags under 6 cm. Miller's own text uses a looser 6.5 cm, about three fingerbreadths. The two cut-offs agree, because anything under 6 cm is abnormal by both, while 6 to 6.5 cm is only borderline.

Treating exactly 6 cm as abnormal. Six is the number people remember, so the bare value looks right. The criterion is a distance below 6 cm, though. A distance of exactly 6 cm sits on the boundary: the ASA criterion does not flag it, and under the 6.5 cm cut-off it is only borderline.

The ASA difficult-airway guideline counts a thyromental distance under 6 cm as concerning. Miller's text says a distance under 6.5 cm, roughly three fingerbreadths from thyroid notch to chin, signals reduced mandibular space and may predict difficult intubation.

Sources: Miller 10e

A tongue large for the oropharynx hides more throat, so each higher class shows fewer structures. In Miller's figure, class I shows the whole uvula and fauces; class II shows the fauces but only part of the uvula; class III loses the fauces, leaving only the uvular base. Faust's table counts the uvular base as class II when the faucial pillars are visible. Barash's figure makes class III soft plus hard palate. So check the pillars: visible means Faust's class II; hidden means Miller's class III.

Class II because uvula is visible. Any uvula in view feels like class II, and one table does put the uvular base there. That table, though, also needs the faucial pillars to be visible. Once the fauces are hidden and only the uvular base is left, the view is class III.

One classification makes class III the soft palate and uvular base. Its class II adds the fauces and part of the uvula. Another puts palate, faucial pillars and uvular base in class II. A third defines class III as soft and hard palate.

Sources: Miller 10eFaustBarash 9e

The laryngoscope must push soft tissue into the submandibular space, and fat in a thick neck crowds the pharynx. Barash ranks neck circumference of 40 cm or more above other signs for mask ventilation, laryngoscopy and intubation. Mallampati III–IV means a tongue large for the oropharynx; Stoelting and Miller count it as a positive intubation predictor in obesity. One Miller study of ramped obese patients found no link with neck circumference, so evidence is mixed. Treat a thick neck as the leading sign, not a certainty.

Choosing Mallampati over neck circumference. Mallampati chosen over neck circumference: Mallampati III–IV is a real obesity predictor and the best-known bedside test, so it feels like the safe pick. But when neck circumference is listed, Barash ranks it as the single biggest predictor in the obese. Mallampati is the fallback only when circumference is absent.

Barash names neck circumference of 40 cm or more the strongest predictor of difficult mask ventilation, laryngoscopy and intubation. Stoelting says a large neck or high Mallampati predicts difficult intubation more reliably. A Miller study found Mallampati III–IV predictive but no link for neck circumference.

Sources: Barash 9eStoelting 8eMiller 10eDifficult Airway Society 2025

Each factor spoils the mask seal or makes upper-airway obstruction more likely: a beard prevents sealing, a snorer's airway obstructs, and excess soft tissue and an edentulous face add to both. The five-factor list comes from a French prospective cohort. Barash ranks by odds ratio: beard first, then BMI, missing teeth and age, snoring last. Miller's airway chapter lists more: obesity at BMI 30 or more, plus male sex and Mallampati III or IV. Obesity counts at either cut-off; female sex does not.

Choosing obesity as the strongest predictor. Obesity seems the obvious airway problem, and in a bariatric patient it is the strongest factor on offer. Among all five predictors, though, a beard has the highest odds ratio and BMI comes second.

A French prospective cohort found five independent predictors. Barash tabulates their odds ratios: beard highest at 3.18, then BMI over 26 at 2.75, with snoring listed last. Miller's airway chapter also lists male sex, Mallampati III or IV, and BMI 30 or more.

Sources: Barash 9eMiller 10eMayo review

Saturation can fall under anaesthesia from apnoea, atelectasis, shunt, airway obstruction or bronchospasm. Giving maximal oxygen widens the safety margin while you look for the cause. In an intubated patient, suspect the tube first. Moving or repositioning the patient can push a correctly placed tube into a main bronchus, so one lung is no longer ventilated. Signs are hypoxaemia, rising airway pressures, uneven chest movement and missing breath sounds on one side. A pneumothorax can look the same. Exhaled CO2 confirms the tube is in the trachea at all.

Blame machine or stop surgery. This looks systematic, and because the fall comes as surgery starts, the machine or the surgeon seems to blame. But it leaves out the immediate step, raising oxygen to maximum, and skips the tube. Tube movement after positioning is a likely reversible cause, and stopping surgery treats nothing.

During anaesthesia, manage desaturation by keeping the airway open and giving 100% oxygen. Hypoxaemia with high airway pressures, uneven chest expansion and absent breath sounds on one side suggests endobronchial intubation. Repositioning can move a tube. Expired CO2 is the gold-standard check of placement.

Sources: Barash 9eMiller 10eFaust

Patients die from hypoxia, not from a missing tube. After an unsuccessful attempt, the difficult-airway algorithm in Faust has you call for help and keep oxygenating by facemask while you consider waking the patient. Repeated laryngoscopy can obstruct the airway and cost you mask ventilation. So the Difficult Airway Society guideline moves on once intubation is declared failed or the mask stops working. A second-generation supraglottic airway restores oxygenation and lets the team stop, think and usually wake the patient.

Another videolaryngoscopy attempt. Videolaryngoscopy improves first-pass success, so another look feels productive. But mask ventilation is already difficult and the patient is desaturating. Another attempt delays oxygenation and can make the airway worse. Restore oxygenation with a supraglottic airway first, then decide.

When intubation fails, rescue with a second-generation supraglottic airway. After unsuccessful attempts, consider calling for help and continue facemask ventilation. In one case, an oral airway, jaw thrust and two-person technique failed to achieve adequate mask ventilation, but an LMA immediately gave a clear airway.

Sources: Difficult Airway Society 2025FaustBarash 9e

Settle it by ruling out the alternatives. The Difficult Airway Society guideline allows three attempts plus one by a more experienced colleague, as repeated instrumentation adds trauma and oedema; further laryngoscopy, with or without the collar, is therefore out. Blood and secretions blind a fibreoptic scope. With ventilation failing, oxygenation becomes the goal: a supraglottic airway only if offered and still ventilating, otherwise front-of-neck access, which leaves the neck undisturbed. The guideline moved from cannula to scalpel technique, so take scalpel if offered, cannula if it is the only route.

Attempting fibreoptic intubation to protect the spine. Fibreoptic intubation appeals because it can pass a tube without moving a possibly injured cervical spine. Here it fails: blood in the pharynx obscures the scope's view, and the attempt limit has already been exhausted while ventilation is deteriorating, so oxygenation, not another intubation, is the priority.

The Difficult Airway Society guideline limits intubation to three attempts plus one by a more experienced operator, and starts priming for emergency front-of-neck airway when supraglottic ventilation is difficult, favouring scalpel over cannula. A textbook adds that blood and secretions defeat even expert bronchoscopists.

Sources: Difficult Airway Society 2025Miller 10e

The trigger is failure to oxygenate, not failure to intubate. Once the tube, the supraglottic device and the facemask have all failed, only an airway made below the larynx can deliver oxygen. Miller's textbook describes reversing rocuronium with sugammadex so that breathing returns. This works only with favourable body habitus, adequate preoxygenation and modest propofol and opioid doses. The Difficult Airway Society guideline says sugammadex reversal is not a reliable rescue after failed intubation. So do not wait on it: cut through the cricothyroid membrane.

Reverse with sugammadex and wake patient. It is tempting because sugammadex reverses rocuronium quickly, and waking the patient sounds like the safe way out. It fails because reversing the block does not open an obstructed upper airway. Fetching and drawing up the drug also delays the front-of-neck airway that the hypoxic patient needs.

If plans A, B and C fail and the patient cannot be intubated or oxygenated, emergency access through the front of the neck by scalpel cricothyroid stab is mandatory. Sugammadex reversal is unreliable; breathing returns only with favourable habitus, oxygen duration and modest induction doses.

Sources: Difficult Airway Society 2025Miller 10e

The cricothyroid membrane is a fibroelastic sheet that runs from the lower border of the thyroid cartilage to the upper edge of the cricoid ring. You can feel both cartilages from the front of the neck, so the membrane is quick to find and enter, either with a percutaneous cannula or by an open technique. A skilled operator can do this fast. That speed is why cricothyrotomy, rather than tracheostomy, is the usual surgical airway in a dire emergency.

Entering below the cricoid cartilage. The cricoid is the best-remembered landmark, and the gap just below it feels like the right entry point, near a tracheostomy site. However, that gap is the cricotracheal ligament, which joins the cricoid to the first tracheal ring. The target membrane lies above the cricoid, not below it.

Cricothyrotomy means opening an airway through the cricothyroid membrane, which is attached to the thyroid cartilage above and the cricoid below. A separate ligament joins the cricoid to the first tracheal ring. In emergencies the membrane can be entered with a percutaneous catheter.

Sources: Barash 9eMiller 10eFaust

Anaesthesia is not induced first because intubation after induction is predicted to be difficult or impossible. Kept awake, the patient goes on breathing unaided, and in neck disease neurology can be checked throughout, so Miller rates it safest there. Barash allows light sedation only while the patient stays cooperative. The textbooks offer either videolaryngoscope or flexible bronchoscope; the DAS awake intubation guideline, an outside source beyond the textbooks, decides between them: restricted mouth opening, a big tongue or a fixed flexed neck favour the bronchoscope.

Videolaryngoscopy after induction. Videolaryngoscopy is tempting because textbooks list it for predicted difficult intubation and spinal disease. But this option does not say awake, so it gives up spontaneous breathing and neurological checks. Also, when mouth opening is this narrow, the DAS guideline, an outside source beyond the textbooks, prefers the flexible bronchoscope.

Miller uses awake bronchoscopic intubation when intubation after induction looks difficult or impossible, and calls it safest in severe neck disease. Barash allows an awake or lightly sedated technique in cooperative patients. The DAS guideline, outside the textbooks, favours the bronchoscope for restricted mouth opening.

Sources: Miller 10eBarash 9eOutside our books: Difficult Airway Society guidelines for awake tracheal intubation (ATI) in adults (2020)

Swollen floor-of-mouth and neck tissues stay open only through the patient's own muscle tone. Anaesthetic drugs and relaxants abolish that tone, so the distorted airway collapses and obstructs completely. Staying awake preserves spontaneous breathing until a tube is placed. Barash rates awake tracheostomy under local anaesthesia the safest route. Miller calls tracheostomy before drainage classic but dated, and prefers fibreoptic intubation, nasal when trismus prevents mouth opening. Both routes are awake: use fibreoptic when available, otherwise awake tracheostomy.

Slow inhalational induction. A slow gas induction that keeps spontaneous breathing feels like a careful middle path, and inhalational induction does appear among the alternatives. But any depth of anaesthesia relaxes the muscles holding the swollen airway open. The airway can block before the tube passes, and there is no awake fallback left.

Barash rates awake tracheostomy under local anaesthesia safest. Miller calls pre-drainage tracheostomy dated, favouring fibreoptic intubation (often nasal for trismus) and warning that airway-tone-reducing drugs can cause complete obstruction. Faust advises awake fibreoptic intubation or local tracheotomy when conventional intubation is doubtful.

Sources: Barash 9eMiller 10eFaust

A stricture fixes the lumen below the cords. A tube sized for a normal trachea may not pass it, and forcing one can turn partial obstruction into total loss of the airway. The DAS awake intubation guideline is an outside source. It warns that narrowing may prevent intubation and advises a smaller tube with front-of-neck access prepared. Miller's also uses a smaller-than-usual tube in paediatric stridor. For stenosis it prefers rigid bronchoscopy, which can get past the lesion and ventilate, done in theatre with surgeons present.

Standard-size tube through stricture. Bypass looks the most drastic, so it feels like the least appropriate choice. But how drastic an option is does not decide this question. Bypass avoids instrumenting the narrowed segment at all. The method that actually fails is pushing a normal-sized tube through a lumen too small for it.

Miller's favours rigid bronchoscopy for tracheal stenosis, in theatre with surgeons ready, as it can pass the obstruction and ventilate; it also uses smaller-than-usual tubes for stridor. DAS guidance adds that narrowing may prevent intubation, so use a smaller tube and prepare front-of-neck access.

Sources: Outside our books: Difficult Airway Society guidelines for awake tracheal intubation (ATI) in adults (2020)Miller 10e

A fistula lets positive-pressure breaths escape through the airway defect. Ventilation is lost, a tension pneumothorax can build, and soiled secretions spill into the healthy lung. Spontaneous breathing until a double-lumen tube isolates the good lung avoids all three. Barash and Miller both rank awake double-lumen intubation best. Miller adds that it needs a cooperative, well-topicalised patient; when that fails, a modified rapid sequence with bronchoscopic tube guidance is acceptable in a normal airway. Barash warns that a plain rapid sequence risks contamination and tension pneumothorax.

Standard rapid sequence induction. A full stomach makes rapid sequence induction the reflex choice, and the airway was easy before. But paralysis commits you to positive pressure before isolation is confirmed. Breaths leak through the fistula, tension pneumothorax may develop and soiling spreads. Miller accepts only a modified version with bronchoscopic double-lumen guidance.

Barash calls awake, spontaneously breathing double-lumen intubation ideal, citing considerable contamination and tension-pneumothorax risk with rapid sequence. Miller calls awake fibreoptic double-lumen intubation possibly safest, allowing modified rapid sequence with bronchoscopic guidance in normal airways. Both insist isolation precedes positive pressure.

Sources: Miller 10eBarash 9e

With a small jaw, the tongue falls backwards, so losing muscle tone can make mask ventilation nearly impossible and intubation hard. Stopping breathing with propofol and a relaxant therefore risks failed intubation and oxygenation. The sources differ in technique but agree on principle. Stoelting often places a supraglottic airway awake, then deepens with an inhaled agent. Faust prefers awake intubation where feasible, otherwise sevoflurane with spontaneous breathing. The small jaw also defeats direct laryngoscopy, so an indirect view must be ready from the start.

Spontaneous breathing, then direct laryngoscopy. It keeps the child breathing during inhaled induction, so seems safe, but fails at laryngoscopy. The small jaw and posteriorly placed tongue usually prevent a direct view, and repeated attempts add harm. The cords must be seen with a fibrescope or videolaryngoscope prepared beforehand.

Stoelting warns these children may be nearly impossible to mask ventilate, so spontaneous breathing must be kept. It commonly uses an awake supraglottic airway before inhalational induction and advises against direct laryngoscopy. Faust prefers sevoflurane with spontaneous breathing when awake intubation is not possible.

Sources: Stoelting 8eFaust

Miller's calls the airway maximum uncertain, citing totals of 4 to 9 mg/kg; the outside DAS awake intubation guideline fixes it at 9 mg/kg lean body weight because toxic plasma levels appeared from 6.0 mg/kg. Convert: 1 ml of 1% = 10 mg, so ml × percentage × 10 = mg; one 10% spray = 10 mg. Gagging starts at tongue-base pressure receptors, so mouth gel misses; a few sprays alone leave larynx and trachea untreated; big volumes of strong solution overshoot.

Thirty 10% sprays alone. Thirty 10% sprays sound simple, but they load the tongue base alone, leave larynx and trachea untreated and push the total towards the toxic band. Nebulised 4% 4 ml plus five 10% sprays reaches every target with a lower total.

The DAS guideline caps lidocaine at 9 mg/kg lean body weight after toxic levels at 6.0–9.3 mg/kg, and counts 1 ml of 1% or one 10% spray as 10 mg. Miller's targets tongue base, pharynx and larynx, not the mouth, allowing combinations within the maximum.

Sources: Outside our books: Difficult Airway Society guidelines for awake tracheal intubation (ATI) in adults (2020)Miller 10e

Two risks compete: aspiration, and vitreous loss when eye pressure rises. Placing a cuffed tube quickly deals with aspiration. The biggest pressure spikes come from coughing, bucking and Valsalva in a light or partly paralysed patient, not from the drugs, so depth and complete blockade matter most. Suxamethonium was avoided because it briefly raises eye pressure, and Miller still adds a caveat for an open anterior chamber. A series of penetrating injuries showed no extrusion, so Barash and Miller now accept it within a controlled rapid sequence.

Awake intubation to preserve airway reflexes. It is tempting because preserved airway reflexes protect a fed trauma patient from aspiration. With a normal airway it adds nothing, and topical anaesthesia and passing the tube provoke coughing and straining. Those cause the largest rises in eye pressure, which can expel the eye's contents.

Barash advises IV induction with a neuromuscular blocker for cases that cannot wait. Rocuronium 1.2 mg/kg is useful. Both books accept suxamethonium in open-eye injury within a controlled rapid sequence, warning that inadequate depth or blockade raises pressure more than the drug does.

Sources: Barash 9eMiller 10e

Blood from the tonsillar bed is swallowed, often in volumes nobody notices, so the stomach is full and aspiration is the main risk. Barash describes cricoid pressure during rapid sequence induction as controversial but sometimes helpful. Miller says it is the usual practice. Both books agree the stomach is full, so rapid sequence induction is the default. Hypovolaemia calls for less induction agent or for etomidate. The relaxant must reach intubating conditions within 60 to 90 seconds: succinylcholine 1.5 mg/kg or high-dose rocuronium 0.9–1.2 mg/kg.

Etomidate with ordinary-dose rocuronium. It looks correct because it pairs rapid sequence induction with etomidate in a pale, hypotensive child. The rocuronium dose is the problem. It is the ordinary intubating dose, not the high rapid-sequence dose, so the airway stays unprotected for longer while the stomach holds blood.

Miller advises fluids before induction and reduced induction agent, or etomidate, if hypovolaemic. Because of swallowed blood, it treats cricoid pressure with rapid sequence induction as routine, accepting succinylcholine 1.5 mg/kg or rocuronium 0.9–1.2 mg/kg. Barash insists on full-stomach precautions.

Sources: Miller 10eBarash 9e

Both morbid obesity and symptomatic reflux make it more likely that stomach contents will reach the lungs. Obesity also makes airway obstruction more likely, for example through sleep apnoea. Sedation dulls protective reflexes but leaves the trachea open. An oral or nasal airway, or a supraglottic device, only keeps the airway open. A cuffed tube in the trachea is the only definitive airway because it seals the trachea against soiling. So when the airway must be protected, choose intubation under general anaesthesia.

Sedation with a supraglottic device. It looks like a middle path. The child gets an airway device and stays lightly sedated, which seems gentle and fits MRI. But a supraglottic device does not seal the trachea, so it is not a definitive airway. It does not protect a child with reflux from aspiration.

Aspiration risk makes sedation a poor choice, and the listed risks include morbid obesity and symptomatic reflux. Patients prone to aspiration or obstruction may need an endotracheal tube. Only a cuffed tube sitting in the trachea counts as a definitive airway.

Sources: Barash 9eStoelting 8eMiller 10e

Pressing on the cricoid ring closes the upper oesophagus, so regurgitated stomach contents cannot reach the pharynx. A lighter force is used while the patient is awake and is raised once consciousness is lost. Miller and the latest difficult airway guideline both give the 10 N and 30 N targets. The upper limit comes from the obstetric airway guideline, which is outside the textbooks. It warns that going well beyond the target, for example to 44 N, is linked to airway obstruction.

30 N as the excessive force. 30 N is the highest figure most people remember, and it can make laryngeal mask placement harder, so it feels like the harmful level. But 30 N is the recommended target after loss of consciousness, not too much force. The excessive force linked to airway obstruction is 44 N.

Miller and the difficult airway guideline recommend 10 N cricoid force while awake, rising to 30 N after loss of consciousness. The obstetric airway guideline, an external source, adds that excessive force, such as 44 N, is associated with airway obstruction.

Sources: Outside our books: Obstetric Anaesthetists' Association and Difficult Airway Society guidelines for the management of difficult and failed tracheal intubation in obstetrics (2015)Miller 10eDifficult Airway Society 2025

Fire needs fuel, ignition and an oxidiser. The laser ignites; a plain tube, its cuff and dry gauze are fuel. Barash caps inspired oxygen at 0.3 and Miller advises that level or lower if possible, so they agree: titrate to the lowest concentration the patient tolerates, never above the cap, and no nitrous oxide. A laser-resistant tube limits fuel; dyed saline in the cuff flags a strike early; wet sponges burn less readily. Without any tube there is nothing to ignite, but aspiration and ventilation become harder.

Thirty per cent oxygen with nitrous oxide. Thirty per cent oxygen echoes the textbook ceiling, so it looks right. But nitrous oxide is itself an oxidiser that supports combustion. Adding it re-enriches the airway atmosphere that the low oxygen was meant to lean out. The books say avoid it entirely.

Both books keep oxygen at or below 0.3 with air, not nitrous oxide. They advise a laser-safe tube, a dyed-saline cuff as an early rupture warning, and moistened sponges, which burn less readily. Tubeless techniques remove the fuel but risk aspiration.

Sources: Miller 10eBarash 9e

A pulse of high-pressure oxygen leaves a narrow needle or catheter very fast. By Bernoulli's principle, the pressure beside that fast stream falls, so room air is drawn into it. The patient therefore receives the jet plus the air it pulls in. The tidal volume is larger than the oxygen alone could give, but the oxygen concentration is lower. Inhalational anaesthesia cannot be given during jet ventilation, so it is run with intravenous anaesthesia.

Gas density (heliox-style flow) explanation. Gas density sounds relevant because heliox helps turbulent flow through narrowed airways, where flow across an orifice depends on density. But that is about flow through a stenosis, not how an injector works. What defines an injector is that it entrains room air.

Each oxygen pulse from the jet or injector needle draws in room air by the Venturi effect, which follows from Bernoulli's principle. This raises the delivered volume and lowers the oxygen concentration. The air–oxygen mix ventilates the patient. Inhalational anaesthesia is impossible during jet ventilation.

Sources: Miller 10eBarash 9eFaust

During the light, excitable phase of emergence the larynx overreacts to stimulation. Moving the cuff then can trigger coughing and laryngospasm. Deep anaesthesia suppresses these reflexes. Full return of reflexes lets the patient protect their own airway. Deep removal still depends on the agent. One textbook reports that in children breathing spontaneously, desflurane caused worse airway events than isoflurane, especially when the mask came out before emergence. Sevoflurane is the least irritant. So when deep removal is planned, it is best done under a non-irritant agent.

Assuming the mask protects against regurgitation. It is tempting because the laryngeal mask is credited with keeping blood and surgical debris out of the airway during supraglottic surgery. That is protection from material above the cuff. It does not make the device safe in a patient at risk of regurgitating stomach contents.

Remove under deep anaesthesia, or once protective reflexes return with mouth-opening on command; removal during excitation risks coughing and laryngospasm. In children, desflurane caused more airway events than isoflurane, especially with mask removal before emergence. Sevoflurane is least irritant.

Sources: Barash 9eMiller 10e

Vital capacity is the largest breath a patient can take on demand. It reflects residual neuromuscular block, central respiratory drive and respiratory muscle strength together. Enough reserve means the patient can cough, sigh, clear secretions and keep breathing without help once the tube and ventilator support are gone. Resting tidal volume shows only quiet breathing, not reserve. Gas-exchange indices such as the dead-space ratio and the alveolar–arterial gradient guide weaning from long-term ventilation in intensive care. They are not the routine tests before postoperative extubation.

Dead-space ratio of 0.6. A dead-space ratio of 0.6 sits exactly at the table's limit, so it looks correct. The table marks it as a measure for weaning from mechanical ventilation in intensive care. It is not a routine awake postsurgical criterion; vital capacity is the listed bedside volume test.

The textbook's objective criteria for routine awake extubation are vital capacity at least 10 mL/kg, peak negative inspiratory pressure beyond –20 cmH2O and tidal volume over 6 mL/kg. A dead-space ratio up to 0.6 is reserved for intensive-care weaning.

Sources: Barash 9e

Croup (laryngotracheobronchitis) narrows the airway below the cords. The lining swells all the way round, which gives the steeple sign on X-ray. Inhaled racemic adrenaline constricts the vessels in that lining, so the swelling shrinks and the stridor eases. That response fits a lesion made of mucosal oedema. Steroids were once disputed, and both Barash and Miller still call them controversial. Barash records the current view that a short course helps. So steroids support adrenaline as an add-on and do not replace it.

Diagnosing croup from toddler age. It is tempting because croup is thought of as a toddler's illness, so a 3-year-old seems to settle it. But age is only background. A response to treatment that targets the mechanism, shrinking oedematous subglottic mucosa, is the feature the texts link to croup.

Croup is described as circumferential subglottic soft-tissue swelling that gives a steeple sign. Nebulised racemic adrenaline helps by constricting mucosal vessels and reducing upper-airway swelling. Steroids are debated, but a short course is now thought useful.

Sources: Barash 9eMiller 10e

A preformed RAE tube or flexible LMA lies under the blade of the tonsil gag. When the gag opens fully, it can squeeze, bend or shift the airway device, and textbooks describe this as common at gag insertion. A narrowed lumen raises resistance. Peak pressure therefore climbs, less tidal volume reaches the lungs and less carbon dioxide comes back. The rigid standard LMA is especially easy to crush under the gag. A wire-reinforced flexible device fits beneath it much better.

Tube migration from neck extension. It is tempting because tube migration also changes peak pressure and capnography. But the problem started when surgery began, which points to the gag. Neck extension tends to pull the tube back rather than push it deeper. A compressed tube explains both signs at that moment.

When the surgeon opens the mouth gag, an RAE tube or LMA often kinks or moves. The rigid standard LMA is easily crushed under the gag. Tube migration shows up as changed peak pressure and capnography, and extending the neck withdraws the tube.

Sources: Miller 10eBarash 9eFaust

When an object only partly blocks a bronchus, the airway widens on inspiration and gas slips past it. On expiration the airway narrows, the object seals the lumen, and gas cannot leave. Each breath adds volume beyond the block, so that segment or lung over-distends into obstructive emphysema. Pressure rises and risks barotrauma. Nitrous oxide enters the trapped gas faster than nitrogen leaves it, so the space grows. Spontaneous breathing, or long expiratory times under controlled ventilation, limits the pressure build-up. Imaging may also show infiltrate or collapse.

Collapse beyond the obstruction. Collapse is also a recognised imaging finding, and 'obstruction leads to collapse' is a reflex answer. But collapse needs a complete block so the trapped gas is absorbed. A partly blocking object that lets air in and not out causes air trapping and over-inflation, which is the ball-valve effect.

Barash says nitrous oxide is avoided so that air does not become trapped beyond the obstruction. It favours spontaneous breathing to limit ball-valve pressure, and lists air trapping, infiltrate and collapse on imaging without ranking them. Faust advises adequate expiratory time to prevent ball-valve barotrauma.

Sources: Barash 9eFaust

Aspirated material injures the alveolar-capillary barrier, so plasma leaks into the lung as permeability oedema. Gas exchange fails at once, causing hypoxaemia, tachypnoea and bronchospasm. The infiltrate takes hours to become visible on a film, so a clear early radiograph cannot exclude the diagnosis. Symptoms come before film changes, so after a minor aspiration, watch for several hours for hypoxaemia, cough, wheeze or new shadowing before discharge. After supine aspiration, shadowing most often appears in the right lower lobe's superior segment.

Attributing it to acute chest syndrome. The clear film pushes people away from aspiration and towards another cause of hypoxaemia with lung injury. Acute chest syndrome is a complication of sickle cell disease, not of gastric contents aspirated at intubation. Aspiration explains both the early hypoxaemia and the delayed radiographic changes.

Aspiration causes capillary-permeability pulmonary oedema; hypoxaemia is common, with possible tachypnoea and bronchospasm. Radiograph may stay normal for 6–12 hours. After small aspiration, outpatient follow-up is reasonable only if no hypoxaemia, cough, wheeze or film change develops within 4–6 hours.

Sources: Stoelting 8eBarash 9e

When a patient breathes in hard against a closed glottis, the pressure inside the chest becomes very negative. More blood then returns to the right heart. This raises hydrostatic pressure in the pulmonary capillaries and pushes fluid into the interstitium and alveoli. The same negative pressure increases left ventricular afterload, so the ventricle ejects less and left atrial and pulmonary venous pressures rise, which adds to the leak. In recovery, laryngospasm is the usual trigger. Any upper-airway occlusion can cause it.

Pulmonary embolism. A smoker who becomes agitated and suddenly hypoxic after abdominal surgery makes people think of embolism. But embolism does not explain bilateral basal crackles. The hypoxia also came straight after laryngospasm, which is the classic trigger for oedema caused by airway obstruction.

Postobstructive (negative-pressure) pulmonary oedema is uncommon but important after laryngospasm or other upper-airway obstruction following extubation, and laryngospasm is probably its commonest cause in recovery. The negative pressure raises pulmonary hydrostatic pressure and also loads the left ventricle.

Sources: Miller 10e

Total thyroidectomy can remove or injure the parathyroids, so parathyroid hormone falls and calcium drifts down over days. One major text places symptoms at 24 to 96 hours; another notes they occasionally start within hours but typically not before 24 to 72 hours, so both treat tetany as a delayed event. Laryngeal muscle is very sensitive to low calcium, making stridor and laryngospasm early tetanic signs that calcium reverses. A haematoma compresses the trachea straight after surgery, so in recovery bleeding, not cramping tetany, is the expected problem.

Evacuating a haematoma. Evacuating a haematoma is the reflex answer to breathing trouble after neck surgery, and it is correct when compression appears straight after the operation. Stridor that begins a day or more later fits falling calcium, and reopening the wound will not treat tetany.

Hypocalcaemic symptoms appear within 24 to 96 hours, usually not before 24 to 72 hours, rarely within hours. Stridor progressing to laryngospasm is an early sign. Once the airway is secure, give intravenous calcium gluconate or chloride. Haematoma compression occurs immediately after surgery.

Sources: Barash 9eMayo reviewStoelting 8e

The thyroid bed lies against the trachea, so bleeding there compresses the airway from outside and the wound swells; haematoma is the commonest external compressor after thyroid, parathyroid or carotid surgery. Laryngeal oedema, the usual cause of post-extubation stridor, narrows the airway from within and leaves the neck flat. Nerve palsy shows in the voice: one recurrent nerve gives hoarseness, both give stridor or aphonia, so a speaking patient lacks bilateral palsy. Hypocalcaemic stridor appears 24 to 96 hours later.

Blaming hypocalcaemia for stridor in recovery. Hypocalcaemia is tempting because parathyroid tissue is at risk in these operations and low calcium can produce stridor that progresses to laryngospasm. But tetany takes a day or more to develop, so stridor in recovery is mechanical (haematoma, oedema or nerve palsy), not hypocalcaemic.

Haematoma is the usual external compressor of the airway after thyroid and parathyroid surgery, while laryngeal oedema commonly causes post-extubation stridor. Hypocalcaemic symptoms emerge at 24 to 96 hours. Unilateral recurrent nerve damage causes hoarseness; bilateral damage causes stridor or aphonia.

Sources: Miller 10eBarash 9e

Surgical damage to the recurrent laryngeal nerves tends to hit the abductor fibres, which open the cords. When both sides are affected, the unopposed adductors bring the cords to the midline and close the glottis, causing stridor, airway obstruction and little or no voice. Unilateral damage causes hoarseness. A haematoma obstructs the airway by compressing the trachea, so the neck is swollen and tense. Laryngeal oedema is the commonest cause of stridor after extubation. A normal neck with a lost voice points to the nerves.

Neck haematoma. Haematoma is the classic airway emergency after neck surgery. It obstructs by compressing the trachea, so it produces a swollen, tense neck. Once the neck has been examined and found normal, it is excluded. It stays possible only when the question gives no neck finding.

Injury to both recurrent laryngeal nerves closes the glottis because cord adduction goes unopposed, and the patient needs immediate intubation. Laryngeal oedema usually explains stridor after extubation. A large haematoma can compress the trachea. Nerve injury on one side shows as hoarseness.

Sources: Miller 10eMayo review

The recurrent laryngeal nerve supplies the muscles that open the vocal cords. When one nerve is paralysed, that cord sits near the midline and the voice suffers. The other cord still moves, so breathing is kept and usually no treatment is needed. If both nerves are lost, both cords sit near the midline, causing aphonia and obstruction that need immediate intubation. Low calcium and haematoma threaten the airway through laryngospasm or tracheal compression. They cause stridor rather than hoarseness alone.

Hypocalcaemia as cause of hoarseness. After parathyroidectomy in a renal patient, a falling calcium about a day later is expected, so it feels like the answer. But low calcium affects the sensitive laryngeal muscles and causes stridor, laboured breathing and laryngospasm. That is an airway problem, not hoarseness with a safe airway.

Damage to one nerve causes hoarseness without obstruction, usually recovers and needs no treatment. Damage to both causes aphonia that needs intubation. Airway symptoms from low calcium usually appear at 24 to 72 hours as stridor and laryngospasm. A large haematoma can compress the trachea.

Sources: Barash 9eStoelting 8eMayo review

The hypoglossal nerve crosses the endarterectomy field and can be stretched, compressed or heated. The textbooks list it among the nerves to check after extubation but give no sign. Outside sources, not the textbooks, supply the sign: a peripheral lesion weakens the tongue muscles on the same side, so the protruded tongue swings toward the injured side, with slurred speech and poor swallowing. A 'dysphonia' here means dysarthria; true hoarseness reflects injury to the recurrent laryngeal branch of the vagus. The deviated tongue decides.

Stroke from a hemispheric lesion. Stroke is the feared complication after carotid surgery, so a deviated tongue seems to fit. But a hemispheric lesion is supranuclear: the tongue points away from it, without atrophy. Slurred speech, poor swallowing and tongue deviation straight after this neck operation fit a peripheral hypoglossal injury.

The anaesthesia textbook lists the hypoglossal among the nerves to examine soon after extubation and links one-sided recurrent laryngeal injury to hoarseness. An outside review links isolated hypoglossal disease to swallowing and speech difficulty with tongue deviation, and says infranuclear damage affects the same side.

Sources: Outside our books: Hypoglossal Nerve Neuropathies—Analysis of Causes and Anatomical Background (2024)Miller 10e

Swollen supraglottic tissue leaves a narrow channel that can close completely. Anything distressing, such as a needle, X-ray or examination, may cause total obstruction in a child who is just coping, so avoid it until the airway is controlled. Slow sevoflurane mask induction keeps the child breathing spontaneously as anaesthesia deepens. The cannula goes in afterwards, and every case is secured with a tracheal tube. Outside the textbooks, an adult review prefers awake fibreoptic intubation; without it, adults too get inhalational induction.

Cannulating and paralysing before the airway is controlled. Placing a cannula first looks like routine emergency care and seems safer for giving drugs. But the needle upsets the child, and agitation can turn partial obstruction into complete obstruction before anyone controls the airway. Access goes in only once sevoflurane has deepened anaesthesia.

Paediatric texts say to disturb the child as little as possible and intubate every case after a slow sevoflurane induction sitting up. Outside the textbooks, adult reviews favour awake fibreoptic intubation and accept inhalational induction when topicalisation is hard.

Sources: Miller 10eFaustBarash 9eOutside our books: Airway Management for an Adult Epiglottic Abscess (2020)Outside our books: Airway management of adult epiglottitis: a systematic review and meta-analysis (2024)

Heat and smoke damage the face, mouth and upper airway, and swelling is expected but not yet present. A tube placed early, while the anatomy is still accessible, is safer than one attempted through an oedematous airway, so visible injury signs justify intubation even when observations are normal. CO poisoning with neurological impairment is a separate indication, as airway protection and oxygenation are at stake. Everyone receives 100% inspired oxygen first, which speeds CO displacement from haemoglobin. A calm child with only soot gets oxygen and close watching.

Intubating at once for soot alone. Soot round the nose and mouth looks like an airway burn, so intubating at once feels decisive. But in an awake child breathing calmly with no stridor, hoarseness or neurological change, soot alone calls for 100% oxygen and close, repeated observation. Intubate once airway-threat or neurological signs appear.

Signs of inhalation injury include facial burns, singed nasal hair, hoarseness, stridor and carbonaceous sputum. Early intubation is advised for symptomatic inhalation injury, threatening oropharyngeal burns, anticipated swelling, or CO poisoning with neurological impairment. Breathing 100% oxygen cuts the CO half-life to about an hour.

Sources: Miller 10e

Blood from the tonsillar bed is often swallowed, so the bleeding seen at the mouth underestimates the true loss. Pallor and agitation mean the child is already hypovolaemic. Inducing anaesthesia in a child who is still under-filled can cause cardiovascular collapse, and without a line there is no route for fluid or drugs. The stomach is also full of blood. So restore volume first, then do a rapid-sequence induction with reduced doses. Empty the stomach only once the airway is secured in theatre.

Immediate gas induction in theatre. This option is tempting because gas induction is the usual paediatric route and it gets the child to the surgeon quickly. It fails because a mask induction in a hypovolaemic child with a stomach full of blood risks collapse and aspiration, with no line to treat either.

Both texts say IV access and volume replacement, including blood products when needed, should come before induction. Swallowed blood means the patient has a full stomach, so cricoid pressure is applied during rapid-sequence induction. Hypovolaemia may call for lower induction doses or etomidate.

Sources: Barash 9eMiller 10e

The fistula forms where the tracheostomy tube presses against the innominate artery. Pulsation of the cannula is an early warning sign. Overinflating the cuff, and pulling the tube forward, presses the tracheal wall against the bleeding point and slows the haemorrhage. That first-aid tamponade does not control the bleeding definitively. So the tracheostomy is then replaced by an orally placed tracheal tube to protect the airway, and the vessel is controlled surgically.

Finger pressure and straight to theatre. Pressing with a finger and heading straight to theatre sounds decisive, and it also compresses the bleeding point. But the books start with the cuff already in the trachea. Other steps come only if cuff overinflation fails, and the airway must be secured before surgery.

Miller lists cuff overinflation as the first step. If that fails, the tracheostomy is exchanged for an oral endotracheal tube. Treatment also includes pulling the tube forward to tamponade, then placing an oral tube to secure the airway before surgical control of the bleeding.

Sources: Miller 10e

Awake flexible-scope intubation barely moves the neck and keeps protective reflexes, so Miller calls it often safest for spinal instability, but only when the patient can cooperate. Stoelting holds that blood need not stop the scope, yet Miller's clinical experience is that a distorted, blood-filled airway defeats even experts, so with active bleeding the scope is the wrong tool. Barash adds that plain direct laryngoscopy succeeds poorly when difficulty is predicted. A frightened, bleeding child must therefore be anaesthetised first, in theatre, where a surgeon can cut if intubation fails.

Awake flexible-scope intubation. It is the classic textbook answer for an unstable cervical spine because it keeps the neck almost still. It fails here because it needs a cooperative patient. Blood and secretions in a distorted airway also blind the scope, so it cannot be used in an uncooperative, bleeding child.

Barash: when intubation looks difficult, direct laryngoscopy succeeds poorly and advanced devices are preferred. Awake techniques suit cooperative patients; uncooperative ones need anaesthesia first, and extensive airway injury may need a surgical airway. Miller: blood-filled airways defeat bronchoscopy. Stoelting: keep in-line stabilisation throughout.

Sources: Barash 9eMiller 10eStoelting 8e

A fire needs fuel, an ignition source and an oxidiser. Pulling the tube removes the fuel and shutting off the gases removes the oxidiser, so do both at once: Miller turns the gases off first, Barash pulls the tube first. Saline then quenches embers, before any breath or new tube. Once the fire is out, Miller ventilates with 100% oxygen; the ASA advisory, from outside the textbooks, avoids added oxygen and nitrous oxide if possible, since embers flare in oxygen. Choose air if offered, oxygen if hypoxic, never nitrous oxide.

Turn oxygen down, leave tube in. A low inspired oxygen fraction is the right precaution during laser work, so turning it down feels logical. Once a flame exists, any oxygen still flowing through a burning tube keeps feeding it. The flow must stop completely and the tube must come out, not be turned down.

Barash: remove the tube, stop the gases, clear flammable material, pour saline. Miller: gases off, remove the tube, flush with saline, then 100% oxygen by mask and rigid bronchoscopy. The ASA advisory (outside source): restart ventilation without added oxygen or nitrous oxide if possible.

Sources: Barash 9eMiller 10eOutside our books: Practice Advisory for the Prevention and Management of Operating Room Fires: An Updated Report by the American Society of Anesthesiologists Task Force on Operating Room Fires (2013)Outside our books: Prevention of and response to surgical fires (2019)

Stridor soon after extubation usually comes from swelling of the airway lining. It is more likely after an oversized tube, a long intubation or repeated intubation attempts. Nebulised racemic adrenaline puts a vasoconstrictor directly onto the swollen mucosa, which shrinks the oedema and widens the airway. Humidified oxygen supports oxygenation in the meantime. Corticosteroids also reduce oedema and belong in the treatment package. However, dexamethasone needs hours to reach full effect, so it cannot be the step that relieves the obstruction now.

IV steroid as the first step. Steroids really do treat airway oedema and appear in every treatment list, so they look like a complete answer. But dexamethasone takes hours to work fully. The child is stridulous now, and the nebulised vasoconstrictor is what acts on the swelling at once.

For stridor in recovery, the treatment listed is humidified oxygen, nebulised racemic adrenaline and IV corticosteroids. Adrenaline probably works through local vasoconstriction that reduces oedema. Risk factors include an oversized tube, prolonged intubation and repeated attempts. Dexamethasone takes several hours for full effect.

Sources: Barash 9eMiller 10e

Most obstruction in recovery comes from soft tissue or a partly closed glottis, and it often reopens without drugs: jaw thrust together with CPAP of 5–15 cmH2O is frequently enough. Escalation is stepwise. If jaw thrust and CPAP fail, succinylcholine (0.1–1.0 mg/kg IV or 4 mg/kg IM) relaxes the cords. If that also fails, give a full induction dose with an intubating relaxant and intubate. Pushing a tube through cords held shut by spasm is contraindicated because it injures the airway.

Immediate succinylcholine and intubation. Succinylcholine is the drug everyone links to laryngospasm, so it looks decisive. But it is the second step, used only after jaw thrust and CPAP have failed. A child at 89% with otherwise normal vital signs needs simple airway opening first, not immediate paralysis and intubation.

Try non-invasive airway opening before reintubating; jaw thrust with CPAP (5–15 cmH2O) often suffices. If that fails, succinylcholine gives immediate muscle relaxation (0.1–1.0 mg/kg IV or 4 mg/kg IM). Forcing a tube through a laryngospasm-closed glottis is contraindicated and risks injury.

Sources: Miller 10e

If laryngospasm persists after airway manoeuvres, desaturation and bradycardia follow, so the cords must be relaxed quickly. Without a cannula, the drug must be absorbed from muscle, giving a slower onset of 3 to 4 minutes and needing a larger dose: 4 mg/kg IM in the books; Barash allows up to 5. IV doses differ: Miller gives 0.1–1.0 mg/kg, enough just to relax the cords; Barash gives 1 to 2 mg/kg. Either is acceptable with a line; without one, both books say 4 mg/kg IM.

Intraosseous access or 3 mg/kg infant dose. Intraosseous access is a real paediatric rescue route, and 3 mg/kg is the neonatal and infant IV dose, so it feels familiar. But for laryngospasm with no line, both books give intramuscular suxamethonium at 4 mg/kg. The 3 mg/kg figure is an infant IV dose, not this rescue.

Miller: after failed jaw thrust and CPAP, give succinylcholine 0.1–1.0 mg/kg IV or 4 mg/kg IM. Barash: 1–2 mg/kg IV, or 4–5 mg/kg IM without IV access; paediatric IM dose 4 mg/kg, onset 3–4 minutes.

Sources: Miller 10eBarash 9e

Unrelieved laryngospasm closes the glottis, so oxygen cannot reach the lungs and saturation falls; in children that desaturation is followed by bradycardia. Infants also react differently to airway irritation: the vagal and glossopharyngeal reflex that raises blood pressure and heart rate in adults tends to slow the heart in infants and small children. An outside review, not a textbook, adds that severe or untreated spasm can progress to cardiac arrest.

Tachycardia from hypoxia. Tachycardia is tempting because adults usually respond to hypoxia and airway stimulation with a fast heart and high blood pressure. Infants do not follow the adult pattern. When their airway is irritated and their saturation falls, the heart slows, and that bradycardia warns that cardiac arrest may be near.

The textbooks state that if positive pressure, oxygen, jaw thrust and deepening fail, desaturation and then bradycardia develop, and that infants respond to airway stimulation with bradycardia rather than the adult hypertension and tachycardia. An outside review, not a textbook, adds possible cardiac arrest.

Sources: Barash 9eMiller 10eOutside our books: Postoperative respiratory adverse events in pediatric anesthesia: risk factors, clinical implications, and management strategies (2025)

The blockage comes from blood under pressure in a closed neck compartment. It squeezes the airway and also obstructs venous and lymphatic outflow, so oedema keeps building in the airway wall. Opening the skin closure lets the clot out and drops that pressure at once. Transfer cannot do that. Opening the wound only buys time, though. Once blood has tracked into the pharyngeal wall, it will not fully relieve the obstruction. So be ready to secure the airway definitively, then control the bleeding vessels.

Transfer to theatre before decompressing. Theatre sounds definitive, and one textbook does prefer returning there when time permits. This patient is already obstructing, though. Transfer and induction cost minutes while pressure and oedema rise. Theatre comes after bedside decompression, not instead of it. Stopping anticoagulation is also needed, but it relieves nothing now.

Stoelting advises returning to theatre when time permits, but opening the wound at the bedside when necessary to relieve obstruction. Miller advises releasing clips or sutures and evacuating the haematoma. It warns this only buys time once blood has infiltrated the pharyngeal tissue.

Sources: Stoelting 8eMiller 10e

Forceful breaths against a blocked upper airway drive intrapleural pressure sharply negative. This lowers interstitial hydrostatic pressure and raises venous return and left ventricular afterload, so fluid floods the lung. Stoelting finds an open airway and oxygen usually enough because the oedema settles by itself. Miller adds diuresis as standard supportive care. Barash gives the diuretic only to patients who are also fluid-overloaded. So: airway and oxygen for all, a diuretic as Miller advises, and positive pressure only when the oedema is severe.

Reintubating every case immediately. Stridor and pink froth just after extubation look like an airway catastrophe, so reintubating feels safest. But this oedema usually settles by itself. All three books keep intubation and mechanical ventilation for severe cases. First-line care is an open airway, oxygen and diuresis.

Stoelting says an open airway and oxygen usually suffice because the oedema settles by itself. Miller treats with oxygen and diuresis, adding positive-pressure ventilation when severe. Barash gives a diuretic when the patient is hypervolaemic, and intubation with PEEP in severe cases.

Sources: Stoelting 8eMiller 10eBarash 9e

In Down syndrome, instability of the joint between the skull, atlas and axis lets the upper cervical vertebrae shift with head movement. Laryngoscopy usually extends the neck, risking spinal cord injury and severe neurological harm. Normal films and absence of symptoms do not exclude this risk, so every Down syndrome neck should be handled with care. Macroglossia, a high-arched palate, micrognathia and obesity also make ventilation and intubation harder, but this can be planned for. Cord injury is the greater danger, so it takes priority.

High-arched palate as main concern. A high-arched palate is a real Down syndrome feature and does make intubation harder, so it looks like the airway answer. It is true but comes second. It only makes laryngoscopy harder, while neck instability can injure the spinal cord. That makes the neck the first concern.

Avoid needless neck flexion or extension at intubation because of occipito-atlanto-axial instability. Keep the neck neutral even when films are normal, as extension during laryngoscopy can injure the cord. Orofacial anomalies and obesity separately predict difficult ventilation and intubation.

Sources: Mayo reviewFaustMiller 10e

Long-term hyperglycaemia leads to glycation of proteins and abnormal cross-linkage of collagen, which stiffens the cervical spine, atlanto-occipital and temporomandibular joints. Because the mouth cannot open fully and the head and neck move less freely, direct laryngoscopy is harder, and so is intubation. The same process affects the small joints of the hand. If a patient cannot press the palms completely together and a space is left between them (the prayer sign), the airway joints are probably affected as well.

Obesity as the cause. Obesity is a well-known predictor of a difficult airway, and diabetes brings weight to mind. But the airway problem specific to diabetes, even in a young type 1 patient, is joint stiffness from glycosylation, not fat. A slim diabetic can still be very hard to intubate.

In long-standing type 1 diabetes, glycosylation stiffens the jaw, atlanto-occipital and cervical spine joints, making intubation difficult. Direct laryngoscopy is difficult in up to 40% of juvenile diabetics having renal transplantation. The prayer sign is suggested as an extra screening test.

Sources: Barash 9e

Old anaesthetic records show the airway only as it was then. Subsequent neck radiation can alter those tissues, so a past easy intubation no longer reassures. Head or neck radiation is a listed condition raising the risk of difficult laryngoscopy, mask ventilation and supraglottic device ventilation, and prior neck radiation also predicted impossible bag–mask ventilation. Other features differ: edentulous patients are easy to intubate but harder to mask; a beard mainly hinders mask ventilation; dental veneers chiefly risk tooth damage, not difficult laryngoscopy.

Choosing the edentulous patient as hardest. An elderly patient with no teeth looks hard to manage, and losing the teeth does spoil the mask seal. But with no incisors in the way, laryngoscopy and passing the tube get easier. A low Mallampati class adds no difficulty. The question asks about intubation, not mask ventilation.

Previous head or neck radiation raises the risk of difficult laryngoscopy, mask ventilation and supraglottic ventilation. Prior neck radiation predicted impossible bag–mask ventilation, as did a beard. Patients with no teeth tend to be easy to intubate. Veneers mainly matter because they are easily damaged.

Sources: Barash 9eMiller 10e

Two infant–adult tables agree on the pattern. The larynx sits higher in the neck, and the epiglottis is long, narrow, omega shaped and stiff. Below the cords, the cricoid is a solid, complete ring of cartilage, so it, not the glottis, is the tightest segment. The trachea is short. 'Floppy' is not the books' word, but a long epiglottis is still a feature they support. A posterior larynx, a long trachea and a glottic narrowest point are not what they describe. Elimination therefore favours the long epiglottis.

Glottis as narrowest point. The glottis is the narrow opening you see at laryngoscopy, so it feels like the tightest point. The books instead name the cricoid ring as the narrowest part of the infant upper airway. It is a complete, solid circle of cartilage below the cords.

The infant–adult tables describe the infant epiglottis as relatively longer, narrower, stiffer and omega shaped. They put the larynx higher in the neck, name the cricoid ring as the narrowest part of the upper airway and describe the trachea as short.

Sources: Barash 9e

The classic three-axis model works like this. A pad under the occiput flexes the neck, which lines up the pharyngeal and laryngeal axes. Tilting the head back at the atlanto-occipital joint then brings the oral axis close to that line. Barash notes that Adnet challenged this model, and Miller says other explanations have been proposed. Whichever model is right, the evidence still shows the sniffing position gives the best laryngoscopic view. Extending the whole neck loses the cervical flexion half of the manoeuvre.

Extension at both neck and head. Extending at both levels feels like the head-tilt used to open an obstructed airway, and the atlanto-occipital half of it is correct. But extending the cervical spine throws away the flexion that lines up the pharyngeal and laryngeal axes, so this is overextension, not sniffing.

Miller calls cervical flexion with atlanto-occipital extension ideal for laryngoscopy. Barash gives about 35 degrees of neck flexion and 15 degrees of head extension, with about 7 cm support under the occiput. The axis model is debated, but evidence still favours sniffing.

Sources: Miller 10eBarash 9e

The superior laryngeal nerve divides in two. Its internal branch carries only sensation, from the tongue down to the upper surface of the vocal folds. Its external branch carries only motor fibres, to the cricothyroid, which tenses the cords. The recurrent laryngeal nerve does the rest: it moves all the other intrinsic muscles, including both cricoarytenoids, and it carries sensation from below the cords. So sensation below the cords, or any muscle other than the cricothyroid, points to the recurrent nerve.

External branch supplying posterior cricoarytenoid. The posterior cricoarytenoid sits on the cricoid and is the laryngeal muscle people know best, so it feels like a natural partner for a laryngeal nerve branch. But it is an intrinsic muscle other than the cricothyroid, so the recurrent laryngeal nerve supplies it, not the external branch.

Faust describes the external branch as purely motor and supplying the cricothyroid, and the internal branch as purely sensory. The recurrent nerve supplies the other laryngeal muscles and sensation below the cords. Barash adds that the cricothyroid tenses the vocal cords.

Sources: FaustBarash 9e

Laryngeal sensation divides at the vocal cords. The superior laryngeal nerve's internal branch is purely sensory, supplying mucosa down to the cords, including their upper surface. The external branch is purely motor to cricothyroid, so it is never a target for sensory block. Below the cords, the subglottis and trachea are supplied by the recurrent laryngeal nerve. A needle through the cricothyroid membrane deposits drug below the cords, in recurrent territory, so the block numbs the trachea and cords, not the supraglottis.

Internal branch of superior laryngeal nerve. It is the laryngeal sensory nerve people remember best, and it is part of most awake-intubation block sets. But its sensory field stops at the cords, and it is reached by its own separate block. A puncture through the cricothyroid membrane below the cords does not block it.

The sources agree that the internal laryngeal branch supplies sensation down to the upper surface of the cords, and the recurrent laryngeal nerve supplies the cords and trachea. Translaryngeal injection, also called transtracheal, at the cricothyroid membrane anaesthetises the trachea and cords.

Sources: Barash 9eFaustMiller 10e

Each recurrent laryngeal nerve drives the abductor muscles of its own cord. When one nerve fails, that cord cannot abduct and comes to rest near the midline. The intact nerve keeps the opposite cord opening and closing, so it can still meet the fixed cord for voice. One mobile cord leaves enough glottic gap to breathe, so the patient is hoarse with a weak cough but the airway stays open. Only when both nerves fail do both cords lie near the midline and dangerously narrow the airway.

Laryngeal oedema for a one-nerve injury. Laryngeal oedema tempts because the question pairs it with stridor after thyroid surgery. Stridor is caused by oedema, a haematoma or injury to both nerves, not by a single nerve injury. With one nerve lost, the paralysed cord sits paramedian, the other still moves, and the patient is only hoarse.

Unilateral injury leaves the affected cord median or paramedian. The patient is hoarse with a weaker cough but breathes without obstruction and usually copes well. If both nerves are lost, both cords are paralysed and the upper airway can become dangerously obstructed.

Sources: Miller 10eStoelting 8e

The mask sits above the cords, so the larynx and trachea are never instrumented, causing less mucosal trauma and sore throat. Less stimulation brings fewer cough and pressor responses, steadier haemodynamics, lower anaesthetic needs and no relaxant. Barash reports fewer laryngospasm episodes at emergence because the cords are untouched. Miller adds that a device above the cords cannot bypass spasm once it starts, so the mask makes spasm less frequent but cannot rescue it. First-generation masks leave the oesophagus unguarded and do not prevent aspiration.

Assuming the LMA protects against aspiration. It is tempting because the cuff surrounds the laryngeal inlet and keeps out blood from above, so it looks protective. But its seal pressure is low, and first-generation masks barely guard against regurgitated stomach contents. A cuffed tracheal tube is still the protective choice.

One text reports less sore throat, coughing, emergence laryngospasm and bronchospasm. The other lists easy, rapid placement, steadier haemodynamics, lower anaesthetic need and no relaxant. It also warns that the mask gives no protection from laryngospasm, and first-generation designs protect little against aspiration.

Sources: Barash 9eMiller 10e

The classic mask and tube are silicone; other makers use silicone or PVC. Both are synthetic, so the device contains no latex. Silicone withstands cleaning, so the classic mask is reusable, with single-use versions as an additional option. It is inserted like a swallowed bolus: the cuff is pushed along the palate into the hypopharynx, so the glottis need not be seen. The cuff sits around the laryngeal inlet but does not reliably protect the airway from gastric contents.

Assuming all LMAs are disposable. Disposable PVC laryngeal masks are now everywhere in theatre, so many people assume all LMAs are single-use. That is wrong: the original classic silicone mask was designed to be cleaned and used again many times, and disposable models were added later.

The classic mask is reusable silicone; other manufacturers use silicone or PVC. It is reusable many times and comes in sizes from neonate to large adult. Insertion copies swallowing. Supraglottic airways do not reliably prevent aspiration, so a full stomach is a contraindication.

Sources: Barash 9eMiller 10e

The cuff must fill the hypopharynx to seal around the larynx, so the device must match the child's pharyngeal size. Body weight is the usual guide. These paediatric weight bands come not from textbooks but from two outside sources, a paediatric sizing trial and a validation study, both using the manufacturer's bands. The manufacturer advises the largest size that sits comfortably in the mouth. A mask that is too small needs an overfilled cuff to seal, risking pharyngolaryngeal injury, nerve damage and failed placement.

Size 2 because 20 kg is close. Size 2 is tempting because 20 kg feels close to its top limit, and a smaller mask can seem safer in a child. But size 2 only covers children under 20 kg. Above that weight the band moves to 2.5, and an undersized mask leaks or needs cuff overinflation.

Two sources outside the textbooks, a paediatric sizing trial and a validation study, give the manufacturer's weight bands: size 2 for 10–20 kg, 2.5 for 20–30 kg, size 3 for 30–50 kg. The manufacturer favours the largest comfortable size; undersising causes cuff overinflation and injury.

Sources: Outside our books: Hyomental distance measured ultrasonography versus weight-based criteria for laryngeal mask size selection in children: a randomized controlled trial (2025)Outside our books: Validation of manufacturers' laryngeal mask airway size selection standard: a large retrospective study (2021)Barash 9eMiller 10e

The device sits rigidly in the pharynx. It restores ventilation and guides a tube towards the glottis, but the tube still has to find the laryngeal inlet without being seen. If the tube goes into the oesophagus or will not advance, intubation fails even though ventilation through the mask may still work. Anything that distorts the laryngeal inlet can therefore defeat it. Because the device is rigid, it puts sustained pressure on surrounding tissue, which is why it is taken out once tube placement is confirmed.

Avoid any rigid device in cervical instability. Cervical instability sounds like an absolute reason to avoid any rigid airway device, so a blanket ban feels safe. No source forbids it. It is described as a bridge to intubation in patients whose cervical spines are fragile and prone to fracture.

Intubating laryngeal masks rescue ventilation when intubation and mask ventilation fail, and allow tracheal access. Blind intubation through them can fail through oesophageal passage or non-advancing tubes. Being rigid and compressing adjacent tissue, they should be removed early.

Sources: Barash 9eMiller 10eStoelting 8e

Food and fluid collect above an obstruction or in a dilated oesophagus that cannot push contents along. They can stay there for days after eating, so the fasting time says nothing about whether the oesophagus is empty. In systemic sclerosis, poor oesophageal motility comes with a weak lower oesophageal sphincter, and reflux is common. Induction removes the protective airway reflexes, so retained material can reach the lungs. Full-stomach precautions are therefore the central anaesthetic concern.

Difficult airway from small mouth. Scleroderma brings to mind a small mouth and a stiff jaw, so the airway feels like the main issue. But a difficult airway is only expected when fibrosis affects the mouth, jaw or cervical spine. Oesophageal dysmotility with a weak sphincter makes aspiration risk almost universal in these patients.

Achalasia carries a high aspiration risk perioperatively, requiring full-stomach precautions, as the dilated oesophagus retains food for days. Swallowing or motility disorders, including oesophageal cancer, predispose to aspiration. In systemic sclerosis, 70% have reflux, and dysmotility with a hypotonic sphincter significantly raises aspiration risk.

Sources: Stoelting 8eBarash 9eMiller 10e

Reflux occurs when the barrier at the oesophagogastric junction fails. Conventional teaching, from an outside reflux review rather than anaesthesia textbooks, lists calcium channel blockers among drugs altering the frequency of transient sphincter relaxation. A recent genetic study, also outside the textbooks, calls drug-induced sphincter relaxation the textbook view but found amlodipine linked to less reflux, so the classic claim is now questioned for amlodipine. Separately, ageing weakens cough and airway reflexes, raising aspiration risk once reflux occurs.

Weak cough as the reflux risk factor. Older people do cough less effectively, so this looks like an age-linked risk. But a weak cough and blunted airway reflexes do not cause acid to reflux. They decide whether refluxed material is aspirated into the lungs. It answers the aspiration question, not the reflux one.

Calcium channel blockers alter transient lower oesophageal sphincter relaxations; sphincter relaxation is the textbook view, yet a genetic study linked amlodipine to less reflux. An anaesthesia textbook associates weaker cough and airway reflexes in older patients with aspiration.

Sources: Outside our books: Genetic evidence for amlodipine's protective role in gastroesophageal reflux disease: A focus on CACNB2 (2025)Outside our books: Risk factors for gastroesophageal reflux disease and analysis of genetic contributors (2018)Miller 10e

The stimulus provokes a generalised seizure. First a brief vagal phase slows the heart and lowers pressure. Then sympathetic discharge drives tachycardia, ectopy and hypertension for several minutes. Stoelting calls this the typical response, so it follows almost every treatment. Faust lists transient arrhythmias, which come from the same surge, first among its complications. Branch by timing: in the acute period the haemodynamic surge dominates and aspiration and fractures are uncommon; memory disturbance is a later, post-treatment effect.

Aspiration as the commonest ECT complication. Aspiration is tempting because the airway is unprotected during a seizure with raised intragastric pressure, and Faust gives it a figure. That figure is small, well below the arrhythmia rate and the post-seizure hypertension, which is the usual response rather than an occasional event.

Stoelting describes the usual response as brief bradycardia, then tachycardia and hypertension lasting several minutes. Faust lists transient arrhythmias at 10–40%, gastric aspiration at 2.5% and musculoskeletal injury including fractures at 0.4%, with memory disturbance among later adverse events.

Sources: Stoelting 8eFaust

No textbook addresses this consent; the reasoning comes from outside sources. A brainstem tumour causing stridor is a fixed obstruction that may worsen. Cranial radiotherapy means many sessions over several weeks, so every session repeats a high-risk induction. Face and head immobilisation and shielding distance make rescue harder in the treatment room. A planned tracheostomy gives a definitive airway that can be relied on each time. Emergency tracheostomy is the worst case each session must prepare for. Both belong in the discussion.

Consenting only for intensive care afterwards. Intensive care after a session sounds like prudent high-risk consent, but it misses the main hazard: losing a fixed, worsening airway at each of many inductions in a remote room. The discussion must name the airway rescue and the definitive airway plan, not just aftercare.

Outside the textbooks, two sources put tracheotomy need in bilateral cord paralysis above half (60% in one). Radiotherapy shielding distance, positioning and immobilisation devices may hinder emergency access. Head and face immobilisers are unpleasant for children and may raise airway concerns for anaesthetists.

Sources: Outside our books: Survey of anesthesia, sedation and non-sedation practices for children undergoing repetitive cranial or craniospinal radiotherapy (2022)Outside our books: Anaesthesia for paediatric radiotherapy: a narrative review (2025)Outside our books: Management of Pediatric Bilateral Vocal Fold Paralysis: A State-of-the-Art Review (2024)Barash 9eOutside our books: Bilateral vocal cord palsy with syringomyelia and Chiari I malformation (2016)