Laryngospam and bronchospam - MD anaesthesia pg exam

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Laryngospasm and Bronchospasm - MD Anaesthesia PG Exam

LARYNGOSPASM

Definition

Laryngospasm is a forceful, involuntary tonic spasm of the laryngeal musculature causing complete or partial occlusion of the laryngeal inlet, with descent of the epiglottis and glottic closure.

Anatomy & Mechanism

The reflex arc involves:

Afferent: Internal branch of the Superior Laryngeal Nerve (SLN) - stimulated by secretions/blood/irritants on the laryngeal mucosa superior to the vocal cords
Motor response:
- Lateral cricoarytenoid (adduction + medial rotation of arytenoids) - via Recurrent Laryngeal Nerve
- Thyroarytenoid (shortening/closure of vocal cords) - via Recurrent Laryngeal Nerve
- Cricothyroid (tensing of cords) - via external branch of SLN
Closure can occur at true vocal cords, aryepiglottic folds, and vestibular (false) folds
Splanchnic nerve stimulation has also been implicated in triggering vocal cord closure

Repetitive suprathreshold SLN stimulation causes heavy after-discharge activity, making spasm persist beyond the original stimulus.

Types

Type	Description
Complete	Total glottic closure - no air movement; can resist PPV up to 140 mmHg
Incomplete	Partial closure - inspiratory stridor audible, some air movement possible

Incidence

Overall: ~0.79% of all anaesthetics (136,929 patient study)
Paediatric: 0.4-10% during induction/emergence; most common at 1-3 months of age (~1 in 50 anaesthetics in young children)
Higher in infants than adults

Risk Factors

Recent URI (upper respiratory infection)
Passive tobacco smoke exposure (children)
Pre-existing reactive airway disease
Younger age - children > adults
Inadequate depth of anaesthesia during airway manipulation
Inhalational > IV anaesthesia induction
Secretions/blood in the larynx
Emergence phase - the transitional period when not fully awake but not deeply anaesthetised
Less experienced anaesthesiologist (non-paediatric specialist)

Clinical Features

Stridor (inspiratory, high-pitched)
Suprasternal and supraclavicular retractions
Paradoxical chest movements ("rocking" pattern)
Loss of capnography waveform and absence of reservoir bag movement
Progressive SpO2 desaturation
Bradycardia (in children especially, due to hypoxia)

When It Occurs

Most common at tracheal extubation (transitional emergence)
Can occur during induction, any phase, or in the PACU (patient awakening, chokes on secretions)
Important: occurs WITHOUT an endotracheal tube in place; if a tube is present, may not be recognised

Consequences if Untreated

Severe hypoxaemia
Negative-pressure pulmonary oedema (NPPE)
Hypoxic cardiac arrest

Hypercarbia depresses adductor activity and severe hypoxaemia (PaO2 <50 mmHg) also inhibits laryngospasm - but relying on this is dangerous.

Treatment - Step-by-Step

Step	Action
1. Remove stimulus	Suction secretions/blood, reposition mask
2. 100% O2 + CPAP 15-20 cmH2O	Tight-fitting mask, positive pressure
3. Jaw thrust (Larson's maneuver)	Vigorous jaw thrust - pressure to the area between the angle of mandible, mastoid process, and base of skull; also provides painful stimulus to trigger crying in children (laryngospasm cannot persist when the child vocalises)
4. Deepen anaesthesia	IV Propofol (subanaesthetic dose 0.5-1 mg/kg) - depresses laryngeal reflexes; IV Lidocaine 1-1.5 mg/kg
5. If failed - Succinylcholine	IV: 0.1-1.0 mg/kg (Miller's) / 0.5-1 mg/kg (Morgan); IM: 4-6 mg/kg (if no IV access) with atropine
6. If still failed	Full induction dose + intubating dose of muscle relaxant → emergency intubation. Forceful intubation through closed glottis is contraindicated

Alternative paralysis: Rocuronium 0.4 mg/kg IV (if succinylcholine contraindicated)

Note: PPV alone should NOT be relied upon - complete vocal cord closure can resist pressures up to 140 mmHg. Aggressive PPV risks gastric distension and aspiration.

Prevention

Extubate either fully awake (eyes open) OR deeply anaesthetised (breathing spontaneously, not swallowing/coughing) - avoid the intermediate phase
Position somnolent paediatric patients lateral in PACU to drain secretions away from cords
Topical/IV Lidocaine before extubation
Adequate depth before laryngeal stimulation
Treat active URI before elective surgery

BRONCHOSPASM

Definition

Bronchospasm is diffuse airway smooth muscle contraction causing increased airway resistance, manifested as wheezing and elevated peak airway pressures during anaesthesia.

Incidence & Significance

Bronchospasm in ~9% of asthmatics perioperatively; ~25% may wheeze after induction
1.7% of asthmatics sustain a poor respiratory outcome
ASA Closed Claims: 40 bronchospasm cases, 88% involved brain damage or death
Only 50-60% of cases had pre-existing asthma/COPD - many occurred de novo
In France, 7% of anaesthesia-related deaths attributed to bronchospasm
Non-allergic mechanism involved in ~80% of cases

Risk Factors

Known asthma or COPD
Active wheezing at induction
Desflurane inhalation induction (potent airway irritant)
Isoflurane inhalation induction
Histamine-releasing drugs (atracurium, morphine, meperidine)
Airway manipulation under light anaesthesia
Pain or emotional stress under light anaesthesia
Surgical stimulation of lung parenchyma/airways
High spinal/epidural (blocks T1-T4 sympathetic tone → unopposed parasympathetic bronchoconstriction)

Clinical Features / Monitoring Signs

Wheezing (expiratory)
Rising peak airway pressures (plateau pressure may remain unchanged - distinguishes from reduced compliance)
Decreasing exhaled tidal volumes
Delayed rise of end-tidal CO2 (shark-fin capnography pattern - expiratory obstruction)
Incomplete exhalation / air trapping
In severe cases: hypercapnia and hypoxaemia

Differential Diagnosis of Intraoperative Wheezing

Bronchospasm must be distinguished from:

ETT kinking / obstruction by secretions / overinflated cuff
Endobronchial (right mainstem) intubation
Active expiratory efforts (straining)
Pulmonary oedema or embolism
Pneumothorax

Perioperative Management

Preoperative

Continue bronchodilators up to day of surgery
Treat active bronchospasm with: inhaled β2-agonists + IV glucocorticoids before elective surgery
Steroid supplementation if on chronic steroids (>5 mg/day prednisone equivalent)
Avoid H2-blockers (H2 activation normally causes bronchodilation; H2 blockade + H1 stimulation can worsen bronchoconstriction)
Anticholinergics not routine unless excessive secretions or ketamine induction planned

Induction Agents - Preferred

Agent	Comment
Propofol	Bronchodilation; first choice
Ketamine	Bronchodilation via sympathomimetic effect; choice if haemodynamically unstable
Etomidate	Acceptable
Barbiturates/opioids/benzodiazepines	No bronchodilation benefit

Inhalational Agents

Agent	Effect
Sevoflurane	Most potent bronchodilator; smoothest inhalation induction in asthmatics
Isoflurane	Bronchodilator; but more cough/bronchospasm during inhalation induction
Desflurane	AVOID in asthmatics - increases airway resistance; potent irritant

Intubation Tips

Achieve deep anaesthesia (2-3 MAC volatile agent for 5 min) before intubation
IV or intratracheal Lidocaine 1-2 mg/kg before intubation
Note: intratracheal lidocaine itself can cause bronchospasm if induction depth inadequate
Succinylcholine is generally safe; rarely causes histamine release
Atracurium should be avoided in asthmatics (histamine release)

Intraoperative Treatment of Bronchospasm

Step	Treatment
1	Increase concentration of volatile agent (all have bronchodilator properties)
2	Administer aerosolised β2-agonist (salbutamol/albuterol) via ETT
3	IV Hydrocortisone (especially in known steroid-responsive patients)
4	Low-dose IV Epinephrine infusion (refractory bronchospasm)

Ventilator Settings During Bronchospasm

Tidal volume: 6 mL/kg
Prolong expiratory time (reduce respiratory rate, increase I:E ratio)
Permissive hypercapnia (acceptable if no cardiovascular/neurological contraindication)
Warmed, humidified gases

Extubation in Asthmatics

Deep extubation (before return of airway reflexes) preferred to reduce bronchospasm on emergence
Lidocaine bolus 1.5-2 mg/kg before emergence to obtund airway reflexes
Reversal with neostigmine is safe if preceded by appropriate anticholinergic (atropine/glycopyrrolate)
Sugammadex avoids cholinergic effects (preferred reversal); rare anaphylaxis reported

COMPARISON TABLE: Laryngospasm vs Bronchospasm

Feature	Laryngospasm	Bronchospasm
Site	Supraglottic/glottic	Lower airways (bronchi/bronchioles)
Sound	Inspiratory stridor (or silent)	Expiratory wheeze
Airway pressure	Not measurable (extubated)	Raised peak airway pressure
SpO2	Rapidly falls	Falls more gradually
Capnography	Flat/absent waveform	Shark-fin (delayed expiratory rise)
Key trigger	Secretions/blood on cords, light anaesthesia at extubation	Histamine-releasing drugs, airway manipulation, asthma
Specific treatment	Succinylcholine	β2-agonist, epinephrine
Common induction	Inhalational > IV	After ETT placement in light anaesthesia
Paediatric predilection	Yes (infants most common)	Less age-specific

HIGH-YIELD EXAM POINTS

Larson's maneuver - jaw thrust with firm pressure at the "laryngospasm notch" (between mastoid process, angle of mandible, base of skull)
Succinylcholine dose for laryngospasm: IV 0.5-1 mg/kg, IM 4-6 mg/kg (with atropine if IM)
Rocuronium 0.4 mg/kg is an alternative to succinylcholine for laryngospasm
Complete vocal cord closure resists PPV up to 140 mmHg - do NOT rely on PPV alone
Negative-pressure pulmonary oedema is a complication of laryngospasm (forced inspiratory effort against closed glottis)
Desflurane is the most irritant volatile - AVOID in asthmatics for induction
Sevoflurane = most potent bronchodilator volatile agent
Ketamine = bronchodilator + haemodynamic stability = choice in asthmatic with haemodynamic compromise
Atracurium - avoid in asthma (histamine release)
Extubate either fully awake OR deeply anaesthetised - the "intermediate zone" is most dangerous for laryngospasm
NPPE (Negative Pressure Pulmonary Oedema): treat with CPAP, may need PPV; develops within 60 min post-laryngospasm
Incidence of laryngospasm in paediatrics: most common at 1-3 months of age

Sources: Miller's Anesthesia 10e, Barash Clinical Anesthesia 9e, Morgan & Mikhail's Clinical Anesthesiology 7e

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