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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