Laryngospasm 5 mark answer

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Laryngospasm

Definition

Laryngospasm is a forceful, involuntary spasm of the laryngeal musculature resulting in partial or complete closure of the glottic opening. It is caused by tonic contractions of the lateral cricoarytenoid, thyroarytenoid, and cricothyroid muscles along with descent of the epiglottis over the laryngeal inlet, producing airway obstruction. - Miller's Anesthesia, 10e / Morgan & Mikhail, 7e

Incidence

Occurs in 0.4% to 10% of children during induction and emergence from anesthesia.
In adults, accounts for 23% of all critical postoperative respiratory events at extubation.
Most common in infants 1-3 months of age and in young children (approximately 1 in 50 anesthetics).
Barash Clinical Anesthesia, 9e

Nerve Supply / Mechanism

Triggered by sensory stimulation of the superior laryngeal nerve (branch of the vagus).
Incomplete laryngospasm: partial closure - air movement possible but with significant effort and inspiratory stridor.
Complete laryngospasm: total closure - no air movement, loss of capnography waveform, absent reservoir bag movement.

Precipitating Factors (Triggers)

Airway irritants - blood, secretions, vomitus, or foreign body in the glottis.
Extubation at a light plane of anesthesia - the most common precipitant (in the transitional, "neither awake nor deeply asleep" stage).
Recent upper respiratory tract infection (URI) or passive exposure to cigarette smoke.
Airway instrumentation - suctioning of the posterior oropharynx, LMA manipulation, or passing an ETT through the larynx.
Pelvic or abdominal visceral stimulation during light anesthesia.
Inhalational anesthesia (vs. IV) - higher risk.

Clinical Features

Inspiratory stridor (partial obstruction) or silent chest (complete obstruction).
Suprasternal and supraclavicular retractions.
Paradoxical ("rocking") chest movements - chest sinks while abdomen rises on inspiration.
Loss of ETCO2 waveform on capnograph.
Absent movement of the reservoir bag.
Progressive oxygen desaturation and bradycardia if untreated.

Treatment (Stepwise)

Step 1 - Remove the stimulus

Suction blood, secretions, or vomitus from the glottis immediately.

Step 2 - 100% O₂ + CPAP + Jaw Thrust

Apply well-fitted mask with 100% oxygen and CPAP 15-40 cmH₂O.
Perform a firm jaw thrust (lifts the mandible anteriorly into the mask) - this simultaneously relieves airway obstruction and provides a painful stimulus. Laryngospasm cannot persist if the patient cries or vocalizes.

Step 3 - Deepen anesthesia

IV propofol (small dose) to deepen the anesthetic level.
IV lidocaine 1-1.5 mg/kg.

Step 4 - Neuromuscular Blockade (if above steps fail and desaturation/bradycardia develops)

IV succinylcholine 0.1-1.0 mg/kg (preferred due to rapid onset and ultra-short action).
If no IV access: IM succinylcholine 4-6 mg/kg (+ atropine to prevent bradycardia).
Alternative: IV rocuronium 0.4 mg/kg.
Then perform emergency tracheal intubation with controlled ventilation.

Note: Never attempt to force a laryngoscope or ETT through a spasmodically closed glottis - this risks direct laryngeal injury. - Miller's Anesthesia, 10e

Prevention

Extubate either deeply asleep (spontaneously breathing, not swallowing or coughing) or fully awake (eyes open, following commands) - avoid the hazardous intermediate stage.
Recovering somnolent pediatric patients in the lateral position allows secretions to pool away from the cords.
Topical lidocaine spray to the glottis before extubation.
Adequate depth of anesthesia during all airway instrumentation.

Complication

Large negative intrathoracic pressures generated during a struggling episode of laryngospasm can cause negative-pressure pulmonary edema, particularly in young, fit, and muscular patients. - Morgan & Mikhail's Clinical Anesthesiology, 7e

Laryngospasm vs bronchospam 10 mark answer

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Laryngospasm vs Bronchospasm

Both are perioperative airway emergencies but differ fundamentally in their anatomical location, mechanism, clinical presentation, and management.

1. Definition

	Laryngospasm	Bronchospasm
Definition	Forceful, involuntary spasm of the laryngeal musculature causing partial or complete glottic closure	Sustained contraction of bronchial smooth muscle causing lower airway narrowing
Anatomical site	Upper airway - glottis and supraglottic structures	Lower airway - bronchi and bronchioles
Nature of obstruction	Fixed, tonic muscular spasm	Dynamic smooth muscle bronchoconstriction

Cummings Otolaryngology; Morgan & Mikhail, 7e

2. Mechanism

Laryngospasm:

Sensory stimulation of the superior laryngeal nerve (branch of vagus) and trigeminal nerve activates intrinsic adductor musculature of the larynx.
Muscles involved: lateral cricoarytenoid, thyroarytenoid, and cricothyroid + descent of the epiglottis over the laryngeal inlet.
Results in complete glottic closure (complete laryngospasm) or partial closure with stridor (incomplete laryngospasm).

Bronchospasm:

Mediated by cholinergic (parasympathetic) stimulation and mast cell mediator release (histamine, leukotrienes).
Blocking sympathetic tone (T1-T4) by high spinal/epidural anesthesia allows unopposed parasympathetic activity, aggravating bronchoconstriction.
Results in increased airway resistance during expiration - air trapping and incomplete exhalation.

3. Precipitating Factors / Risk Factors

Laryngospasm:

Secretions, blood, or vomitus contacting the glottis
Extubation at a light plane of anesthesia (most common cause)
Inhalational anesthesia (higher risk than IV)
Recent upper respiratory tract infection (URI), passive smoke exposure
Surgical stimulation (adenotonsillectomy has the highest risk)
Young age - infants 1-3 months most vulnerable; ~1 in 50 pediatric anesthetics

Bronchospasm:

Pre-existing asthma, eczema, allergic rhinitis (atopic patients)
Airway irritation from ETT, DLT, or bronchial blocker manipulation
Drugs causing histamine release - atracurium, morphine, meperidine
Light plane of anesthesia during intubation
Pulmonary aspiration, mucus plugging
Pain, emotional stress, or stimulation during light anesthesia
URI doubles the risk; nocturnal dry cough confers 10-fold risk
High spinal/epidural blocking T1-T4 sympathetic tone
Morgan & Mikhail, 7e; Cummings Otolaryngology

4. Clinical Features

Feature	Laryngospasm	Bronchospasm
Breath sounds	Inspiratory stridor (partial) or silent chest (complete)	Expiratory wheeze on auscultation
Phase of obstruction	Primarily inspiratory	Primarily expiratory
Chest movement	Paradoxical "rocking" movements; suprasternal and supraclavicular retractions	Hyperinflated chest; prolonged expiration
Capnograph	Loss of ETCO2 waveform (complete)	Delayed, slowly rising ETCO2 waveform (shark-fin pattern); incomplete exhalation plateau
Airway pressures	Not directly monitored on ventilator (extra-thoracic obstruction)	Rising peak inspiratory pressure; plateau pressure may remain unchanged initially
Tidal volumes	Absent reservoir bag movement	Decreasing exhaled tidal volumes
SpO2	Rapid desaturation	Gradual desaturation
Bradycardia	Common (hypoxia-driven, especially in children)	Less immediate

5. Diagnosis / Differential Approach

Laryngospasm is a clinical diagnosis based on:

Absence of breath sounds + inability to ventilate despite mask seal
Timing: typically at extubation or emergence
Stridor or total silence during inspiratory effort

Bronchospasm must be differentiated from:

ETT kinking, secretions, or overinflated balloon cuff
Endobronchial intubation (unilateral breath sounds)
Pulmonary edema or embolism
Pneumothorax
Anaphylaxis (bronchospasm may be its first sign)
Active expiratory efforts (straining)
Morgan & Mikhail's Clinical Anesthesiology, 7e

6. Management

Laryngospasm - Stepwise

Step 1: Remove the triggering stimulus (suction blood/secretions from glottis).

Step 2: 100% O₂ + CPAP 15-40 cmH₂O via well-fitted face mask + firm jaw thrust (relieves obstruction + painful stimulus breaks the spasm; laryngospasm cannot persist if the patient cries/vocalizes).

Step 3: Deepen anesthesia - IV propofol + IV lidocaine 1-1.5 mg/kg.

Step 4 (if above fails + desaturation/bradycardia):

IV succinylcholine 0.1-1.0 mg/kg (drug of choice - rapid onset, ultra-short duration).
No IV access: IM succinylcholine 4-6 mg/kg + atropine.
Alternative: IV rocuronium 0.4 mg/kg.
Then proceed to controlled ventilation ± emergency intubation.

Do NOT forcibly pass a laryngoscope through a closed glottis - this causes direct laryngeal injury.

Bronchospasm - Stepwise

Step 1: Confirm and remove mechanical causes (rule out ETT kinking, endobronchial intubation, mucus plug).

Step 2: Increase volatile anesthetic concentration (all volatiles are bronchodilators; sevoflurane is the most potent).

Step 3: Administer aerosolized β₂-agonist (albuterol/salbutamol 2-8 puffs via ETT adaptor) - first-line drug.

Step 4: Additional agents:

Ipratropium bromide (inhaled anticholinergic)
IV hydrocortisone / IV methylprednisolone (especially in steroid-responsive patients)
Magnesium sulfate IV (bronchodilator via calcium antagonism)
Low-dose IV epinephrine infusion (refractory cases / anaphylaxis)
IV ketamine (bronchodilatory induction agent if not already used)

Step 5: Ventilator adjustments:

Tidal volume 6 mL/kg + prolonged expiratory time (to avoid air trapping)
PaCO₂ may be allowed to rise (permissive hypercapnia) if no cardiovascular/neurological contraindication.

Step 6: Extubation strategy - deep extubation (before return of airway reflexes) reduces bronchospasm on emergence; IV lidocaine 1.5-2 mg/kg bolus helps obtund airway reflexes.

Morgan & Mikhail, 7e; Miller's Anesthesia, 10e; Cummings Otolaryngology

7. Prevention

	Laryngospasm	Bronchospasm
Extubation strategy	Extubate fully awake OR deeply anesthetized (avoid intermediate stage)	Deep extubation preferred in asthmatics
Induction agent	IV induction preferred in at-risk children	Propofol or ketamine (both bronchodilate)
Drugs to use	IV lidocaine spray to glottis	Continue pre-op bronchodilators up to surgery; IV/inhaled β₂-agonists pre-op
Drugs to avoid	Inhalational agents in high-risk children	Atracurium, morphine, meperidine (histamine releasers); H₂-blockers (may worsen)
Position	Lateral position for somnolent pediatric patients in recovery	Avoid high spinal/epidural (T1-T4 blockade)
Anesthesia depth	Adequate depth during all airway manipulation	Adequate depth before intubation; volatile maintenance

8. Complications

	Laryngospasm	Bronchospasm
Acute	Hypoxia, bradycardia, cardiac arrest	Hypoxia, hypercapnia, respiratory failure
Unique	Negative-pressure pulmonary edema (from large negative intrathoracic pressures in muscular/fit patients fighting obstruction)	Air trapping / dynamic hyperinflation, barotrauma, pneumothorax
If untreated	Brain injury, death	Status asthmaticus, cardiac arrest

Summary Table

Parameter	Laryngospasm	Bronchospasm
Site	Upper airway (glottis)	Lower airway (bronchi/bronchioles)
Mechanism	Laryngeal adductor spasm via SLN	Smooth muscle contraction via parasympathetics + mediators
Sound	Inspiratory stridor / silence	Expiratory wheeze
Capnograph	Lost waveform	Shark-fin / slow rising plateau
Key drug	Succinylcholine	Salbutamol (β₂-agonist)
Adjunct	Propofol, lidocaine	Volatile agent, magnesium, hydrocortisone
Reversal agent	Succinylcholine (neuromuscular block)	Epinephrine (refractory/anaphylaxis)
Unique complication	Negative-pressure pulmonary edema	Dynamic hyperinflation / air trapping

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