Perioperative Laryngospasm
2006/02/15
R3 張維修
Epidemiology
Olsson & Hallen; laryngospasm during
anesthesia, GA, 1984
over an 11-year period: 1967 to 1978
all age: 136,929 patients
1. An overall incidence: 8.7/1000 patients
children (0-9 y/o): 17.4/1000
infants (birth to 3 m/o): 28.2/1000
2. adolescence: male > female
male: 12.1/1000; female: 7.2/1000

Epidemiology
3.

Children with
Extubation: 42/1,000
Presence of NG tube: 48.5/1,000
Oral endoscopy and esophagoscopy:
48.5/1,000
an upper respiratory infection or
bronchial asthma: 95.8/1000
Anatomy
Anatomy
Anatomy

1.
2.
3.
4.
5.
Intrinsic laryngeal muscle:
Posterior cricoarytenoid m.: the only
abductor
Lateral cricoarytenoid m.:adductor
Thyroarytenoid m.:shortening
Cricothyroid m.:lengthening
Interarytenoid m.:adduction
Anatomy
Sensory nerve innervation: C.N. X (vagus
nerve)
Internal branch of the superior
laryngeal nerve (SLN): the area above
the true cord
Recurrent laryngeal nerve: below the
true vocal cord to upper part of the
trachea
Anatomy
Motor nerve innervation: C.N. X (vagus
nerve)
External branch of superior laryngeal
nerve: inferior pharyngeal constrictors
and cricothyroid muscle
Recurrent laryngeal nerve: other
intrinsic laryngeal muscle
Physiology

Laryngeal reflex: (glottic closure reflex; quick
protective response)
laryngeal closure (vocal cord adduction, short
lived), protect lungs from aspiration of
foreign material
Laryngospasm: a prolonged form of vocal
cord of adduction (closure of the true vocal
cords alone or the true and false vocal cords)
Physiology

Receptor: mechanoreceptors,
chemoreceptor, and thermal receptor
Density: greater around the laryngeal
opening, true vocal fold (posterior >
anterior)
Physiology

1.
2.
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4.
Afferent impulses
Stimulation of the nasal mucosa, soft
palate and pharynx
Stimulation of the epiglottis and larynx
Stimulation of the tracheobronchial
tree
Stimulation of the abdominal viscera
and diaphragm
Pathophysiology

1.
2.
3.

Animal study:
50 to 75 d/o mongrel puppies: a period of
transient laryngeal hyperexcitability
increases the risk of laryngospasm;
central synaptic immaturity,
transient reduction of central latency and
a reduction in central inhibition
In human, certain levels of light anesthesia
may create a state of central disinhibition
Pathophysiology

During GA: irritating inhalation agents,
excessive secretions, or manipulation of the
airway
A ball-valve effect: Fink
after the true and false vocal cord close
translaryngeal inspiratory pressure gradient
increases
supraglottic soft tissue become rounded and
redundant and drawn into the laryngeal inlet
Pathophysiology

Suzuki and Sasaki: laryngospasm heavy
after-discharge activity, elicited by
repetitive suprathreshold stimulation of
SLN, not by single-shock excitation
Adduction motor neuron: SLN`s
afferent limb stimulus intensity↑;
output function (motor excitation) ↑
Pathophysiology

Ikari & Sasaki
glottic closure reflex in dogs
expiratory phase > inspiratory phase
PCO2↑; adductor activity↓; adductor neuron
activity↓
PO2↓(less than 50 mmHg); adductor neuron
activity↓; postsynaptic potential ↓
Asphyxia prevents prolonged laryngospasm
(severely hypoxia or hypercarbia)
Pathophysiology
Fink, 1956, Anesthesiology

Laryngospasm: three levels
1.
The vocal cords
2.
The false cords
3.
The AE folds
Pathophysiology
Pathophysiology

A ball valve effect
Ball: preepiglottic body (from hyoid to notch
of the thyroid cartilage)
Valve: upper surface of the false cords
Translaryngeal inspiratory pressure gradient
increased
Intrinsic muscle
Extrinsic muscle: thyrohyoid muscle,
sternohyoid muscle, sternothyroid muscle
Pathophysiology
Pathophysiology

Vocal cord adduction can be treated
with positive ventilation pressure
Ball-valve effect during laryngospasm:
forced inflation of the pharynx merely
distends the pyriform fossae and
presses the arytenoid against each
other
Pathophysiology
Pathophysiology

Induction of anesthesia: Inspiratory
stridor; passive closure of the glottic
shutter during inspiration; abductor are
relaxed
Smaller laryngeal apetures: infant and
young children > older children or
adults
Diagnosis

Incomplete airway obstruction
Complete airway obstruction
Diagnosis-incomplete airway
obstruction

An audible inspiratory or expiratory
sound (a precordial stethoscope; early
diagnosis, routine monitor for pediatric
patient)
Tracheal tug, paradoxical respiratory
movements of the thorax and abdomen
(ineffective chest wall movement,
exaggerated abdominal movement)
Diagnosis-complete airway
obstruction

Severe laryngospasm: absence of
breath sound despite adequate chest
wall movement (sine qua non)
Tracheal tug, paradoxical respiratory
movements of the thorax and abdomen
(ineffective chest wall movement,
exaggerated abdominal movement)
Diagnosis-
Australian Incident Monitoring
Study (AIMS): 189/4000, 2005-Feb

1.
2.
3.
145/189 (77%): clinically obvious and
easily diagnosed
23%
27/189 (14%): non-laryngospasm
airway obstruction
9/189 (5%): vomiting/regurgitation
7/189 (4%): desaturation
Precipitating causes of
laryngospasm-Australian Incident Monitoring Study
(AIMS): 189/4000
Morbidity and Mortality of
laryngospasm

Severe hypoxaemia
Pulmonary aspiration
Post-obstructive pulmonary edema (severe
intrapleural negative pressure)
Arrhythmia
Delay recovery
Bradycardia
Cardiac arrest
AIMS
Treatment

Incomplete airway obstruction
Complete airway obstruction
Incomplete airway obstruction

First
Removing the irritating surgical stimulus
Removing debris from the larynx
100%O2; airway maneuver (chin lift/jaw
thrust)
Second
Deepening anesthesia
Third
A tight-fitting face mask with continuous
positive airway pressure as 100% O2
Complete airway obstruction

Fink: ball-valve
First
Airway maneuver:
forcing the chin forward with strong pressure
from behind the ascending rami of the jaw
→ dislocate TMJ anteriorly
→ lengthen thyrohyoid muscle
→ unfold the soft supraglottic tissue
Complete airway obstruction
Complete airway obstruction

Second: muscle relaxant
Intravenous: atropine and succinylcholine
Intramuscular: succinylcholine (4mg/kg)
vocal cords relax within one minute; last
several minutes to intubation
Intralingual: atropine and succinylcholine
(not recommended for children with
halothane/nitrous oxide/O2; ventricular
arrhythmia)
Complete airway obstruction

Redden and colleagues: (1990, Anesth
Progress)
injection of succinylcholine by an
extraoral submental approach in
children
2% succinylcholine (3.0mg/kg)
Resulted in satisfactory intubation
conditions
Complete airway obstruction

Intrinsic muscles of the larynx: sensitive
to succinylcholine
Chung & Rowbottom: (1993;
Anaesthesia)
Laryngoscopy; iv succinylcholine (0.1
mg/kg) in children with laryngospasm
lasted 2 minutes after injection
Complete airway obstruction

Third
Intubation without muscle relaxation
spray vocal folds directly with lidocaine
(direct effect of local analgesia or to a
prolonged effect of hypoxia)
Complete airway obstruction

Fourth
Cricothyrotomy or emergent
tracheostomy
Prevention

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4.
Prevention is the best therapy for
laryngospasm
Identified the risk factor:
Surgical type
Patient age
Pre-existing condition
Anaesthetic technique
Risk factor-surgical type

Otolaryngological and oral surgery
Upper aerodigestive tract endoscopy
Hypospadias repair
Anal surgery
Risk factor-patient age

An overall incidence: 8.7/1000 patients
Children (0-9 y/o): 17.4/1000: 2X
Infants (birth to 3 m/o): 28.2/1000: 3X
Risk factor-pre-existing
condition

Pre-existing respiratory problem;
asthma
Upper airway infection
A history of previous anaesthetic
complications
NG tube in situ
Risk factor-anaesthetic
technique

Light stages of anesthesia:
inhalation induction, tracheal intubation, extubation
Light anesthesia
Inhalation induction of with pungent anesthetics such
as isoflurane, desflurane, enflurane
Barbiturates (parasympathetic overactivity)
Intubation v.s. face or laryngeal mask
Blood or secretions in the upper airway at the time of
extubation (Major cause of post-op laryngospasm)
Prevention

Baraka A. 1978, Intravenous lodicaine
controls extubation laryngospasm in children,
Anesth Analg
Intravenous lidocaine 2 mg/kg
one minute before extubation
slowly over a 30-second period
(central interruption of the reflex pathway; a
direct peripheral action on the sensory or
motor nerve terminals)
Prevention

Directly apply local anesthetic to the laryngeal
area or supraglottic mucosa
Lidocaine (30mins); Cocaine 4% solution
Vagolytic agent: IM atropine; elimination of
undesirable secretions
Extubation while the patient is still deeply
anaesthetized
hypoventilation, aspiration, respiratory
obstruction
Algorithm- Signs
Algorithm- Think of
Algorithm- Management
Algorithm- Further care
Conclusion

Easily detected and managed
If poorly managed, potential morbidity
and mortality
Prevention is the best therapy for
laryngospasm
References

Landsman IS. Mechanisms and treatment of
laryngospasm. Int Anesthesiol Clin.
1997;35(3):67-73
Roy WL, Lerman J. Laryngospasm in
paediatric anesthesia. Can J Anaesth
1988;35:93-98
Visvanathan T, Kluger MT, Webb RK,
Westhorpe RN. Crisis management during
anaesthesia: laryngospasm. Qual Saf Health
Care. 2005 Jun;14(3):e3
References

Olsson GL, Hallen B. Laryngospasm during
anaesthesia. A computer-aided incidence study in
13,929 patients. Acta Anaesthesiol Scand
1984;28:567-575
Rex MAE. A review of the structural and functional
basis of laryngospasm and a discussion of nerve
pathways involved in reflexes and its clinical
significance in man and animals. Br j Anaesth 1970;
42:891-899
Fink BR. The etiology and treatment of laryngospasm.
Anesthesiology 1956;17:569-577
The end
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