Laryngospasm: Review of Different Prevention and Treatment Modalities

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Pediatric Anesthesia 2008 18: 281–288 doi:10.1111/j.1460-9592.2008.02448.

Review article
Laryngospasm: review of different prevention and
treatment modalities
ACHIR A. ALALAMI MD, CHAKIB M. AYOUB AND
ANIS S. BARAKA MD
Department of Anaesthesia, American University of Beirut Medical Center, Beirut, Lebanon

Summary
Laryngospasm is a common complication in pediatric anesthesia. In
the majority of cases, laryngospasm is self-limiting. However, some-
times laryngospasm persists and if not appropriately treated, it may
result in serious complications that may be life-threatening. The
present review discusses laryngospasm with the emphasis on the
different prevention and treatment modalities.
Keywords: laryngospasm; review; anesthesia; treatment; prevention;
modalities

Introduction Epidemiology
Laryngospasm is mainly seen in children. It is a The overall incidence of laryngospasm is 0.87%. The
reflex closure of the upper airway as a result of incidence in children in the first 9 years of age is
the glottic musculature spasm. It is essentially a 1.74% with a higher incidence of 2.82% in infants
protective reflex that acts to prevent foreign between 1 and 3 months (4).
material entering the tracheobronchial tree. The The incidence of morbidity resulting from laryn-
exaggeration of this reflex may result in complete gospasm can vary as follows: cardiac arrest 0.5%,
glottic closure and consequently impeding respira- postobstructive negative pressure pulmonary edema
tion (1). This leads to hypoxia and hypercapnea. In 4%, pulmonary aspiration 3%, bradycardia 6% and
the majority of patients, the prolonged hypoxia oxygen desaturation 61% (4,6–8).
and hypercapnea abolishes the spastic reflex and
the problem is self-limited (2–4). However, in
Mechanism
certain cases, the spasm is sustained as long as
the stimulus continues and morbidity such as Most laryngeal reflexes are elicited by stimulation of
cardiac arrest, arrhythmia, pulmonary edema, the afferent fibers contained in the internal branch of
bronchospasm or gastric aspiration may occur the superior laryngeal nerve. These reflexes control
(4–6). the laryngeal muscle contractions which protect the
The present review discusses the general aspects airway during swallowing. Laryngospasm may
of laryngospasm with the emphasis on the different occur secondary to loss of inhibition of the laryngeal
prevention and treatment modalities. closure reflex as a result of abnormal excitation (3).

Correspondence to: Achir A. Alalami MD, Chief resident of Clinical manifestation


Anaesthesiology, Department of Anaesthsiology, American Uni-
versity Hospital, Riad El Solh, 1107-2020, Beirut, Lebanon (email: Laryngospasm can be partial, when there is
[email protected]). some degree of air entry and it is recognized by

 2008 The Authors


Journal compilation  2008 Blackwell Publishing Ltd 281
2 82 A . A . A L A L A M I E T A L.

inspiratory stridor (6). Laryngospasm can be com-


Anesthesia-related factors
plete, with no air movement and absence of breath
sounds. It is early recognized by feeling with the Insufficient depth of anesthesia during both induc-
hand or placing the ear over the mouth (9,10). In tion and emergence predisposes to laryngospasm.
both partial and complete laryngospasm, signs of During anesthesia including tracheal intubation,
airway obstruction such as tracheal tug, paradoxical laryngospasm tends to occur after extubation, while
movement of the chest and abdomen are noticed anesthesia by spontaneous breathing using a face or
(6,11,12). Late signs such as oxyhemoglobin desatu- laryngeal mask may result in laryngospasm during
ration, bradycardia and central cyanosis may ensue induction or maintenance (8,11,17).
(8). In addition, airway irritation with volatile anes-
thetics, mucus or blood and airway manipulation
with suction catheter or laryngoscope blade may
Differential diagnosis
also induce laryngospasm (11,17).
Laryngospasm should be differentiated from other Among the intravenous (i.v.) induction agents,
causes of airway obstruction such as bronchospasm barbiturates such as thiopentone have been shown to
or supraglottic obstruction (8). Both supraglottic increase the incidence of laryngospasm (4,6,18–22).
obstruction and partial laryngospasm are associated Ketamine is rarely associated with laryngospasm
with inspiratory stridor and intercostal retractions (0.4%) (5,23). However, Ketamine may cause hyper-
with rapidly deteriorating oxygenation. These two salivation which can precipitate laryngospasm by
complications can be differentiated by directly visua- irritating the vocal cords (23). Also, anesthesia
lizing the vocal cords while the patient is making induction with propofol is less associated with
inspiratory efforts (9). However, in the clinical laryngospasm than sevoflurane induction (24).
situation, inserting a laryngoscope to visualize the Volatile anesthetics have been associated with
vocal cords in such situation may worsen laryngo- laryngospasm in pediatric anesthesia (2.3%) (5,6).
spasm. Jaw thrust or head tilt maneuver with or Among all the volatile agents, the highest incidence
without insertion of oral or nasal airway while of laryngospasm is associated with desflurane
applying gentle positive pressure would relieve both (50%). Isoflurane is more associated with laryngo-
supraglottic obstruction and partial laryngospasm. If spasm than enflurane, halothane and sevoflurane
these fail to treat the obstruction, complete laryngo- (6,7,25,26). There is no difference in the incidence of
spasm should be suspected and appropriate treat- laryngospasm between sevoflurane and halothane
ment should be initiated (10). In this issue if the (27).
journal, Anghelescu and Burgoyne (13) discuss the Finally, laryngospasm is more likely to occur in
incidence and treatment of laryngospasm at the St children which are supervised by less experienced
Jude Children’s Research Hospital in Memphis. Anes- anesthesiologists (28).
thesiologists must also differentiate laryngospasm
from breath-holding by the presence of rocking-type
Patient-related factors
movement of the chest wall and abdomen (14).
Laryngospasm can be psychogenic which is most The incidence of laryngospasm following general
often seen in anxious adolescents and young adults. anesthesia is inversely correlated with age (29).
It presents with sudden paroxysms of stridor or Children with upper respiratory tract infection or
wheezing in response to exercise or emotional stress active asthma have irritable airway and are appro-
and is treated with reassurance and midazolam ximately 10-fold more prone to develop laryngo-
sedation (15,16). spasm.
Airway hyperactivity lasts for up to 6 weeks after
respiratory infection, thus elective surgery can be
Risk factors
delayed for 6 weeks (4,5,18,30–32).
Risk factors can be classified into three categories: Chronic smokers have increased airway reflex
anesthesia-related factors, patient-related factors and sensitivity and are more prone to develop laryn-
surgery-related factors: gospasm. A period of abstinence from smoking of at

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Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 18, 281–288
R E V I E W O F D I F F E R EN T P R E V E N T I O N A N D T R E A T M E N T M O D A L I T I E S 2 83

least 48 h and possibly up to 10 days may be The advantage of deep tracheal extubation over
required to reduce the risk of airway problems awake extubation in children undergoing tonsillec-
(33). There is a 10-fold increase in the incidence of tomy is that patients are less likely to cough and
laryngospasm in children who are exposed to strain which can cause bleeding from the tonsilar
tobacco smoke. Therefore, preoperative visit should bed and consequently increasing the risk of laryn-
include questioning about ‘passive smoking’ (20, gospasm. On the other hand, awake tracheal extu-
History of gastroesophageal reflux is also a risk bation offers the advantage of protecting the airway
factor for developing laryngospasm. (34,35). Finally, against aspiration during this vulnerable period.
patients with elongated uvula and those with history Patel et al. (48) undertook a study comparing
of choking during sleep may also develop laryn- awake vs anesthetized tracheal extubation of
gospasm under general anesthesia (11,36,37). patients after tonsillectomy and adenoidectomy.
They used the criteria of awake extubation when
patients demonstrated facial grimace, had adequate
Surgery-related factors
tidal volumes and respiratory rate, coughed with
There is a close association between laryngospasm open mouths or opened their eyes. They concluded
and the type of surgery (4,8). Tonsillectomy and that there is no difference in laryngospasm incidence
adenoidectomy have the highest incidence of lar- between the two techniques. On the other hand,
yngospasm (21–26%) (1,19,38–43). Other types of Pounder et al. (49) studied the incidence of respira-
surgery such as appendicectomy, cervical dilation, tory complications in children undergoing minor
hypospadias surgery and skin transplant in chil- surgery and found greater oxyhemoglobin desatu-
dren are highly associated with laryngospasm (4). ration in the awake extubation group than in the
Thyroid surgery has been associated with laryn- deep extubation group (P < 0.05). They also found
gospasm secondary to superior laryngeal nerve 16% incidence of laryngospasm in the awake group
injury or to (44) iatrogenic removal of parathyroid vs 4% incidence in the anesthetized group
glands causing hypocalcemia that predisposes to (P > 0.05). The ‘No Touch’ technique was initially
laryngospasm (45). Esophageal procedures may described by Lee (6,50). It is virtually an awake
cause laryngospasm secondary to stimulation of tracheal extubation. This technique consists of
distal afferent esophageal nerves (4,46). suctioning of the blood and secretions from the
pharynx, turning the patient to the lateral position
while anesthetized, discontinuing the volatile anes-
Prevention
thetics and avoiding any stimulation until the
Identifying the patients at risk for laryngospasm and patients open their eyes and spontaneously wake
taking the necessary precautions are the most up to be followed by tracheal extubation. Tsui et al.’s
important measures to prevent laryngospasm. (40) study applied this technique to 20 children
Inhalational induction of anesthesia should be undergoing tonsillectomy and adenoidectomy and
carried out by a nonirritant anesthetic such as found no incidence of laryngospasm. However, this
sevoflurane. Also, during sevoflurane induction of study has several shortcomings. First, there was no
anesthesia, it has been recommended to insert the control group with the deep extubation technique.
i.v. line 2 min after the loss of lid reflex to ensure an Second, the size of the group was small (20 patients).
adequate level of anesthesia and to decrease the Concerning tracheal extubation, Lee suggested
incidence of laryngospasm (47). Laryngoscopy and that the tracheal tube be removed while the lungs
tracheal intubation should also be attempted after are inflated by positive pressure; this technique
deepening the level of anesthesia in order to avoid decreases the adductor response of the laryngeal
laryngospasm. muscles and reduces the incidence of layngospasm
Many controversies exist among anesthesiologists (12). Also, positive pressure inflation of the lungs
about the best technique of tracheal extubation before tracheal extubation is followed by forced
which reduces the incidence of laryngospasm. Both exhalation ‘artificial cough’ after extubation which
awake and anesthetized extubation have advantages expels any secretions or blood and this in turn
and disadvantages. decreases vocal cord irritation and laryngospasm.

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Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 18, 281–288
2 84 A . A . A L A L A M I E T A L.

Many drugs have been used to prevent laryngo- 25% in the control group (P < 0.05). They suggest
spasm following general anesthesia. that magnesium acts by both increasing anesthesia
Premedication with anticholinergic agents to pre- depth and providing muscle relaxation in prevent-
vent larygospasm is controversial. However, anti- ing laryngospasm (41).
cholinergics decrease secretions which play a role in Few anesthesiologists in modern practice would
triggering laryngospasm and thus they play an use 5% carbon dioxide (CO2) for preventing laryn-
indirect role in reducing the incidence of laryngo- gospasm, assuming that it could be found on the
spasm (6,29,38,51). Also, premedication with an oral anesthesia machine. This can be performed by
benzodiazepine decreases upper airway reflexes and inhaling the 5% CO2 for 5 min prior to tracheal
thus may decrease laryngospasm during induction extubation. The mechanism is that the respiratory
of anesthesia (47,51,52,53). drive to exhale the carbon dioxide overrides the
The role of lidocaine in preventing laryngospasm laryngospasm reflex. This was a study performed on
is controversial. The i.v. administration of lidocaine cats and thus human studies are needed to prove its
for prevention of laryngospasm was initially des- efficacy and safety (55).
cribed by Baraka. He studied 40 children under- Finally, acupuncture has been described for the pre-
going tonsillectomy and adenoidectomy and found vention of laryngospasm. The incidence of laryngo-
that none of the 20 children who had received an i.v. spasm of was 5.3% in the study group compared
injection of lidocaine 2 mgÆkg)1 1 min before extu- with 23.7% in the control group (P < 0.05). This
bation developed laryngospasm after tracheal extu- method although reducing the incidence of laryngo-
bation, while four of 20 children of the control group spasm, it did not totally abolish it. In addition, the
developed severe laryngospasm after extubation of anesthesiologist would need to learn the proper
the trachea (42). However, Leicht et al. studied 100 techniques of acupuncture (19) (Table 1).
children after tonsillectomy in which i.v. lidocaine
1.5 mgÆkg)1 was administered before tracheal extu-
Treatment
bation when patients started swallowing. They
found no difference in the incidence of layngospasm For laryngospasm which occurs during anesthesia
between the study and control groups. They sug- induction or emergence, the treatment is the same:
gested that the beneficial effects of lidocaine dem- identifying and removing the offending stimulus,
onstrated by Baraka may be attributed to a central applying jaw thrust maneuver, inserting an oral or
increase in the depth of anesthesia. Thus, in order to nasal airway and positive pressure ventilation with
benefit from the effect of central nervous depression 100% oxygen. If these techniques suffice to treat
produced by lidocaine, tracheal extubation must be the spasm, partial laryngospasm is diagnosed. If
performed before signs of swallowing occur (43). the obstruction is not relieved, complete laryngo-
Koc et al. have also reported that 2% topical spasm should be suspected and the next step
lidocaine sprayed to the glottis at 4 mgÆkg)1 or 2% should be calling for help and deepening the level
intraveous lidocaine given at 1 mgÆkg)1 5 min before of anesthesia with i.v. or inhalational anesthetic.
extubation are fairly effective in preventing laryn- Propofol can be used at doses 0.25–0.8 mgÆkg)1
gospasm following tonsillectomy and adenoidec- because of its rapid and predictable action, but if
tomy (39). Also spraying the glottis with 2% there is no i.v. line inhalational anesthesia can be
lidocaine at 4 mgÆkg)1 has an important clinical used (29,56–59). If this technique fails and oxy-
application in decreasing the incidence of larygo- hemoglobin desaturation ensues (SpO2 < 85%) sux-
spasm during awake intubation in neonates (54). amethonium can be given at doses of 0.1–3 mgÆkg)1
Gulhas et al. described the use of magnesium to followed by mask ventilation and, or tracheal
prevent laryngospasm after tonsillectomy and ade- intubation (60–62).
noidectomy in children. They gave 15 mgÆkg)1 mag- The use of propofol at 0.5 mgÆkg)1 i.v. to treat
nesium sulphate in 30 ml 0.9% NaCl over 20 min laryngospasm has been shown to be safe and free of
after tracheal intubation in 20 patients and found cardiovascular events, however, some patients may
that the incidence of laryngospasm during tracheal develop transient apnea which needs airway sup-
extubation in this group was 0% compared with port and ventilation (29). The question of whether to

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Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 18, 281–288
R E V I E W O F D I F F E R EN T P R E V E N T I O N A N D T R E A T M E N T M O D A L I T I E S 2 85

Table 1 suxamethonium administration following hypoxia


A simplified algorithm for prevention of laryngospasm
may be associated with severe bradycardia and even
cardiac arrest. Thus, it is highly recommended to
give atropine at 0.02 mgÆkg)1 i.v. prior to adminis-
tration of suxamethonium to treat laryngospasm
(6,8,38).
In case of cardiac arrest following suxamethonium
administration, tracheal intubation should be fol-
lowed by ventilation with 100% oxygen and epi-
nephrine should be given at 5–10 lgÆkg)1 i.v. in
incremental doses until there is a response (61).
An intubating dose of suxamethonium (1–
3 mgÆkg)1 i.v.) has been used to treat laryngospasm
until a report by Chung and Rowbottom showed
that the use of 0.1 mgÆkg)1 i.v. of suxamethonium
was successful in treating laryngospasm. The two
advantages of this small dose of suxamethonium are
the maintenance of spontaneous breathing thus
avoiding further hypoxia and the avoidance of
bradycardia following repeated doses (60).
When laryngospasm occurs during inhalational
induction without previous i.v. access several
options can be used. Many studies have shown that
the intramuscular (i.m.) administration of a non-
depolarizing muscle relaxant is not suitable for
emergency intubation mainly because of slow
absorption (63–66). Warner recommends that i.m.
suxamethonium can be administered at 4 mgÆkg)1
followed by tracheal intubation, claiming that maxi-
mum relaxation of i.m. suxamethonium that takes
3 or 4 min is not necessary to treat laryngospasm
use propofol or suxamethonium is a matter of because the onset of neuromuscular blockade is
timing. Propofol should be used prior to suxame- more rapid in the larynx compared with peripheral
thonium because it is successful in treating laryn- muscles (67). However, Donati et al. (64) advise
gospasm in 76.9% of cases (29,58,59). In addition, against the use of i.m. suxamethonium for intubation
propofol offers many advantages over suxame- without i.v. access. They suggest establishing an i.v.
thonium. First, is the lack of interaction of a access for the administration of drugs to treat
depolarizing drug with a previously administered laryngospasm. If this does not succeed, help should
nondepolarizing muscle relaxant. Second, avoiding be sought to establish an i.v. access including the
suxamethonium will eliminate the possibility of femoral vein. Weiss et al. (68) recommend using the
prolonged paralysis in patients with pseudocho- intraosseous route as an efficient and quick access to
linesterase deficiency. Finally, propofol can be used give neuromuscular blocking drugs with faster
when suxamethonium is contraindicated, such as in central circulation times and better pharmacokinet-
patients with muscular dystrophy, recent burns, ics compared with a peripheral i.v. route.
spinal cord transection or hyperkalemia (58,61). For laryngospasm which occurs after tracheal
Suxamethonium still has a crucial role when pro- extubation, Owen showed that infusing doxapram
pofol is unsuccessful (59) and its administration at 1.5 mgÆkg)1 over 20 s to five patients rapidly
should not be delayed until the patient becomes abolished postextubation laryngospasm. He sug-
severely desaturated (SpO2 < 85%). This is because gested that doxapram abolishes laryngospasm by

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Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 18, 281–288
2 86 A . A . A L A L A M I E T A L.

increasing the respiratory drive. However, the effect


of doxapram was seen in only five patients and a
study of large number of patients would be needed
to confirm its efficacy and practicability (69).
Sibaii also, reported two cases of postextubation
laryngospasm that were treated with i.v. nitrogly-
cerin at 4 gÆkg)1. However, whether laryngospasm
was self-limited or was actually treated by nitro-
glycerin needs to be answered. It is well known that
nitroglycerin relaxes the smooth muscles, but the
laryngeal muscles are skeletal muscles and may not
be a target of nitroglycerin action (17).
There is a technique which was first described
40 years ago by Guadagni and was later described
by Larson. It involves placing the middle finger of
Figure 2
each hand in what they term the ‘laryngospasm Superior laryngeal nerve block (71). (A 25 G needle is used to
notch’ (Figure 1). This technique consists of firmly make contact with the hyoid bone, walking off the inferior margin
pressing inward toward the base of the skull with of the bone and advancing 1–2 mm until it pierces the hyoid
ligament).
both fingers, while at the same time applying jaw
thrust maneuver (27). This opens the airway and
induces periosteal pain by pressing on the styloid nerve, a branch of vagus nerve, provides anesthesia
process which helps relaxing the vocal cords by the for supraglottic mucosa via its internal branch.
autonomic nervous system (27,70). Blocking this nerve may be useful for both preven-
Finally, Monso et al. reported three cases of tion and treatment of laryngospasm (71). These are
postextubation laryngospasm that were successfully case reports; hence a study of large number of
treated with superior laryngeal nerve block patients is needed to confirm its efficacy (Table 2).
(Figure 2). Also, Mevorach described the successful In conclusion, knowledge of the risk factors
use of superior laryngeal nerve block in treating whether patient-related, anesthesia or surgery-
postextubation laryngospasm that was refractory to related is the most important factor for prevention
medical treatment (11,71). The superior laryngeal of laryngospasm. During tracheal intubation, the

Table 2
A simplified algorithm for treatment of laryngospasm

Figure 1
Laryngospasm notch (located behind the lobule of the pinna of the
ear, bounded anteriorly by the ascending ramus of the mandible
adjacent to the condyle, posteriorly by the mastoid process of the
temporal bone and cephalad by the base of the skull).

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R E V I E W O F D I F F E R EN T P R E V E N T I O N A N D T R E A T M E N T M O D A L I T I E S 2 87

patient must be deeply anesthetized to avoid laryn- 14 Miller R. Older pediatric patients. Pediatric anesthesia. In:
Miller RD, ed. Miller’s Anesthesia, 6th edn. Philadelphia:
gospasm. There is still controversy whether awake
Elsevier Churchill Livingstone, 2005: 2382.
including the ‘no touch technique’ or anesthetized 15 Golden SE. The management and treatment of recurrent
tracheal extubation should be used in order to postoperative laryngospasm. Anesth Analg 1997; 84: 1389–1396.
prevent laryngospasm. i.v. lidocaine or propofol 16 Patterson D. The management and treatment of recurrent
postoperative laryngospasm. Anesth Analg 1996; 83: 1110–
administration before tracheal extubation may 1111.
decrease the incidence of laryngospasm. Also, pro- 17 Sibai AN, Yamout I. Nitroglycerin relieves laryngospasm. Acta
pofol can relieve laryngospasm in most of the Anaesthesiol Scand 1999; 43: 1081–1083.
18 Schreiner MS, O’Hara I, Markakis DA et al. Do children who
patients. In case of failure, i.v. or i.m. suxamethoni- experience laryngospasm have an increased risk of upper
um can be used. Finally, the patients who have respiratory tract infection? Anesthesiology 1996; 85: 475–480.
suffered laryngospasm should be assessed for the 19 Lee CK, Chien TJ, Hsu JC et al. The effect of acunpucture on
the incidence of postextubation laryngospasm in children.
possibility of developing pulmonary aspiration or
Anaesthesia 1998; 53: 910–924.
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23 Mcglone RG, Howes MC, Joshi M. The Lancaster experience
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Accepted 24 September 2007

 2008 The Authors


Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 18, 281–288

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