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    Laryngospasm

    R3

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    Introduction A protective reflexive glottic closure

    prevent aspiration

    Its exaggeration impedes respiration

    Self-limited mostly: prolonged hypoxia andhypercapnea abolish the reflex

    If sustained, morbidity (e.g. cardiac arrest,

    PE,etc.) and mortality ensue

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    Epidemiology Inversely related with age

    The overall incidence: 0.87%

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    Anatomy

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    Anatomy

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    Physiology A multitude of mechanoreceptors,

    chemoreceptors and thermoreceptors arethroughout the larynx

    The density is greatest around the laryngeal

    opening The posterior aspect of the true vocal folds has

    greater density than the anterior

    Stimulation of these receptors induce short-livedglottic adduction to protect from aspiration

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    Mechanism Afferent fibers within the internal branch of the SLN

    Spasmodic dysphonia: involuntary spasms in thelaryngeal muscles during speech production Neuroimaging(20:20) and postmortem histopathology(20:3)

    Axonal and myelin content in the genu of internal capsule

    Mineral depositions in parenchyma and vessel walls of the post.limb of the int. capsule, putamen, globus pallidus and cerebellum

    Efferent response to the entire vagus apnea,bronchoconstriction, bradycardia, peripheral vasculartone change

    There is a speculation: such a response leads to suddeninfant death, possibly in reaction to LPR

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    Risk Factor Patient-related

    Young age

    Anxiety GERD URI or active asthma

    2~10 folds the risk

    Chronic smoker

    Airway anomaly Surgery-related

    T and/or A LMS Thyroid surgery

    SLN injury Hypoparathyroidism

    Esophageal procedure Distal afferent nerves

    Anesthesia-related Insufficient depth of

    anesthesia during induction i.v. induction agents

    Barbiturate Ketamine saliva

    LMA > ETT > face mask

    Airway irritation Volatile anesthetics Mucus or blood after

    extubation

    Children supervised by lessexperienced anesthesiologist

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    Prevention Identify patients at risk is the most important

    Nonirritant inhalational anesthetic, e.g.sevoflurane Deep anesthesia before intubation Extubate while the lungs are inflated by positive

    pressure Adductor response of laryngeal muscle Artificial cough

    5% CO2 inhalation for 5 min before extubaionCO2 exhalation drive > the laryngospasmreflex Acupuncture

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    Prevention Drugs

    Premedication with oral BZD upperairway reflex during induction

    Anticholinergics secretion

    Lidocaine

    Spray to larynx at 4 mg/kg (1 mL 10% lidocaine fora 25 kg pt)

    30 min in duration

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    Intravenous Lidocaine

    Gilbert first used i.v. lidocaine as an

    adjunct to general inhalation agents in1951

    Controversial in preventing laryngospasm Some said i.v. at 1 mg/kg 5 min before

    extubation fairly effective as topical use

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    Deep versus Awake Extubation Controversial

    Awake extubation

    Protect the airway from aspiration

    Deep extubation Less likely to cough and strain, which can

    cause bleeding throat irrtation

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    Treatment Partial laryngospasm

    Identify and remove the stimulus

    Apply jaw thrust maneuver Insert oral or nasal airway Positive pressure ventilation with 100% O2

    Complete laryngospasm

    Call for help Deepen the anesthesia level

    If laryngospasmoccurs without i.v. line intraosseousroute offer a faster central circulation than peripheral

    Lidocaine SLN block 5 mL of 2% lidocaine + 5 mL NS nebulized by 100% O2 Transtracheal injection of 1~2 mL 4% lidocaine

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    Superior Laryngeal Nerve Block

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    The LaryngospasmNotch

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    Follow Up Assess for the possibility of developing

    Pulmonary aspiration

    Postobstructive negative pressure pulmonaryedema

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    Paroxysmal Laryngospasm Extremely rare and is diagnosed by history:

    spontaneous sudden onset of stridulousdyspnea, resolve within minutes

    Frequently have a positional component, maywake the patient

    Extremely distressing, impending doom

    LPRmucosal hypersensitivitymaladaptedreflex arc

    Aggressive elimination of LPR satisfactorilytreated the majority of patients

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    Reference Head & Neck Surgery - Otolaryngology, 4th Edition ABERRANT RECURRENT LARYNGEAL NERVE REINNERVATION AS A CAUSE

    OF STRIDOR AND LARYNGOSPASM Ann Otol Rhinol Laryngol 113:2004

    Aerosolized Lidocaine for Relief of Extubation LaryngospasmANESTH ANALG2005;101:1563

    An approach to the management of paroxysmal laryngospasm The Journal ofLaryngology & Otology ( 2008), 122, 5760.

    Focal white matter changes in spasmodic dysphonia: a combined diffusion tensorimaging and neuropathological study Brain (2008), 131, 447-459

    Intervention steps for treating laryngospasmin pediatric patients PediatricAnesthesia 2008 18: 297302

    Laryngospasm: review of different prevention and treatment modalities PediatricAnesthesia 2008 18: 281288

    Laryngospasmin pediatric practice Pediatric Anesthesia 2008 18: 279280 Risk factors for laryngospasmin children during general anesthesia Pediatric

    Anesthesia 2008 18: 289296 The use of preoperative lidocaine to prevent stridor and laryngospasmafter

    tonsillectomy and adenoidectomy Otolaryngol Head Neck Surg 1998;118:880-2. Transtracheal lignocaine: effective treatment for postextubation stridor Anesth

    Intensive Care 2007; 35:128-131

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    Thank you for listening