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. 3. 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 1. 2. 3. 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 Thank you!
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