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Sodium Azide-Associated Laryngospasm After Air Bag Deployment
The Journal of Emergency Medicine, Vol. 39, No. 3, pp. e113– e115, 2010 Copyright © 2010 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter
doi:10.1016/j.jemermed.2007.10.030
Clinical Communications: Adults SODIUM AZIDE-ASSOCIATED LARYNGOSPASM AFTER AIR BAG DEPLOYMENT David Francis,
MD,*
Samuel A. Warren, MD,† Keir J. Warner, BS,‡ William Harris, Michael K. Copass, MD,† and Eileen M. Bulger, MD‡
MD,†
*Department of Otolaryngology, †Department of Emergency Medicine, and ‡Department of Trauma Surgery, Harborview Medical Center, University of Washington, Seattle, Washington Reprint Address: Keir J. Warner, BS, Harborview Medical Center, 325 Ninth Avenue, Box 359796, Seattle, WA 98104
e Abstract—The advent and incorporation of the air bag into motor vehicles has resulted in the mitigation of many head and truncal injuries in motor vehicle collisions. However, air bag deployment is not risk free. We present a case of sodium azide-induced laryngospasm after air bag deployment. An unrestrained male driver was in a moderate-speed motor vehicle collision with air bag deployment. Medics found him awake, gasping for air with stridorous respirations and guarding his neck. The patient had no external signs of trauma and was presumed to have tracheal injury. The patient was greeted by the Anesthesiology service, which intubated him using glidescope-assisted laryngoscopy. The patient was admitted for overnight observation and treatment of alkaline ocular injury and laryngospasm. Although air bags represent an important advance in automobile safety, their use is not without risk. Bruising and tracheal rupture secondary to air bag deployment have been reported in out-of-position occupants. Additionally, alkaline by-products from the combustion of sodium azide in air bags have been implicated in ocular injury and facial burns. Laryngospasm after sodium azide exposure presents another diagnostic challenge for providers. Therefore, it is incumbent to maintain vigilance in the physical examination and diagnosis of occult injuries after air bag deployment. © 2010 Elsevier Inc.
ment is not risk free. The mechanical force generated in deployment (approximately 40 –191 joules) has been implicated in ophthalmologic, facial, head, neck, spine, thoracic, upper extremity, abdominal, and lower extremity injuries (1–18). Airway compromise stemming from air bag deployment has been reported secondary to thyroid cartilage fracture and blunt trauma (8). Although most are mechanical, some injuries are chemical. The mechanism of insufflation occurs as a charge of sodium azide is ignited, producing sufficient nitrogen gas to fill the 56-L air bag in 30 ms. This conversion creates a plume of sodium hydroxide, sodium carbonate, and other alkaline byproducts. Alkaline injury to the eye has been reported frequently in the literature. Such injuries occur independently of air bag rupture, because the air bag is necessarily vented for the purpose of dissipating deceleration force. However, chemical injury in a motor vehicle crash resulting in laryngospasm has not been reported. Presented here is a case of laryngospasm after air bag deployment. CASE REPORT
e Keywords—sodium azide; air bag; laryngospasm; trauma; airway
An unrestrained 22-year-old male driver was involved in a 35-mph rear-ended collision with frontal air bag deployment. He did not lose consciousness. Paramedics found him alert, guarding his neck, with “gasping” stridorous respirations at 28 breaths/min prohibiting speech, and pulse oximetry in the low 90s. He was provided a
INTRODUCTION Although designed to mitigate head and truncal injuries in high-speed motor vehicle collisions, air bag deploy-
RECEIVED: 26 March 2007; FINAL ACCEPTED: 12 October 2007
SUBMISSION RECEIVED:
3 June 2007; e113
e114
D. Francis et al.
non-rebreather high-flow oxygen mask, which maintained his oxygen saturation above 90%. All other vital signs were within normal limits. His neck examination was unremarkable for tracheal deviation, abrasions, lacerations, or subcutaneous emphysema. He was transported by advanced life support with spinal immobilization to our Level 1 trauma center, with presumed laryngotracheal injury. The patient had no history of respiratory disease, atopy, or drug allergies. In the Emergency Department, he had biphasic stridor with an arterial blood gas pH 7.39, PaCO2 39, and PaO2 331. Rapid-sequence endotracheal intubation was performed by Anesthesiology using glidescope-assisted laryngoscopy, etomidate, and succinylcholine. The airway was ASA grade II with normal-appearing vocal cords, and the endotracheal tube was inserted without event. Otolaryngology performed fiberoptic laryngoscopy and found an erythematous supraglottis, but no traumatic airway injury. Ocular pH was assessed and noted to be 9, and neutralized with 3 L of ocular irrigation using normal saline. The patient took no prescribed medications, and urinary toxicology was negative for recreational drugs. No other injuries were noted on secondary survey. He was admitted to the trauma intensive care unit for observation, mechanical ventilation (AMV, peak inspiratory pressure [PIP] ⫽ 30), and dexamethasone therapy for laryngospasm. He was extubated uneventfully on hospital day 1 and discharged from the hospital on day 2.
DISCUSSION Without a history of respiratory illness or respiratory symptoms, it is reasonable to conclude that his stridor resulted from the collision. Etiologies of foreign body airway obstruction or traumatic injury to the laryngotracheal airway were eliminated, making laryngospasm the best explanation for his condition. Exposure to the airborne air bag propellant was confirmed by an ocular pH of 9. Any proposed mechanism for acute laryngospasm secondary to automobile air bag deployment is speculative. Laryngospasm is a primitive defense mechanism in response to an irritant and functions to protect the lower respiratory tree. Although there are reports of air bags causing traumatic head and neck injuries that result in airway emergencies, there is a paucity of airway complications in an atraumatic neck (7,8). There are rare case reports of acute new-onset asthma attributed to air bag deployment; however, the pathophysiologic explanation for new-onset asthma is unclear (19,20). Many laryngologists argue that these reports represent the inception of paradoxical vocal fold dysfunction (PVFD) rather than asthma. Although an incompletely understood entity,
it is a disorder of the larynx characterized by the inappropriate adduction of the vocal cords during inspiration, resulting in glottic airway obstruction. Both organic and inorganic etiologies have been proposed; however, trauma as the inciting incident and a conversion-type reaction has been described and seems most plausible in this scenario (21). In this case, the proposed laryngeal adductor spasm seems to be related to the caustic by-products of the sodium azide reaction released during deployment. Inhalation of these agents resulted in a particulate reaction and a superficial burn to the larynx. Mechanistically, laryngospasm occurs when a foreign body sensation triggers afferent signals from the recurrent and superior laryngeal nerves, which provide sensation to the laryngeal mucosa, thereby producing reflex closure of the glottis. The laryngeal adduction reflex triggered by acid, base, pressure, or water, has been strong enough to be lethal (22). Whereas this phenomenon is most often described in the anesthesia literature associated with intubation and extubation, analogous reactions related to immersion and thermal inhalational injuries occur (23). There are alternative explanations for his condition. Anxiety-induced laryngospasm is well documented in the laryngology literature, particularly in cases of PVFD (21,24). It is possible that the case reports of new-onset asthma after air bag deployment may instead represent PVFD exacerbation. Another explanation for his laryngospastic event was pressure change within his larynx. Air bags expand utilizing the aforementioned chemical reaction, which necessarily produces substantial pressure change. If this pressure was translated transorally, it might result in substantial irritation and activation of the laryngeal sensory reflex and produce laryngospasm. All these potential etiologies for our patient’s airway emergency result in adductor spasm of his vocal cords. The treatment for this condition is muscle relaxation, which usually occurs spontaneously. In this case, administration of the short-acting depolarizing skeletal muscle relaxant succinylcholine was the event that reversed his laryngospasm definitively. Steroid treatment has no obvious role in the treatment of laryngospasm, a noninflammatory process. Therefore, his treatment was appropriate yet serendipitous, as the process of securing his airway treated his condition. Sodium azide is a noxious versatile compound and its combustion is the presumed etiology for laryngospasm in this incident. Chemically, it is an inhibitor of cytochrome oxidase and has been used as a biocidal additive for stock reagents in laboratories and as an herbicide and nematocide in the agricultural industry. Its volatile combustibility has been exploited in explosive detonators and in air bags. In collisions with a set change in velocity, frontal sensors activate a charge of this compound, producing a
Air Bag-Induced Laryngospasm
volume of gas that inflates an air bag in approximately 30 ms to protect the head and thorax from severe injury from the vehicle interior. Air bags seem to be effective, as their institution has reportedly reduced the incidence of severe injuries to the head and thorax by 30% and mortality by 19% in highspeed frontal crashes (22,25,26). Nonetheless, there are by-products of sodium azide, which, in this case, seem to have resulted in an airway emergency.
CONCLUSIONS Air bags represent an important advance in automobile safety; however, it is incumbent on health care personnel to report and be prepared to manage potential medical complications secondary to their deployment.
REFERENCES 1. McGwin G Jr, Owsley C. Risk factors for motor vehicle collisionrelated eye injuries. Arch Ophthalmol 2005;123:89 –95. 2. Duma SM, Rath AL, Jernigan MV, Stitzel JD, Herring IP. The effects of depowered airbags on eye injuries in frontal automobile crashes. Am J Emerg Med 2005;23:13–9. 3. Cox D, Vincent DG, McGwin G, MacLennan PA, Holmes JD, Rue LW 3rd. Effect of restraint systems on maxillofacial injury in frontal motor vehicle collisions. J Oral Maxillofac Surg 2004;62: 571–5. 4. Murphy RX Jr, Birmingham KL, Okunski WJ, Wasser T. The influence of airbag and restraining devices on the patterns of facial trauma in motor vehicle collisions. Plast Reconstr Surg 2000;105: 516 –20. 5. Stewart TC, Girotti MJ, Nikore V, Williamson J. Effect of airbag deployment on head injuries in severe passenger motor vehicle crashes in Ontario, Canada. J Trauma 2003;54:266 –72. 6. Pintar FA, Yoganandan N, Gennarelli TA. Airbag effectiveness on brain trauma in frontal crashes. Annu Proc Assoc Adv Automot Med 2000;44:149 – 69. 7. Hirshoren N, Hocwald E, Eliashar R. Isolated traumatic thyroid hemorrhage secondary to air bag deployment. Otolaryngol Head Neck Surg 2004;130:791–3. 8. Epperly NA, Still JT, Law E, Deppe SA, Friedman B. Supraglottic and subglottic airway injury due to deployment and rupture of an automobile airbag. Am Surg 1997;63:979 – 81.
e115 9. Smith JA, Siegel JH, Siddiqi SQ. Spine and spinal cord injury in motor vehicle crashes: a function of change in velocity and energy dissipation on impact with respect to the direction of crash. J Trauma 2005;59:117–31. 10. Ball ST, Vaccaro AR, Albert TJ, Cotter JM. Injuries of the thoracolumbar spine associated with restraint use in head-on motor vehicle accidents. J Spinal Disord 2000;13:297–304. 11. Morgenstern K, Talucci R, Kaufman MS, Samuels LE. Bilateral pneumothorax following air bag deployment. Chest 1998;114: 624 – 6. 12. Dunn JA, Williams MG. Occult ascending aortic rupture in the presence of an air bag. Ann Thorac Surg 1996;62:577– 8. 13. Jernigan MV, Duma SM. The effects of airbag deployment on severe upper extremity injuries in frontal automobile crashes. Am J Emerg Med 2003;21:100 –5. 14. Huelke DF, Moore JL, Compton TW, Samuels J, Levine RS. Upper extremity injuries related to airbag deployments. J Trauma 1995;38:482– 8. 15. Fusco A, Kelly K, Winslow J. Uterine rupture in a motor vehicle crash with airbag deployment. J Trauma 2001;51:1192– 4. 16. Yoganandan N, Pintar FA, Gennarelli TA, Maltese MR. Patterns of abdominal injuries in frontal and side impacts. Annu Proc Assoc Adv Automot Med 2000;44:17–36. 17. Estrada LS, Alonso JE, McGwin G Jr, Metzger J, Rue LW 3rd. Restraint use and lower extremity fractures in frontal motor vehicle collisions. J Trauma 2004;57:323– 8. 18. McGovern MK, Murphy RX Jr, Okunski WJ, Wasser TE. The influence of air bags and restraining devices on extremity injuries in motor vehicle collisions. Ann Plast Surg 2000;44:481–5. 19. Hambrook DW, Fink JN. Airbag asthma: a case report and review of the literature. Ann Allergy Asthma Immunol 2006;96:369 –72. 20. Gross KB, Koets MH, D’Arcy JB, Chan TL, Wooley RG, Basha MA. Mechanism of induction of asthmatic attacks initiated by the inhalation of particles generated by airbag system deployment. J Trauma 1995;38:521–7. 21. Guss J, Mirza N. Methacholine challenge testing in the diagnosis of paradoxical vocal fold motion. Laryngoscope 2006;116:1558 – 61. 22. Cummings P, Koepsell TD, Rivara FP, McKnight B, Mack C. Air bags and passenger fatality according to passenger age and restraint use. Epidemiology 2002;13:525–32. 23. Valdez TA, Desai U, Ruhl CM, Nigri PT. Early laryngeal inhalation injury and its correlation with late sequelae. Laryngoscope 2006;116:283–7. 24. Patel NJ, Jorgensen C, Kuhn J, Merati AL. Concurrent laryngeal abnormalities in patients with paradoxical vocal fold dysfunction. Otolaryngol Head Neck Surg 2004;130:686 –9. 25. Braver ER, Kyrychenko SY, Ferguson SA. Driver mortality in frontal crashes: comparison of newer and older airbag designs. Traffic Inj Prev 2005;6:24 –30. 26. Viano DC. Restraint effectiveness, availability and use in fatal crashes: implications to injury control. J Trauma 1995;38:538 – 46.
doi:10.1016/j.jemermed.2007.10.030
Clinical Communications: Adults SODIUM AZIDE-ASSOCIATED LARYNGOSPASM AFTER AIR BAG DEPLOYMENT David Francis,
MD,*
Samuel A. Warren, MD,† Keir J. Warner, BS,‡ William Harris, Michael K. Copass, MD,† and Eileen M. Bulger, MD‡
MD,†
*Department of Otolaryngology, †Department of Emergency Medicine, and ‡Department of Trauma Surgery, Harborview Medical Center, University of Washington, Seattle, Washington Reprint Address: Keir J. Warner, BS, Harborview Medical Center, 325 Ninth Avenue, Box 359796, Seattle, WA 98104
e Abstract—The advent and incorporation of the air bag into motor vehicles has resulted in the mitigation of many head and truncal injuries in motor vehicle collisions. However, air bag deployment is not risk free. We present a case of sodium azide-induced laryngospasm after air bag deployment. An unrestrained male driver was in a moderate-speed motor vehicle collision with air bag deployment. Medics found him awake, gasping for air with stridorous respirations and guarding his neck. The patient had no external signs of trauma and was presumed to have tracheal injury. The patient was greeted by the Anesthesiology service, which intubated him using glidescope-assisted laryngoscopy. The patient was admitted for overnight observation and treatment of alkaline ocular injury and laryngospasm. Although air bags represent an important advance in automobile safety, their use is not without risk. Bruising and tracheal rupture secondary to air bag deployment have been reported in out-of-position occupants. Additionally, alkaline by-products from the combustion of sodium azide in air bags have been implicated in ocular injury and facial burns. Laryngospasm after sodium azide exposure presents another diagnostic challenge for providers. Therefore, it is incumbent to maintain vigilance in the physical examination and diagnosis of occult injuries after air bag deployment. © 2010 Elsevier Inc.
ment is not risk free. The mechanical force generated in deployment (approximately 40 –191 joules) has been implicated in ophthalmologic, facial, head, neck, spine, thoracic, upper extremity, abdominal, and lower extremity injuries (1–18). Airway compromise stemming from air bag deployment has been reported secondary to thyroid cartilage fracture and blunt trauma (8). Although most are mechanical, some injuries are chemical. The mechanism of insufflation occurs as a charge of sodium azide is ignited, producing sufficient nitrogen gas to fill the 56-L air bag in 30 ms. This conversion creates a plume of sodium hydroxide, sodium carbonate, and other alkaline byproducts. Alkaline injury to the eye has been reported frequently in the literature. Such injuries occur independently of air bag rupture, because the air bag is necessarily vented for the purpose of dissipating deceleration force. However, chemical injury in a motor vehicle crash resulting in laryngospasm has not been reported. Presented here is a case of laryngospasm after air bag deployment. CASE REPORT
e Keywords—sodium azide; air bag; laryngospasm; trauma; airway
An unrestrained 22-year-old male driver was involved in a 35-mph rear-ended collision with frontal air bag deployment. He did not lose consciousness. Paramedics found him alert, guarding his neck, with “gasping” stridorous respirations at 28 breaths/min prohibiting speech, and pulse oximetry in the low 90s. He was provided a
INTRODUCTION Although designed to mitigate head and truncal injuries in high-speed motor vehicle collisions, air bag deploy-
RECEIVED: 26 March 2007; FINAL ACCEPTED: 12 October 2007
SUBMISSION RECEIVED:
3 June 2007; e113
e114
D. Francis et al.
non-rebreather high-flow oxygen mask, which maintained his oxygen saturation above 90%. All other vital signs were within normal limits. His neck examination was unremarkable for tracheal deviation, abrasions, lacerations, or subcutaneous emphysema. He was transported by advanced life support with spinal immobilization to our Level 1 trauma center, with presumed laryngotracheal injury. The patient had no history of respiratory disease, atopy, or drug allergies. In the Emergency Department, he had biphasic stridor with an arterial blood gas pH 7.39, PaCO2 39, and PaO2 331. Rapid-sequence endotracheal intubation was performed by Anesthesiology using glidescope-assisted laryngoscopy, etomidate, and succinylcholine. The airway was ASA grade II with normal-appearing vocal cords, and the endotracheal tube was inserted without event. Otolaryngology performed fiberoptic laryngoscopy and found an erythematous supraglottis, but no traumatic airway injury. Ocular pH was assessed and noted to be 9, and neutralized with 3 L of ocular irrigation using normal saline. The patient took no prescribed medications, and urinary toxicology was negative for recreational drugs. No other injuries were noted on secondary survey. He was admitted to the trauma intensive care unit for observation, mechanical ventilation (AMV, peak inspiratory pressure [PIP] ⫽ 30), and dexamethasone therapy for laryngospasm. He was extubated uneventfully on hospital day 1 and discharged from the hospital on day 2.
DISCUSSION Without a history of respiratory illness or respiratory symptoms, it is reasonable to conclude that his stridor resulted from the collision. Etiologies of foreign body airway obstruction or traumatic injury to the laryngotracheal airway were eliminated, making laryngospasm the best explanation for his condition. Exposure to the airborne air bag propellant was confirmed by an ocular pH of 9. Any proposed mechanism for acute laryngospasm secondary to automobile air bag deployment is speculative. Laryngospasm is a primitive defense mechanism in response to an irritant and functions to protect the lower respiratory tree. Although there are reports of air bags causing traumatic head and neck injuries that result in airway emergencies, there is a paucity of airway complications in an atraumatic neck (7,8). There are rare case reports of acute new-onset asthma attributed to air bag deployment; however, the pathophysiologic explanation for new-onset asthma is unclear (19,20). Many laryngologists argue that these reports represent the inception of paradoxical vocal fold dysfunction (PVFD) rather than asthma. Although an incompletely understood entity,
it is a disorder of the larynx characterized by the inappropriate adduction of the vocal cords during inspiration, resulting in glottic airway obstruction. Both organic and inorganic etiologies have been proposed; however, trauma as the inciting incident and a conversion-type reaction has been described and seems most plausible in this scenario (21). In this case, the proposed laryngeal adductor spasm seems to be related to the caustic by-products of the sodium azide reaction released during deployment. Inhalation of these agents resulted in a particulate reaction and a superficial burn to the larynx. Mechanistically, laryngospasm occurs when a foreign body sensation triggers afferent signals from the recurrent and superior laryngeal nerves, which provide sensation to the laryngeal mucosa, thereby producing reflex closure of the glottis. The laryngeal adduction reflex triggered by acid, base, pressure, or water, has been strong enough to be lethal (22). Whereas this phenomenon is most often described in the anesthesia literature associated with intubation and extubation, analogous reactions related to immersion and thermal inhalational injuries occur (23). There are alternative explanations for his condition. Anxiety-induced laryngospasm is well documented in the laryngology literature, particularly in cases of PVFD (21,24). It is possible that the case reports of new-onset asthma after air bag deployment may instead represent PVFD exacerbation. Another explanation for his laryngospastic event was pressure change within his larynx. Air bags expand utilizing the aforementioned chemical reaction, which necessarily produces substantial pressure change. If this pressure was translated transorally, it might result in substantial irritation and activation of the laryngeal sensory reflex and produce laryngospasm. All these potential etiologies for our patient’s airway emergency result in adductor spasm of his vocal cords. The treatment for this condition is muscle relaxation, which usually occurs spontaneously. In this case, administration of the short-acting depolarizing skeletal muscle relaxant succinylcholine was the event that reversed his laryngospasm definitively. Steroid treatment has no obvious role in the treatment of laryngospasm, a noninflammatory process. Therefore, his treatment was appropriate yet serendipitous, as the process of securing his airway treated his condition. Sodium azide is a noxious versatile compound and its combustion is the presumed etiology for laryngospasm in this incident. Chemically, it is an inhibitor of cytochrome oxidase and has been used as a biocidal additive for stock reagents in laboratories and as an herbicide and nematocide in the agricultural industry. Its volatile combustibility has been exploited in explosive detonators and in air bags. In collisions with a set change in velocity, frontal sensors activate a charge of this compound, producing a
Air Bag-Induced Laryngospasm
volume of gas that inflates an air bag in approximately 30 ms to protect the head and thorax from severe injury from the vehicle interior. Air bags seem to be effective, as their institution has reportedly reduced the incidence of severe injuries to the head and thorax by 30% and mortality by 19% in highspeed frontal crashes (22,25,26). Nonetheless, there are by-products of sodium azide, which, in this case, seem to have resulted in an airway emergency.
CONCLUSIONS Air bags represent an important advance in automobile safety; however, it is incumbent on health care personnel to report and be prepared to manage potential medical complications secondary to their deployment.
REFERENCES 1. McGwin G Jr, Owsley C. Risk factors for motor vehicle collisionrelated eye injuries. Arch Ophthalmol 2005;123:89 –95. 2. Duma SM, Rath AL, Jernigan MV, Stitzel JD, Herring IP. The effects of depowered airbags on eye injuries in frontal automobile crashes. Am J Emerg Med 2005;23:13–9. 3. Cox D, Vincent DG, McGwin G, MacLennan PA, Holmes JD, Rue LW 3rd. Effect of restraint systems on maxillofacial injury in frontal motor vehicle collisions. J Oral Maxillofac Surg 2004;62: 571–5. 4. Murphy RX Jr, Birmingham KL, Okunski WJ, Wasser T. The influence of airbag and restraining devices on the patterns of facial trauma in motor vehicle collisions. Plast Reconstr Surg 2000;105: 516 –20. 5. Stewart TC, Girotti MJ, Nikore V, Williamson J. Effect of airbag deployment on head injuries in severe passenger motor vehicle crashes in Ontario, Canada. J Trauma 2003;54:266 –72. 6. Pintar FA, Yoganandan N, Gennarelli TA. Airbag effectiveness on brain trauma in frontal crashes. Annu Proc Assoc Adv Automot Med 2000;44:149 – 69. 7. Hirshoren N, Hocwald E, Eliashar R. Isolated traumatic thyroid hemorrhage secondary to air bag deployment. Otolaryngol Head Neck Surg 2004;130:791–3. 8. Epperly NA, Still JT, Law E, Deppe SA, Friedman B. Supraglottic and subglottic airway injury due to deployment and rupture of an automobile airbag. Am Surg 1997;63:979 – 81.
e115 9. Smith JA, Siegel JH, Siddiqi SQ. Spine and spinal cord injury in motor vehicle crashes: a function of change in velocity and energy dissipation on impact with respect to the direction of crash. J Trauma 2005;59:117–31. 10. Ball ST, Vaccaro AR, Albert TJ, Cotter JM. Injuries of the thoracolumbar spine associated with restraint use in head-on motor vehicle accidents. J Spinal Disord 2000;13:297–304. 11. Morgenstern K, Talucci R, Kaufman MS, Samuels LE. Bilateral pneumothorax following air bag deployment. Chest 1998;114: 624 – 6. 12. Dunn JA, Williams MG. Occult ascending aortic rupture in the presence of an air bag. Ann Thorac Surg 1996;62:577– 8. 13. Jernigan MV, Duma SM. The effects of airbag deployment on severe upper extremity injuries in frontal automobile crashes. Am J Emerg Med 2003;21:100 –5. 14. Huelke DF, Moore JL, Compton TW, Samuels J, Levine RS. Upper extremity injuries related to airbag deployments. J Trauma 1995;38:482– 8. 15. Fusco A, Kelly K, Winslow J. Uterine rupture in a motor vehicle crash with airbag deployment. J Trauma 2001;51:1192– 4. 16. Yoganandan N, Pintar FA, Gennarelli TA, Maltese MR. Patterns of abdominal injuries in frontal and side impacts. Annu Proc Assoc Adv Automot Med 2000;44:17–36. 17. Estrada LS, Alonso JE, McGwin G Jr, Metzger J, Rue LW 3rd. Restraint use and lower extremity fractures in frontal motor vehicle collisions. J Trauma 2004;57:323– 8. 18. McGovern MK, Murphy RX Jr, Okunski WJ, Wasser TE. The influence of air bags and restraining devices on extremity injuries in motor vehicle collisions. Ann Plast Surg 2000;44:481–5. 19. Hambrook DW, Fink JN. Airbag asthma: a case report and review of the literature. Ann Allergy Asthma Immunol 2006;96:369 –72. 20. Gross KB, Koets MH, D’Arcy JB, Chan TL, Wooley RG, Basha MA. Mechanism of induction of asthmatic attacks initiated by the inhalation of particles generated by airbag system deployment. J Trauma 1995;38:521–7. 21. Guss J, Mirza N. Methacholine challenge testing in the diagnosis of paradoxical vocal fold motion. Laryngoscope 2006;116:1558 – 61. 22. Cummings P, Koepsell TD, Rivara FP, McKnight B, Mack C. Air bags and passenger fatality according to passenger age and restraint use. Epidemiology 2002;13:525–32. 23. Valdez TA, Desai U, Ruhl CM, Nigri PT. Early laryngeal inhalation injury and its correlation with late sequelae. Laryngoscope 2006;116:283–7. 24. Patel NJ, Jorgensen C, Kuhn J, Merati AL. Concurrent laryngeal abnormalities in patients with paradoxical vocal fold dysfunction. Otolaryngol Head Neck Surg 2004;130:686 –9. 25. Braver ER, Kyrychenko SY, Ferguson SA. Driver mortality in frontal crashes: comparison of newer and older airbag designs. Traffic Inj Prev 2005;6:24 –30. 26. Viano DC. Restraint effectiveness, availability and use in fatal crashes: implications to injury control. J Trauma 1995;38:538 – 46.