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Etomidate use during emergency intubation of trauma patients
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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 15, Number 1 • January 1997
In the ED, the patient denied any other complaint except for neck pain. She was otherwise healthy with an insignificant medical history. She denied the use of alcohol or street drugs. On physical examination, the patient was an alert, cooperative girl who was in obvious discomfort. Head, ear, eye, nose, and throat examination findings were unremarkable. The patient had severe midline cervical pain. Lungs were clear to auscultation, heart was regular with $1S2, and the patient had no chest wall bruising or pain to palpitation. Her abdominal was soft and nontender. Extremity examination found no bruising or tenderness, and the patient was able to move all extremities with normal strength. Knee jerks were two plus and equal, and She had normal sensation throughout. Cervical films and computed tomography showed a nondisplaced fracture of the C6 lamina which extended through the pedicle and the facet. There was also a vertical fracture through the body of C6 and evidence of ligamentous injury between C5 and C6. The patient was admitted to the trauma service and on day 2 a halo vest was placed under local anesthesia by neurosurgery. She was discharged from the hospital 4 days later. After wearing the halo vest for 10 weeks the halo was removed and the patient was reimaged, with flexion and extension films showing slight angulation and kyphotic deformity with interspinous laxity remaining between C5 and C6. After 2 weeks of a cervical collar and mild range of motion exercises, She had repeat flexion and extension films done under fluoroscopy. This study showed that the angulation and laxity had increased. Although the patient remained neurologically intact, she was considered to be at high risk for a serious neurological injury, and 3 months after the original injury she underwent an anterior cervical microdiscectomy at C5-C6 with an autograft fusion and plating. Her recovery has since been unremarkable. This case illustrates yet another way to incur a cervical injury. A literature review found no reported cases of injury caused by human body surfing. This could be secondary to lack of prior occurrence or, more likely, lack of documentation and reporting. In the past few years more emergency medicine physicians have become more involved in the planning and provision of medical care to spectators at large events. Fortunately, most injuries that occur at such events are minor and require minimal medical attention. 1 However, as this case demonstrates, the possibility for significant spectator morbidity from injury is quite real, and qualified medical personnel must be readily available to provide emergency care. By definition, injury occurs whenever energy is transmitted above an individual's tolerance. 2 When providing medical care to spectators, it is important to anticipate what injuries are likely to occur and to determine if they are preventable. This is done by close examination of the venue, the environment, the crowd demographics, and any anticipated special modifiers (such as heavy alcohol use or inclement weather). 2 In this case, the environment was a rock concert, a venue where spectators often consume excessive amounts of alcohol or illicit drugs that may impair their coordination and lessen their social inhibitions, leading to an increased risk of injury. Research has shown that the percentage of spectators that seek medical care at rock concerts is higher than at other venues. 3 Here, injury occurred secondary to the transfer of kinetic energy from the human body surfer to our patient, leading to her fracture. Fortunately, she sought immediate help and was lucky that she did not incur a secondary injury such as paralysis during her transfer to further medical care. Upon review of this case, we hope that physicians and other personnel involved in event management would appreciate the potential for serious injury from human body surfing and develop policies to discourage its practice. We would also hope that physicians who are in charge of event safety would educate event
personnel in the importance of early spinal immobilization of spectators with suspected cervical injuries. JEANNETTEM. WOLFE,MD
Department of Emergency Medicine RICHARDANDERSON,MD
Neurosurgery Baystate Medical Center Springfield, MA
References 1. SandersAB, Criss E, Steckl P, et al: An analysis of medical care at mass gatherings. Ann Emerg Med 1986;15:515-519 2. Martinez R: Injury assessment and control. In Callaham M: Current practices in Emergency Medicine (ed 2). Philadelphia, PA, B. C. Decker, 1991, pp 87-90 3. DeLorenzo RA, Gray BA, Bennett P, et al: Effect of crowd size on patient volume at a large, multipurpose, indoor stadium. J Emerg Med 1989;7:379-384
ETOMIDATE USE DURING EMERGENCYINTUBATION OF TRAUMAPATIENTS To the Editor:--Etomidate, an ultrashort-acting, nonbarbiturate hypnotic agent, has been used as an anesthetic induction agent for many years.l,2 Although etomidate has been suggested as a sedative for emergent endotracheal intubation, there are no previous reports regarding its use in the trauma patient in the emergency department (ED) setting. We prospectively evaluated the safety and efficacy of etomidate as a sedative agent for endotracheal intubation in a case series of trauma patients presenting to a level I trauma center, community teaching hospital ED. Twenty patients (13 men and 7 women) with average age of 47 _+ 26 years (range 15 to 83 years) and average weight of 71 -+ 17 kg (range 50 to 102 kg) were studied. Excluded were patients 10 years of age or younger, those with hypersensitivity to etomidate, and those with history of seizure or pregnancy. After intravenous (IV) cannulation, etomidate (Amidate; Abbott Laboratories, North Chicago, IL) was administered in an IV dose of 0.3 mg/kg of estimated body weight. A second dose was administered in 6 (30%) cases to achieve adequate sedation. Sedation was considered adequate in all patients, with onset of deep sleep in less than 30 seconds and duration of sleep less than 5 minutes. Morphine sulfate and midazolam were administered in one case to further prolong sedation. In contrast, muscle relaxation was adequate in 14 (70%), requiring the use of paralytic agents in 6 (30%), vecuronium in 4, and succinylcholine in 2 cases, primarily because of bruxism. Patients were intubated by either the nasal or oral route at the discretion of the emergency physician. The intubation method was nasotracheal in 9 (45%), orotracheal in 10 (50%), and not documented in one case. Although the time to successful intubation was not recorded, the number of intubation attempts was one in 7 patients (36.8%), 2 in 9 patients (47.4%), 3 in 2 patients (10.5%); and 4 in 1 patient (5.3%) (not documented in one). Indications for intubation included closed head injury and agitation in 9, respiratory failure and acidosis in 5, agitation requiring sedation for computerized tomography in 5, inhalation injury in 2, pulmonary contusion in 2, and flail chest in 1. Minimal hemodynamic effects were noted. The initial pulse (116.2 _+ 20.2 beats/rain) and repeat pulse within l0 minutes (113.5 _+ 25.3 beats/min) were not significantly different (P = 0.96, two-tailed t test). Similarly, the initial blood pressure (141.2 _+ 29.4 mm Hg) and repeat blood pressure within 10 minutes (139.3 _+ 28.9 mm Hg) were not significantly different (P = 0.98, two-tailed t test).
CORRESPONDENCE
There were no cases of apnea; however, mild respiratory depression occurred in 8 (40%) requiring ventilatory assistance. Nausea and vomiting occurred in 1 case (5%). Myoclonic activity was absent in 6 cases (30%), and was mild in 12 (60%), moderate in 1 (5%), and severe in 1 (5%). In 5 cases (25%) significant orofacial myoclonus (bruxism) prevented orotracheal intubation. Pain at the injection site occurred in 3 cases (15%). As experts in airway management of the trauma victim, emergency physicians should be aware of the various advantages and disadvantages of etomidate as an alternative sedative agent. Several attributes would appear to make etomidate ideal for the trauma patient, including its high efficacy, rapid onset, short duration of action, cerebroprotective effects, and minimal respiratory or hemodynamic effects. Following a single 0.3 mg/kg IV dose, etomidate induces sleep with onset of 30 to 60 seconds and duration of approximately 5 to 10 minutes. 1 The short duration of action can be advantageous in cases of head injury or intoxication that require repeat neurologic examination. Because of this short duration of action, however, a continuous infusion or additional sedative agent should be administered if the patient is to be paralyzed. Etomidate could be particularly advantageous in the head injured patient, since it has been reported to have cerebroprotective effects similar to barbiturates in that it decreases intracranial pressure, regional cerebral blood flow, and cerebral metabolic rate for oxygen. 3,4 In contrast to barbiturates, etomidate does not diminish arterial blood pressure or cerebral perfusion pressure. 3,4 Persistence of spontaneous respirations could be a major advantage of a sedative agent for intubation, especially in cases of airway difficulty or failed intubation attempts. Etomidate causes less respiratory depression than other agents, such as thiopental. 2 Hypoventilation has been reported in up to 25% of cases, and transient (resolving within 2 minutes) apnea (up to 90 seconds duration) reported in 12% to 16% of cases. 2,5 Choi et al6 noted a CO2 independent stimulation of ventilation with etomidate, suggesting its utility in cases in which maintenance of spontaneous respiration is desired. Etomidate has been reported to have minimal cardiovascular effects even in the setting of hemodynamic instability7 and compares favorably to midazolam, 8 propofol, and thiopentone9 with regard to hemodynamic safety. Although etomidate has been noted to result in variable changes in systemic vascular resistance, cardiac output, and stroke volume,9,~°these alterations are typically within acceptable limits, and the most favorable advantage is decreased myocardial oxygen consumption. 10Although all but one of our patients were normotensive, etomidate did not significantly alter pulse or blood pressure in any patient in our series. Further study of etomidate in the hypotensive trauma patient should be considered. Etomidate has several side effects of which the emergency physician must be aware; the most important disadvantages include pain on injection, myoclonus, and adrenal suppression. The incidence of pain on injection of etomidate has varied from 4% to 70%. 2 This effect is likely related to the solvent, 35% propylene glycol, which is less irritating than previous preparations. Pain on injection is more common in small peripheral veins, and can be minimized by further dilution or premedication with fentanyl or diazepam. 2 Although phlebitis can occur in up to 23% of patients, lj this was not noted in any of our patients. Spontaneous movements, such as tremor, dystonic posturing, and especially, myoclonia, following etomidate have previously been noted in 20% to 87% of patients 2,6,12and may be precipitated by physical contact. 5 The presence of myoclonic movements varies with the solvent (whether propylene glycol, polyethylene glycol, or aqueous ethanol mixture) 1 and can be minimized by premedication with small doses of narcotic (such as fentanyl) or benzodiazepine
99
(such as diazepam) agents. 5 The mechanism of myoclonia may be related to subcortical disinhibition.1 Although initial reports noted the absence of epileptiform activity, a recent study by Reddy et all2 noted electroencephalographic spikes in 22% of cases with myoclonia and recommend the cautious use of etomidate in patients with seizure history. As an imidazole derivative, etomidate is a potent inhibitor of adrenal corticosteroid production, 13 and continuous infusion has been related to increased mortality. 14 Single induction doses of etomidate can result in depressed levels of cortisol and elevated levels of adrenocorticotropic hormone. 15 This adrenal suppression has likely been the most important factor recently limiting etomidate's popularity as an induction agent. Several other minor disadvantages have previously been noted, including nausea and vomiting, minor hemolysis, cardiovascular responses to intubation, bradycardia, and possibly, histamine release. Nausea and vomiting are not uncommon after etomidate administration and are present in up to 50% of patients receiving multiple doses. 1 Detectable levels of hemolysis have been noted in animal studies, 16 thought to be related to the high osmolality of propylene glycol; however, this has not been demonstrated to be of clinical significance in human trials. 1,2 The increases in heart rate and arterial pressure occurring with laryngeal stimulation during intubation are inhibited less with etomidate alone than thiopentone or propofol, j7 Asystole or bradycardia associated with use of etomidate and suxamethonium or vecuronium have been rarely reported, 18,19 and neither were noted in this series. Although etomidate has previously been reported to not result in histamine release, a recent study noted a limited degree of histamine release in 20% of healthy volunteers, resulting in pain, but without hypotension, tachycardia, or allergic reaction. 2° Again, this side effect is thought to be related to the propylene glycol solvem: This case series demonstrates that etomidate can be used safely in the ED trauma patient; although side effects were common, they were rarely clinically significant to influence patient outcome. This descriptive study, however, was limited by the lack of invasive hemodynamic monitoring, assessment of adrenal function, or blinded comparison to other induction agents. Because several side effects, such as pain on injection, myoclonus, and the hemodynamic response to intubation, may be minimized with premedication with fentanyl and/or diazepam, future studies should consider assessing the safety of etomidate with premedication. Future investigations should also compare the relative safety and efficacy of various sedative agents, such as etomidate, midazolam, fentanyl, propofol, or methohexital, in the trauma setting. Etomidate may be a safe and effective sedative agent for intubation of the ED trauma patient. Etomidate's rapid onset, short duration, minimal respiratory depression, cerebroprotective effects, and lack of cardiovascular response are unique advantages for the head injured or hypotensive trauma victim. The disadvantages of etomidate, including myoclonus (the most frequent side effect), pain on injection, the occasional need for sedative premedication or concomitant paralytic agent use, and adrenal suppression, however, may limit its widespread use. Etomidate is not the ideal premedication for intubation, but remains a reasonable alternative, especially in the setting of trauma. MICHAELC. PLEWA,MD RANDALLKING, MD DAVID JOHNSON,MD DOUGLASADAMS,MD St. Vincent Medical Center The Toledo Hospital Emergency Residency Program Mmo ENGOREN,MD Department of Anesthesia St. Vincent Medical Center Toledo, OH
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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 15, Number 1 • January 1997
References 1. GiesedL, Stanley-I'H: Etomidate:Anewintravenousanesthetic induction agent. Pharmacotherapy 1983;3:251-258 2. Gooding JM, Corssen G: Etomidate: An ultrashort-acting nonbarbiturate agent for anesthesia induction. Anesth Analg 1976;55:286269 3. Cold GE, Eskasen V, Eriksen H, et al: CBF and CMRO2 during continuous etomidate infusion supplemented with N20 and fentanyl in patients with supratentorial cerebral tumour: A dose-response study. Acta Anesthesiol Scand 1985;29:490-494 4. Renou AM, Vernhiet J, Macrez P, et al: Cerebral blood flow and metabolism during etomidate anesthesia in man. Br J Anaesth 1978;50:1047-1057 5. Morgan M, Lumley J, Whitwam J: Etomidate a new watersoluble nonbarbiturate intravenous induction agent Lancet 1975;1: 955-956 6. Choi SD, Spaulding BC, Gross JB, et al: Comparison of the ventilatory effects of etomidate and methohexital. Anesthesiology 1985;62:442-447 7. Colvin MP, Savege -i'M, Newland PE, et al: Cardiorespiratory changes following induction of anesthesia with etomidate in patients with cardiac disease. Br J Anaesth 1979;51:551-556 8. MacGillivray RG, Rocke DA, Mahomedy AE: Midazolam for induction of anaesthesia in patients with limited cardiac reserves. A comparison with etomidate. S Afr Med J 1988;73:101-103 9. Gauss A, Heinrich H, Wilder-Smith OH: Echocardiographic assessment of the haemodynamic effects of propofol: a comparison with etomidate and thiopentone. Anaesthesia 1991;46:99-105 10. Kettler D, Sonntag H, Donath U, et al: Hemodynamics, myocardial mechanics, oxygen requirements and oxygen consumption of the human heart during etomidate induction into anaesthesia. Anaesthesist 1974;23:116-121 11. Zacharias M, Clarke RS, Dundee JW, et al: Venous sequelae following etomidate. Br J Anaesth 1979;51:779-783 12. Reddy RV, Moorthy SS, Dierdorf SF, et al: Excitatory effects and electroencephalographic correlation of etomidate, thiopental, methohexital, and propofol. Anesth Analg 1993;77:1008-1011 13. Preziosi P, Vacca M: Adrenocortical suppression and other endocrine effects of etomidate. Life ScJ 1988;42:477-489 14. Ledingham IM, Watt I: Influence of sedation on mortality in critically ill, multiple trauma patients. Lancet 1983; 1:1270 15. AIIolio B, Dorr H, Stuttmannn R, et al: Effect of a single bolus of etomidate upon eight major corticosteroid hormones and plasma ACTH. Clin Endocrinol 1985;22:281-286 16. NebauerAE, Doenicke A, Hoernecke R, et al: Does etomidate cause haemolysis? Br J Anaesth 1992;69:58-60 17. Harris CE, MurrayAM, Anderson JM, et al: Effects of thiopentone, etomidate and propofol on the haemodynamic response to tracheal intubation. Anaesthesia 1988;43(S):32-36 (suppl) 18. Inoue K, Reichelt W: Asystole and bradycardia in adult patients after a single dose of suxamethonium. Acta Anaesthesiol Scand 1986;30:571-573 19. Inoue K, eI-BanayosyA, Stolarski L, et al: Vecuronium induced bradycardia following induction of anaesthesia with etomidate or thiopentone, with or without fentanyl. Br J Anaesth 1988;60:10-17 20. Doenicke A, Lorenz W, Hoernecke R, et al: Histamine release after injection of benzodiazepines and of etomidate. A problem associated with the solvent propylene glycol. Ann Fr Anesth Reanim 1993;12:166-168CORRESPONDENCE
A 3-WEEK-OLD WITH STRIDOR To the Editor:--Stfidor in the newborn is a serious entity. Newborn airways are smaller in caliber and have immature supporting cartilage. 1 The causes of stridor can be intrinsic or extrinsic to the airway. In either case, emergency interventions may be necessary when evaluating such newborns. The following is a presentation of intermittent stridor in a 3-week-old child. On July 31, 1994 a 3-week old white girl presented to a children's emergency department. The parents stated that the child was wheezing and choking when feeding the past 2 days. They elaborated that their baby girl would gasp for air, turn red in the
face, and have bluish coloration around the lips when eating. These episodes would last about 10 to 15 seconds and resolve without sequelae. On presentation the child turned red and appeared to have a choking episode prior to the physical examination. This lasted about 5 seconds. The oral mucosa at first appeared normal, but then a 3- to 4-cm thin grayish tissue arose from the oral pharynx. This tissue disappeared into the pharynx. The mouth was reexamined, and the tissue was again visualized. A tongue blade was pressed lightly against the tissue in the hope of possibly removing the tissue, but there was resistance. A finger sweep was not attempted. A portable bronchoscopy revealed a mass based at the left tonsillar fossa. On day 2 of hospitalization, a barium swallow revealed a left esophageal mass which moved into the nasopharynx and down the esophagus. The child was taken to the operating room, and an oropharyngeal mass pedicled at the left tonsillar fossa was removed. The child was taking by mouth the next day and was discharged 2 days after surgery. The pathology report revealed a mass 2.5 cm in length with a .8-cm diameter, consistent with a hairy polyp. Many lay people interchange the terms "stridor" and "wheezing." Stridor is an audible manifestation of airway obstruction caused by turbulent air flow through a narrowed segment of airway. 2 The anterior nares to the larger bronchi are the narrowest airway areas that cause stridor. 3 Wheezing is also an audible manifestation of turbulent air flow through a narrowed airway. However, wheezing results from narrowed intrathoracic lower airways (small bronchi and bronchioles). 3 Stridor in the newborn, whether reported by the parents or heard on physical exam, is a serious entity because of the small caliber of the newborn airway and its supporting cartilage. This less developed cartilage allows the more flaccid airway to easily twist and collapse with changes in an infant's head position.l The causes of newborn stridor arc numerous and can be either intrinsic or extrinsic to the airway. Congenital anomalies, especially laryngeal anomalies, account for the majority of intrinsic causes. Laryngomalacia is the most common, 3 followed by vocal cord paralysis. 1 Extrinsic causes of stridor are much less common and usually involve aberrant segments of the embryonic aortic arch. 1 In severe cases of extrinsic obstruction, the infant may assume an opisthotonic posture to assist breathing. 4 The workup for any infant who presents with stridor includes the complete history, physical examination, radiographic tests and other ancillary tests, and consultation for definitive treatment. If at any time the infant is in respiratory distress, emergency interventions are necessary. A thorough history from the parents or caretaker is very important. This history should include the time when the stridor began along with any associated symptoms. Always ask if the stridor is temporally related to feeding, because this is usually associated with tracheoesophageal fistula, cleft larynx, vascular ring, congenital anomalies, or neurological disorders. 3 A prenatal and birth history should be obtained, with particular attention to any fetal distress or injury during delivery. The physical examination must be complete. The nasal and oral pharynx should be examined for patency and obstructing lesions. With all newborns, a feeding tube should easily pass through both nares to exclude choanal atresia. Any masses or bruits of the neck should be noted along with any cardiac abnormalities. The pulmonary exam should identify wheezing, retractions, or grunting. The quality of the stridor is important because this may identify the location of the abnormality. A snoring or snorting noise usually implies obstruction at the level of the nasopharynx, while gurgling implies a pharyngeal abnormality. Gurgling can also be the result of a blocked esophageal lumen. Inspiratory high-pitched stridor is usually caused by laryngeal or subglottic obstruction. Tracheal abnormalities result in inspiratory and expiratory stridor.
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 15, Number 1 • January 1997
In the ED, the patient denied any other complaint except for neck pain. She was otherwise healthy with an insignificant medical history. She denied the use of alcohol or street drugs. On physical examination, the patient was an alert, cooperative girl who was in obvious discomfort. Head, ear, eye, nose, and throat examination findings were unremarkable. The patient had severe midline cervical pain. Lungs were clear to auscultation, heart was regular with $1S2, and the patient had no chest wall bruising or pain to palpitation. Her abdominal was soft and nontender. Extremity examination found no bruising or tenderness, and the patient was able to move all extremities with normal strength. Knee jerks were two plus and equal, and She had normal sensation throughout. Cervical films and computed tomography showed a nondisplaced fracture of the C6 lamina which extended through the pedicle and the facet. There was also a vertical fracture through the body of C6 and evidence of ligamentous injury between C5 and C6. The patient was admitted to the trauma service and on day 2 a halo vest was placed under local anesthesia by neurosurgery. She was discharged from the hospital 4 days later. After wearing the halo vest for 10 weeks the halo was removed and the patient was reimaged, with flexion and extension films showing slight angulation and kyphotic deformity with interspinous laxity remaining between C5 and C6. After 2 weeks of a cervical collar and mild range of motion exercises, She had repeat flexion and extension films done under fluoroscopy. This study showed that the angulation and laxity had increased. Although the patient remained neurologically intact, she was considered to be at high risk for a serious neurological injury, and 3 months after the original injury she underwent an anterior cervical microdiscectomy at C5-C6 with an autograft fusion and plating. Her recovery has since been unremarkable. This case illustrates yet another way to incur a cervical injury. A literature review found no reported cases of injury caused by human body surfing. This could be secondary to lack of prior occurrence or, more likely, lack of documentation and reporting. In the past few years more emergency medicine physicians have become more involved in the planning and provision of medical care to spectators at large events. Fortunately, most injuries that occur at such events are minor and require minimal medical attention. 1 However, as this case demonstrates, the possibility for significant spectator morbidity from injury is quite real, and qualified medical personnel must be readily available to provide emergency care. By definition, injury occurs whenever energy is transmitted above an individual's tolerance. 2 When providing medical care to spectators, it is important to anticipate what injuries are likely to occur and to determine if they are preventable. This is done by close examination of the venue, the environment, the crowd demographics, and any anticipated special modifiers (such as heavy alcohol use or inclement weather). 2 In this case, the environment was a rock concert, a venue where spectators often consume excessive amounts of alcohol or illicit drugs that may impair their coordination and lessen their social inhibitions, leading to an increased risk of injury. Research has shown that the percentage of spectators that seek medical care at rock concerts is higher than at other venues. 3 Here, injury occurred secondary to the transfer of kinetic energy from the human body surfer to our patient, leading to her fracture. Fortunately, she sought immediate help and was lucky that she did not incur a secondary injury such as paralysis during her transfer to further medical care. Upon review of this case, we hope that physicians and other personnel involved in event management would appreciate the potential for serious injury from human body surfing and develop policies to discourage its practice. We would also hope that physicians who are in charge of event safety would educate event
personnel in the importance of early spinal immobilization of spectators with suspected cervical injuries. JEANNETTEM. WOLFE,MD
Department of Emergency Medicine RICHARDANDERSON,MD
Neurosurgery Baystate Medical Center Springfield, MA
References 1. SandersAB, Criss E, Steckl P, et al: An analysis of medical care at mass gatherings. Ann Emerg Med 1986;15:515-519 2. Martinez R: Injury assessment and control. In Callaham M: Current practices in Emergency Medicine (ed 2). Philadelphia, PA, B. C. Decker, 1991, pp 87-90 3. DeLorenzo RA, Gray BA, Bennett P, et al: Effect of crowd size on patient volume at a large, multipurpose, indoor stadium. J Emerg Med 1989;7:379-384
ETOMIDATE USE DURING EMERGENCYINTUBATION OF TRAUMAPATIENTS To the Editor:--Etomidate, an ultrashort-acting, nonbarbiturate hypnotic agent, has been used as an anesthetic induction agent for many years.l,2 Although etomidate has been suggested as a sedative for emergent endotracheal intubation, there are no previous reports regarding its use in the trauma patient in the emergency department (ED) setting. We prospectively evaluated the safety and efficacy of etomidate as a sedative agent for endotracheal intubation in a case series of trauma patients presenting to a level I trauma center, community teaching hospital ED. Twenty patients (13 men and 7 women) with average age of 47 _+ 26 years (range 15 to 83 years) and average weight of 71 -+ 17 kg (range 50 to 102 kg) were studied. Excluded were patients 10 years of age or younger, those with hypersensitivity to etomidate, and those with history of seizure or pregnancy. After intravenous (IV) cannulation, etomidate (Amidate; Abbott Laboratories, North Chicago, IL) was administered in an IV dose of 0.3 mg/kg of estimated body weight. A second dose was administered in 6 (30%) cases to achieve adequate sedation. Sedation was considered adequate in all patients, with onset of deep sleep in less than 30 seconds and duration of sleep less than 5 minutes. Morphine sulfate and midazolam were administered in one case to further prolong sedation. In contrast, muscle relaxation was adequate in 14 (70%), requiring the use of paralytic agents in 6 (30%), vecuronium in 4, and succinylcholine in 2 cases, primarily because of bruxism. Patients were intubated by either the nasal or oral route at the discretion of the emergency physician. The intubation method was nasotracheal in 9 (45%), orotracheal in 10 (50%), and not documented in one case. Although the time to successful intubation was not recorded, the number of intubation attempts was one in 7 patients (36.8%), 2 in 9 patients (47.4%), 3 in 2 patients (10.5%); and 4 in 1 patient (5.3%) (not documented in one). Indications for intubation included closed head injury and agitation in 9, respiratory failure and acidosis in 5, agitation requiring sedation for computerized tomography in 5, inhalation injury in 2, pulmonary contusion in 2, and flail chest in 1. Minimal hemodynamic effects were noted. The initial pulse (116.2 _+ 20.2 beats/rain) and repeat pulse within l0 minutes (113.5 _+ 25.3 beats/min) were not significantly different (P = 0.96, two-tailed t test). Similarly, the initial blood pressure (141.2 _+ 29.4 mm Hg) and repeat blood pressure within 10 minutes (139.3 _+ 28.9 mm Hg) were not significantly different (P = 0.98, two-tailed t test).
CORRESPONDENCE
There were no cases of apnea; however, mild respiratory depression occurred in 8 (40%) requiring ventilatory assistance. Nausea and vomiting occurred in 1 case (5%). Myoclonic activity was absent in 6 cases (30%), and was mild in 12 (60%), moderate in 1 (5%), and severe in 1 (5%). In 5 cases (25%) significant orofacial myoclonus (bruxism) prevented orotracheal intubation. Pain at the injection site occurred in 3 cases (15%). As experts in airway management of the trauma victim, emergency physicians should be aware of the various advantages and disadvantages of etomidate as an alternative sedative agent. Several attributes would appear to make etomidate ideal for the trauma patient, including its high efficacy, rapid onset, short duration of action, cerebroprotective effects, and minimal respiratory or hemodynamic effects. Following a single 0.3 mg/kg IV dose, etomidate induces sleep with onset of 30 to 60 seconds and duration of approximately 5 to 10 minutes. 1 The short duration of action can be advantageous in cases of head injury or intoxication that require repeat neurologic examination. Because of this short duration of action, however, a continuous infusion or additional sedative agent should be administered if the patient is to be paralyzed. Etomidate could be particularly advantageous in the head injured patient, since it has been reported to have cerebroprotective effects similar to barbiturates in that it decreases intracranial pressure, regional cerebral blood flow, and cerebral metabolic rate for oxygen. 3,4 In contrast to barbiturates, etomidate does not diminish arterial blood pressure or cerebral perfusion pressure. 3,4 Persistence of spontaneous respirations could be a major advantage of a sedative agent for intubation, especially in cases of airway difficulty or failed intubation attempts. Etomidate causes less respiratory depression than other agents, such as thiopental. 2 Hypoventilation has been reported in up to 25% of cases, and transient (resolving within 2 minutes) apnea (up to 90 seconds duration) reported in 12% to 16% of cases. 2,5 Choi et al6 noted a CO2 independent stimulation of ventilation with etomidate, suggesting its utility in cases in which maintenance of spontaneous respiration is desired. Etomidate has been reported to have minimal cardiovascular effects even in the setting of hemodynamic instability7 and compares favorably to midazolam, 8 propofol, and thiopentone9 with regard to hemodynamic safety. Although etomidate has been noted to result in variable changes in systemic vascular resistance, cardiac output, and stroke volume,9,~°these alterations are typically within acceptable limits, and the most favorable advantage is decreased myocardial oxygen consumption. 10Although all but one of our patients were normotensive, etomidate did not significantly alter pulse or blood pressure in any patient in our series. Further study of etomidate in the hypotensive trauma patient should be considered. Etomidate has several side effects of which the emergency physician must be aware; the most important disadvantages include pain on injection, myoclonus, and adrenal suppression. The incidence of pain on injection of etomidate has varied from 4% to 70%. 2 This effect is likely related to the solvent, 35% propylene glycol, which is less irritating than previous preparations. Pain on injection is more common in small peripheral veins, and can be minimized by further dilution or premedication with fentanyl or diazepam. 2 Although phlebitis can occur in up to 23% of patients, lj this was not noted in any of our patients. Spontaneous movements, such as tremor, dystonic posturing, and especially, myoclonia, following etomidate have previously been noted in 20% to 87% of patients 2,6,12and may be precipitated by physical contact. 5 The presence of myoclonic movements varies with the solvent (whether propylene glycol, polyethylene glycol, or aqueous ethanol mixture) 1 and can be minimized by premedication with small doses of narcotic (such as fentanyl) or benzodiazepine
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(such as diazepam) agents. 5 The mechanism of myoclonia may be related to subcortical disinhibition.1 Although initial reports noted the absence of epileptiform activity, a recent study by Reddy et all2 noted electroencephalographic spikes in 22% of cases with myoclonia and recommend the cautious use of etomidate in patients with seizure history. As an imidazole derivative, etomidate is a potent inhibitor of adrenal corticosteroid production, 13 and continuous infusion has been related to increased mortality. 14 Single induction doses of etomidate can result in depressed levels of cortisol and elevated levels of adrenocorticotropic hormone. 15 This adrenal suppression has likely been the most important factor recently limiting etomidate's popularity as an induction agent. Several other minor disadvantages have previously been noted, including nausea and vomiting, minor hemolysis, cardiovascular responses to intubation, bradycardia, and possibly, histamine release. Nausea and vomiting are not uncommon after etomidate administration and are present in up to 50% of patients receiving multiple doses. 1 Detectable levels of hemolysis have been noted in animal studies, 16 thought to be related to the high osmolality of propylene glycol; however, this has not been demonstrated to be of clinical significance in human trials. 1,2 The increases in heart rate and arterial pressure occurring with laryngeal stimulation during intubation are inhibited less with etomidate alone than thiopentone or propofol, j7 Asystole or bradycardia associated with use of etomidate and suxamethonium or vecuronium have been rarely reported, 18,19 and neither were noted in this series. Although etomidate has previously been reported to not result in histamine release, a recent study noted a limited degree of histamine release in 20% of healthy volunteers, resulting in pain, but without hypotension, tachycardia, or allergic reaction. 2° Again, this side effect is thought to be related to the propylene glycol solvem: This case series demonstrates that etomidate can be used safely in the ED trauma patient; although side effects were common, they were rarely clinically significant to influence patient outcome. This descriptive study, however, was limited by the lack of invasive hemodynamic monitoring, assessment of adrenal function, or blinded comparison to other induction agents. Because several side effects, such as pain on injection, myoclonus, and the hemodynamic response to intubation, may be minimized with premedication with fentanyl and/or diazepam, future studies should consider assessing the safety of etomidate with premedication. Future investigations should also compare the relative safety and efficacy of various sedative agents, such as etomidate, midazolam, fentanyl, propofol, or methohexital, in the trauma setting. Etomidate may be a safe and effective sedative agent for intubation of the ED trauma patient. Etomidate's rapid onset, short duration, minimal respiratory depression, cerebroprotective effects, and lack of cardiovascular response are unique advantages for the head injured or hypotensive trauma victim. The disadvantages of etomidate, including myoclonus (the most frequent side effect), pain on injection, the occasional need for sedative premedication or concomitant paralytic agent use, and adrenal suppression, however, may limit its widespread use. Etomidate is not the ideal premedication for intubation, but remains a reasonable alternative, especially in the setting of trauma. MICHAELC. PLEWA,MD RANDALLKING, MD DAVID JOHNSON,MD DOUGLASADAMS,MD St. Vincent Medical Center The Toledo Hospital Emergency Residency Program Mmo ENGOREN,MD Department of Anesthesia St. Vincent Medical Center Toledo, OH
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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 15, Number 1 • January 1997
References 1. GiesedL, Stanley-I'H: Etomidate:Anewintravenousanesthetic induction agent. Pharmacotherapy 1983;3:251-258 2. Gooding JM, Corssen G: Etomidate: An ultrashort-acting nonbarbiturate agent for anesthesia induction. Anesth Analg 1976;55:286269 3. Cold GE, Eskasen V, Eriksen H, et al: CBF and CMRO2 during continuous etomidate infusion supplemented with N20 and fentanyl in patients with supratentorial cerebral tumour: A dose-response study. Acta Anesthesiol Scand 1985;29:490-494 4. Renou AM, Vernhiet J, Macrez P, et al: Cerebral blood flow and metabolism during etomidate anesthesia in man. Br J Anaesth 1978;50:1047-1057 5. Morgan M, Lumley J, Whitwam J: Etomidate a new watersoluble nonbarbiturate intravenous induction agent Lancet 1975;1: 955-956 6. Choi SD, Spaulding BC, Gross JB, et al: Comparison of the ventilatory effects of etomidate and methohexital. Anesthesiology 1985;62:442-447 7. Colvin MP, Savege -i'M, Newland PE, et al: Cardiorespiratory changes following induction of anesthesia with etomidate in patients with cardiac disease. Br J Anaesth 1979;51:551-556 8. MacGillivray RG, Rocke DA, Mahomedy AE: Midazolam for induction of anaesthesia in patients with limited cardiac reserves. A comparison with etomidate. S Afr Med J 1988;73:101-103 9. Gauss A, Heinrich H, Wilder-Smith OH: Echocardiographic assessment of the haemodynamic effects of propofol: a comparison with etomidate and thiopentone. Anaesthesia 1991;46:99-105 10. Kettler D, Sonntag H, Donath U, et al: Hemodynamics, myocardial mechanics, oxygen requirements and oxygen consumption of the human heart during etomidate induction into anaesthesia. Anaesthesist 1974;23:116-121 11. Zacharias M, Clarke RS, Dundee JW, et al: Venous sequelae following etomidate. Br J Anaesth 1979;51:779-783 12. Reddy RV, Moorthy SS, Dierdorf SF, et al: Excitatory effects and electroencephalographic correlation of etomidate, thiopental, methohexital, and propofol. Anesth Analg 1993;77:1008-1011 13. Preziosi P, Vacca M: Adrenocortical suppression and other endocrine effects of etomidate. Life ScJ 1988;42:477-489 14. Ledingham IM, Watt I: Influence of sedation on mortality in critically ill, multiple trauma patients. Lancet 1983; 1:1270 15. AIIolio B, Dorr H, Stuttmannn R, et al: Effect of a single bolus of etomidate upon eight major corticosteroid hormones and plasma ACTH. Clin Endocrinol 1985;22:281-286 16. NebauerAE, Doenicke A, Hoernecke R, et al: Does etomidate cause haemolysis? Br J Anaesth 1992;69:58-60 17. Harris CE, MurrayAM, Anderson JM, et al: Effects of thiopentone, etomidate and propofol on the haemodynamic response to tracheal intubation. Anaesthesia 1988;43(S):32-36 (suppl) 18. Inoue K, Reichelt W: Asystole and bradycardia in adult patients after a single dose of suxamethonium. Acta Anaesthesiol Scand 1986;30:571-573 19. Inoue K, eI-BanayosyA, Stolarski L, et al: Vecuronium induced bradycardia following induction of anaesthesia with etomidate or thiopentone, with or without fentanyl. Br J Anaesth 1988;60:10-17 20. Doenicke A, Lorenz W, Hoernecke R, et al: Histamine release after injection of benzodiazepines and of etomidate. A problem associated with the solvent propylene glycol. Ann Fr Anesth Reanim 1993;12:166-168CORRESPONDENCE
A 3-WEEK-OLD WITH STRIDOR To the Editor:--Stfidor in the newborn is a serious entity. Newborn airways are smaller in caliber and have immature supporting cartilage. 1 The causes of stridor can be intrinsic or extrinsic to the airway. In either case, emergency interventions may be necessary when evaluating such newborns. The following is a presentation of intermittent stridor in a 3-week-old child. On July 31, 1994 a 3-week old white girl presented to a children's emergency department. The parents stated that the child was wheezing and choking when feeding the past 2 days. They elaborated that their baby girl would gasp for air, turn red in the
face, and have bluish coloration around the lips when eating. These episodes would last about 10 to 15 seconds and resolve without sequelae. On presentation the child turned red and appeared to have a choking episode prior to the physical examination. This lasted about 5 seconds. The oral mucosa at first appeared normal, but then a 3- to 4-cm thin grayish tissue arose from the oral pharynx. This tissue disappeared into the pharynx. The mouth was reexamined, and the tissue was again visualized. A tongue blade was pressed lightly against the tissue in the hope of possibly removing the tissue, but there was resistance. A finger sweep was not attempted. A portable bronchoscopy revealed a mass based at the left tonsillar fossa. On day 2 of hospitalization, a barium swallow revealed a left esophageal mass which moved into the nasopharynx and down the esophagus. The child was taken to the operating room, and an oropharyngeal mass pedicled at the left tonsillar fossa was removed. The child was taking by mouth the next day and was discharged 2 days after surgery. The pathology report revealed a mass 2.5 cm in length with a .8-cm diameter, consistent with a hairy polyp. Many lay people interchange the terms "stridor" and "wheezing." Stridor is an audible manifestation of airway obstruction caused by turbulent air flow through a narrowed segment of airway. 2 The anterior nares to the larger bronchi are the narrowest airway areas that cause stridor. 3 Wheezing is also an audible manifestation of turbulent air flow through a narrowed airway. However, wheezing results from narrowed intrathoracic lower airways (small bronchi and bronchioles). 3 Stridor in the newborn, whether reported by the parents or heard on physical exam, is a serious entity because of the small caliber of the newborn airway and its supporting cartilage. This less developed cartilage allows the more flaccid airway to easily twist and collapse with changes in an infant's head position.l The causes of newborn stridor arc numerous and can be either intrinsic or extrinsic to the airway. Congenital anomalies, especially laryngeal anomalies, account for the majority of intrinsic causes. Laryngomalacia is the most common, 3 followed by vocal cord paralysis. 1 Extrinsic causes of stridor are much less common and usually involve aberrant segments of the embryonic aortic arch. 1 In severe cases of extrinsic obstruction, the infant may assume an opisthotonic posture to assist breathing. 4 The workup for any infant who presents with stridor includes the complete history, physical examination, radiographic tests and other ancillary tests, and consultation for definitive treatment. If at any time the infant is in respiratory distress, emergency interventions are necessary. A thorough history from the parents or caretaker is very important. This history should include the time when the stridor began along with any associated symptoms. Always ask if the stridor is temporally related to feeding, because this is usually associated with tracheoesophageal fistula, cleft larynx, vascular ring, congenital anomalies, or neurological disorders. 3 A prenatal and birth history should be obtained, with particular attention to any fetal distress or injury during delivery. The physical examination must be complete. The nasal and oral pharynx should be examined for patency and obstructing lesions. With all newborns, a feeding tube should easily pass through both nares to exclude choanal atresia. Any masses or bruits of the neck should be noted along with any cardiac abnormalities. The pulmonary exam should identify wheezing, retractions, or grunting. The quality of the stridor is important because this may identify the location of the abnormality. A snoring or snorting noise usually implies obstruction at the level of the nasopharynx, while gurgling implies a pharyngeal abnormality. Gurgling can also be the result of a blocked esophageal lumen. Inspiratory high-pitched stridor is usually caused by laryngeal or subglottic obstruction. Tracheal abnormalities result in inspiratory and expiratory stridor.