Authors: Colin G. Kaide, MD, FACEP, FAAEM, Assistant Professor of Emergency Medicine, Department of Emergency Medicine, The Ohio State University, Columbus; Jason C. Hollingsworth, MD, Emergency Medical Staff Physician, Community Hospital of Indianapolis, Indianapolis, IN.
Peer Reviewer: Perry W. Stafford, MD, FACS, FAAP, FCCM, Chief of Trauma and Surgical Critical Care, Associate Professor of Pediatric Surgery, Department of Pediatric General and Thoracic Surgery, Children’s Hospital of Philadelphia, PA.
In critical situations, the management of the airway is paramount. Virtually all algorithms begin with attention to and protection of the airway. In a patient with a traumatic injury, airway management assumes an essential role to stabilization and survival of the patient, but often presents unique challenges not inherent in other types of patients. The skill of the intubator is put to the ultimate test in the trauma patient, whose airway often is compromised by multiple complicating factors, including hemodynamic instability from multiorgan injury, cervical spine fractures, and direct trauma to the airway.
The process of airway management has evolved considerably to include sophisticated techniques and pharmacologic adjuncts. This two-part article will review the concepts of airway management in the trauma patient, the technique of rapid sequence intubation (RSI), and adjuncts to assist with the management of the difficult or failed airway.—The Editor
The Trauma Airway
The airway in the trauma patient can present many challenges, even for the experienced clinician. These factors can occur individually or together to complicate the care of the trauma patient. (See Table 1.)
Preexisting Difficult Airway. As everyone who works in the field of emergency medicine knows, Murphy’s Law virtually defines our existence—if something can go wrong, it will. Inevitably, a neckless, 375-pound man with advanced ankylosing spondylitis who is driving a compact car will have an unfortunate encounter with a tractor-trailer at 3 a.m. and be transported to your facility as a Level 1 trauma. As you prepare to perform the intubation, you realize that multiple previous airway manipulations have significantly altered the anatomy in the posterior pharynx.
Patients will bring to the trauma room preexisting anatomical variations that can complicate endotracheal intubation (ETI). In any patient who is not critical enough to require an immediate airway intervention, it is imperative to conduct as thorough an evaluation as possible before considering the use of a paralytic agent. The ultimate rule of airway management is to have a thoroughly prepared plan to deal with the patient’s airway, and never paralyze a patient you suspect will be extremely difficult or impossible to intubate. Further, the ability to adequately mask ventilate should be taken into consideration when deciding upon the type and method of airway intervention. Characteristics of patients who may be difficult to mask ventilate or intubate are discussed in detail in the "Difficult Airway" section.1-5
Trauma Immobilization. The physical process of trauma immobilization with a cervical collar and backboard significantly can limit access to the airway and the anterior neck. A properly placed collar inhibits opening of the mouth and, by intention, prevents repositioning of the head and neck. The collar further can obstruct visualization of the anterior neck and potentially lead one to miss laryngeal trauma or distortion of airway anatomy.
It is essential, therefore, to remove the cervical collar and utilize inline stabilization by a dedicated individual during attempts at intubation.
Cervical Spine Considerations. As in virtually all trauma cases, careful consideration must be given to potential injury to the cervical spine and spinal cord. This stated, however, airway management still remains at the top of the resuscitation algorithm. Failure to adequately control an airway due to theoretical concerns of cervical injury violates this standard. The emergency physician charged with the task of securing an airway must employ the best possible available techniques to maintain cervical stability and utilize refined intubation skills while not sacrificing the patient for protection of his spinal cord.
Mechanical Distortion of the Airway or of Contiguous Structures. Direct trauma to the face, larynx, or thorax can alter the normal anatomic relationships of the airway structures and can increase the difficulty of intubation.
Indications for Invasive Airway Intervention
The decision to intubate a patient in the emergency department (ED) can be the most significant and definitive step in the care of the trauma patient. The primary goals of intubation are to improve gas exchange, relieve respiratory distress by decreasing the work of breathing, and protect against aspiration. Secondary goals range from intentional hyperventilation to core rewarming.
Experienced clinicians will be familiar with the intubation criteria listed in Table 2.6
Respiratory Failure. Respiratory failure occurs when a patient is unable to oxygenate or ventilate adequately to meet his/her physiologic needs. The decision to intervene is based on abnormalities found on blood gas analysis and, often more importantly, the clinician’s observation of the patient in respiratory distress.
Oxygenation failure often is defined as the inability to maintain a PaO2 of 60 mmHg on an FiO2 greater than 40%.
Ventilation Failure. The best indicator of hypoventilation is an abnormal pH. A pH less than 7.3 resulting from hypoventilation should prompt intervention. Intervention at a higher pH may be necessary if the patient appears fatigued or has significant comorbidity. Chronic compensated elevation in PaCO2 does not require support. When making a decision based on abnormal blood gas analysis, carbon dioxide retention with a PaCO2 greater than 55 (with previously normal PaCO2) or rise in PaCO2 by 10 acutely in chronic obstructive pulmonary disease (COPD) is an indication for intervention.
Respiratory Muscle Fatigue. The increased work of breathing seen with decreases in lung compliance (e.g., pulmonary contusions, pulmonary edema, consolidation, pneumothorax, or atelectasis) and increases in airway resistance (e.g., bronchospasm or excessive airway secretions) can contribute to early fatigue of respiratory muscles. This can be seen clinically by agitation, diaphoresis, nasal flaring, the use of accessory muscles, and abdominal (seesaw motion) breathing. (See Table 3.)
Intentional Hyperventilation. Although this technique traditionally has been used to attenuate intracranial hypertension by inducing alkalosis to cause cerebral vasoconstriction, it recently has been shown to be appropriate in only limited situations.
Cardiovascular Support. Under normal physiologic conditions, energy expenditure for breathing is low. During states of physiologic stress, such as cardiogenic, hypovolemic, or septic shock, the oxygen demand of the pulmonary mechanism rises significantly. Early intervention with ETI in patients with significant hemodynamic compromise can improve oxygenation to the ischemic tissue and lessen myocardial workload.
Aspiration Protection. When a patient appears obtunded or lacks a gag reflex, ETI becomes vital to decrease the risk of aspiration and its attendant complications.
Mechanical Obstruction. Distortion of the airway can occur in a variety of traumatic injuries. In cases of impending airway obstruction or when obstruction already has occurred, the decision to intervene is a foregone conclusion.
With more subtle injury patterns, an airway may be intact at the time of initial examination, but the risk for potential obstruction can be very high. This situation is typified in the case of burns to the upper airway, where developing edema has the potential to completely obstruct the larynx and other posterior pharyngeal structures. Other examples include direct laryngeal trauma and penetrating wounds to the neck. Hematomas from injury to the carotid artery can expand and distort the airway beyond recognition.
Core Rewarming. A patient can develop substantial hypothermia as the result of a traumatic injury occurring during cold weather or secondary to submersion in cold water. As core temperature drops, many physiologic changes occur, resulting in coagulopathy, hypotension, and an overall decrease in survival. The principles of core rewarming place significant value on the delivery of heated, humidified oxygen to the lungs as a major method of adding heat to the body.7 This is best accomplished via the use of an endotracheal (ET) tube. Humidified oxygen is heated to 45°C (113°F) and delivered continuously. A rise in core temperature of 1-2.5°C (1.8-4.3°F) per hour can be expected. Contrary to widely held belief, intubation of a hypothermic patient never has precipitated the onset of a lethal arrhythmia.
Rapid Sequence Intubation (RSI)
Historical Perspective and Overview. Prior to the emphasis on the development of controlled airway management strategies, airway management outside of the operating room (OR) was, to say the least, practiced with a particular lack of sophistication. Awake, non-pharmacologically assisted, oral intubation was common. Nasotracheal intubation also was utilized as a primary method of intubation or as a rescue technique. In the field, esophageal obturator airways were the standard modality.
If sedation became necessary, serial sedation frequently was utlilized. This method used incremental doses of an opiate such as morphine, along with a benzodiazepine like diazepam or lorazepam, to "soften the patient up a little." The drugs were given until the patient was sleepy enough to allow the introduction of a laryngoscope into the mouth. The problem resulted when the epiglottis or larynx was stimulated, causing rapid central nervous system (CNS) arousal and vomiting. This method is distinctly different from the delivery of rapid-push induction agents used in RSI.
Meanwhile, in the OR, anesthesiologists would take a carefully prepared patient, keep him or her from eating or drinking anything (NPO) for hours, evaluate the airway for a potentially difficult intubation, then deliver a cocktail of carefully measured drugs, which rapidly would induce unconsciousness and muscle relaxation. The completely defenseless patient could be intubated without resistance. If a difficulty arose, backup readily was available, and ultimately, the anesthesiologist had the option of canceling the case and trying another approach to intubation on another day.
In the ED, canceling the case is rarely, if ever, an option. Further, every ED/trauma patient seemingly just finished a dinner consisting of beer and a pizza with everything. He or she then often has the nerve to violate the law of inertia and go partially through the windshield just before becoming entrapped in a car that flipped upside down in three feet of water. So much for NPO, a controlled environment, and an ASA class I (healthy) patient!
This type of setting demands a better approach to the patient in need of emergent definitive airway management.
When the technique of RSI was assimilated into emergency medicine practice from the OR, the word "induction" was replaced with "intubation," thereby focusing the procedure on the establishment of an airway rather than the induction of anesthesia for an operative case. The American College of Emergency Physicians endorses RSI as the standard of practice for airway management.8 Nasotracheal intubation (NTI), which once was the primary method of intubation in the ED, largely has been replaced by RSI. A national survey of emergency medicine residencies showed an average of only 2.8 NTIs during a three-year period by emergency medicine residents.9 RSI is considered routine in most EDs; it is utilized in up to 84% of all ED intubations, with success rates reported at 97%.8,10-14
The role of RSI in trauma has been evolving and it currently is considered the method of choice for emergent airway control in the traumatized patient unless specific contraindications are present.1,4,15
RSI is a method of quickly obtaining optimal intubating conditions via the delivery of an induction agent (to induce unconsciousness) followed in rapid succession by a paralytic agent. The goal of RSI is to facilitate the passage of an ET tube into the trachea quickly and efficiently. RSI eliminates or reduces the need for ventilating the patient during the procedure unless oxygenation is impaired and the bag-valve mask must be used to maintain adequate saturation. This technique should minimize the chances of aspiration of stomach contents during the intubation.
Various methods of teaching RSI for the emergency clinician have been developed, but the use of the "Seven P’s of RSI," as described by Walls and Murphy,1 is the one that is the best developed. The algorithm described below is a modification of the above approach specifically adapted to the ED and includes eight P’s—plan B, prepare, preoxygenate, pretreat, put down, paralyze, pass the tube, prove placement.
Plan B. The first P in this series refers to the predetermined plan for dealing with a difficult or failed orotracheal intubation. It can be very disconcerting (at the very least) to discover a heretofore unknown airway anomaly in what appears to be an easy intubation. A recent article published in the anaesthesia literature found an unanticipated failed intubation occurred in 0.4% of the cases (44 of 11,621 patients).16 Published reports of the ED airway management experience at several teaching hospitals found that rate of difficult intubation was less than 5%.11,12 A complicated situation rapidly can become a disaster if no pre-implemented plan exists to deal with an anomaly. To avoid potential disasters, it is recommended that all EDs have assembled an emergency airway cart for use in trauma patients. It is present at all intubations. For a list of the items in the ultimate, complete, difficult airway cart, see Appendix 1 in The Manual of Emergency Airway Management.17,18 The minimum required equipment utilized by the author as part of a difficult airway cart is listed in Table 4.
Prepare. Taking the time to organize and inventory the working environment directly prior to the actual intubation assures that everything needed to perform the task will be available and in good working order. Not only does this preparation provide peace of mind and decrease stress levels, it can be a time- and life-saving investment.
Preparation includes the following:
• Thoroughly evaluate the patient for a potentially difficult intubation and for difficulty with bag-valve mask ventilation;
• Remove the patient’s dentures;
• Bring the difficult airway cart to the bedside;
• Have the chosen laryngoscope blades ready (two sizes of Macintosh blades, two Miller blades);
• Check the light on the laryngoscope blades;
• Verify the integrity of the balloon on the ET tube; and
• Have suction ready at the bedside. When preparing suction, it is useful to have two suction options available. A standard Yankaur tip works well for loose secretions but does not adequately aspirate such common items as steak, pizza, mushrooms, and other assorted food morsels often found in the posterior pharynx of ED patients. It may be useful to cut the tip off of the Yankaur suction with some trauma shears prior to intubating the patient.
• Verify the integrity of your IV access and start a second IV line. A disastrous situation can result when an induction agent is given, and the IV stops working before the paralytic agent can be pushed. Have your chosen means to secure the ET tube ready to implement.
• Have color-change capnography device at bedside.
Preoxygenate. As early as possible in the course of preparation for intubation, the patient should be placed on 100% FiO2. Standard non-rebreather masks only deliver FiO2 at approximately 70%, because they allow the entraining of room air. The goal is to "denitrogenate" the patient’s functional residual capacity and replace it with oxygen. This step can afford the intubator some buffer time during the procedure. The healthy 70 kg adult can take as long as eight minutes to desaturate to 90%, whereas further desaturation from 90% to 0% can take only two minutes. This reflects the characteristic "slippery slope" found in the oxyhemoglobin saturation curve. Heavier patients and small children typically will desaturate faster.19 The typical ED trauma patient requiring intubation may not have a normal cardiopulmonary function and, therefore, may fail to optimally oxygenate. Further, some pulmonary processes that impair oxygenation also will antagonize the effects of prolonged preoxygenation.
In an ideal setting, a patient should breathe 100% oxygen for five minutes prior to attempts at intubation. Most ED oxygen delivery devices (even non-rebreather masks) achieve only a 75% FiO2; the use of a Capnoflo brand bag-valve mask delivers close to 100%. Patients who are stable enough should receive adequate preoxygenation. However, in the ED, some patients with impending apnea will not tolerate a five-minute period of preoxygenation. Instead, eight vital capacity breaths of 100% oxygen may serve the same nitrogen washout function and effectively retard apnea-induced hemoglobin desaturation.20
When studied, most ED oxygen delivery devices cannot deliver adequate oxygen flow to reach an FiO2 even close to 100%. Non-rebreather masks only achieve a 75% FiO2 because they allow the entraining of room air.
When put to the test, some commonly used resuscitation bag-valve mask systems achieved FiO2s that never exceeded 40% (Code Blue and 1st Response). By using a one-way exhalation valve that does not allow for the entrainment of room air, only the Capno-Flow and the Silicone Resuscitator brand bag-valve mask systems were able to deliver greater than 90% oxygen.21
Pretreat. The pretreatment phase of RSI involves the delivery of medications to modify the physiologic response during and after intubation. One mnemonic used to describe the types of medications frequently used in the pretreatment phase is "LOAD," described by Walls, et al, in the Manual of Emergency Airway Management.26 (See Table 5.)
Put Down. The next step involves the induction of anesthesia with a rapid-acting induction agent. This step is performed virtually simultaneously with the next step, administration of a paralytic agent. Owing to the rapid onset of agents such as etomidate and ketamine, complete loss of consciousness can be achieved in 30-45 seconds. The onset of succinylcholine, the paralytic agent of choice, usually is less than 1 minute. When given in rapid succession, the onset of induction and paralysis can be almost simultaneous.
• Induction agents are given simultaneously to, or in rapid succession with, paralytic agents;
• Apply cricoid pressure (Sellick’s maneuver). Do not release until placement is verified; and
• Do not ventilate until patient is intubated or reoxygenation is required.
Induction Agents — Etomidate (Amidate). If only one drug is available to utilize for RSI in ED patients, etomidate is the agent of choice. With its onset of action in one arm-to-brain circulation (30 seconds), a duration of action of only 3-10 minutes, and very little effect on cardiovascular hemodynamics, etomidate is ideally suited for sick, potentially hypotensive or grossly unstable patients. It has gained significant popularity for use in ED RSI.27 (See Table 6a.)
Etomidate is a non-barbiturate sedative-hypnotic agent unrelated to other induction agents. This medication typically is delivered by a single dose of 0.3 mg/kg given by rapid IV push, often simultaneous with, or directly preceding, a paralytic agent. The reported incidence of etomidate-induced myoclonus (up to 30%) is of little significance since all movement will be obliterated with the coadministration of a rapid-acting paralytic drug. Benzodiazepines and opiates have been employed to attenuate etomidate-induced myoclonus. Studies in adults have found that the only consistent effects are achieved with fentanyl at doses of 500 mcg.28 Transient adrenocortical dysfunction lasting 12 hours after a single bolus dose of 0.3 mg/kg of etomidate has been reported. This effect appears to have little clinical relevance since serum cortisol levels remain within normal parameters during the period of dysfunction.29
If etomidate is given without a paralytic agent, most patients will continue to breathe. Although sufficient intubating conditions often are produced with etomidate alone, myoclonus (especially involving the jaw) can interfere with the process, requiring rescue paralysis.
Ketamine (Ketalar). Ketamine, a dissociative anesthetic derived from PCP, is unique in that it is the only agent which provides analgesic, amnestic, and anesthetic (sedative-hypnotic) properties.
Despite an inherent myocardial depressant effect, ketamine stimulates the release of endogenous epinephrine, causing an increase in heart rate, blood pressure, myocardial oxygen consumption, and bronchodilation.
This agent is best suited for hypotensive patients, owing to the cardiovascular support provided by this drug. Current recommendations caution against the use of ketamine in patients with head injury. Although an increase in intracranial pressure is reported, this appears to result from an increase in cerebral blood flow. Increases in brain perfusion potentially can offset the increased ICP, calling into question the clinical relevance of this untoward effect.
The frequency of emergence hallucinations, reported with the use of ketamine in adults may be overstated. The addition of a benzodiazepine may control or minimize any effects that may occur. Further, in the ED patient who will remain ventilated, sedated, and paralyzed, emergence reactions have little significance.
Thiopental (Pentothal). Pentothal is a classic induction agent with very rapid onset and short duration of action. It can lower intracranial pressure. Since it can drop blood pressure significantly with one dose, it is not a good agent for unstable or hypotensive patients. This agent has amnestic and anesthetic properties with paradoxical antianalgesic effects sometimes observed.
Propofol (Diprivan). Propofol can produce potentially severe hypotension in cardiovascularly compromised or blood volume depleted patients. Availability of other choices makes propofol suboptimal for ED RSI in all but the most cardiovascularly stable patients.
Paralyze. This step involves the delivery of a rapid-acting paralytic agent given simultaneously, or in close succession with, an induction agent.
Paralytic agents induce profound muscle relaxation by inhibiting the action of acetylcholine (Ach) at the neuromuscular endplate. These drugs are either depolarizing or non-depolarizing, depending on their interaction with the Ach receptor. (See Table 6b.)
Depolarizing agents such as succinylcholine fit into the Ach receptor and act to initially cause depolarization of the motor endplate and induce contraction, manifesting clinically as fasciculations. Subsequently, the receptor is blocked by the succinylcholine, preventing Ach from binding and producing further contraction. The paralysis lasts until succinylcholine is degraded by acetylcholinesterase.
Non-depolarizing agents such as vecuronium and rocuronium competitively inhibit the Ach receptor, occupying it and then exiting the site. These agents are removed from the neuromuscular junction and broken down in the liver. Their duration and onset of action generally are longer than succinylcholine.
Succinylcholine (Anectine/Quelicin). Succinylcholine is the first line agent for paralysis in RSI. No agent consistently has demonstrated comparable rapidity of onset and short duration of action. In otherwise normal individuals, the use of succinylcholine results in only minimal changes in serum potassium of 0.5-1 mEq/L.19,30 The magnitude of this effect is enhanced in two groups of patients. The first group is those who have had massive tissue destruction such as severe burns, massive trauma, and rhabdomyolysis. Owing to the large surface area of damaged muscle that is capable of leaking potassium, severe, rapidly fatal hyperkalemia can develop. Mortality rates can reach 30%, even with treatment.31
The second group is comprised of patients who develop an up-regulation of acetylcholine receptors. When muscles lose their normal input from motor nerves, the acetylcholine receptors normally located in the motor endplates increase in density and spread over the surface of the muscle. Stimulation from succinylcholine causes an exaggerated release of potassium. Conditions which cause this effect include: CNS injury (CVA); spinal cord injury; neuromuscular diseases with muscle wasting (e.g., muscular dystrophy, etc.); disuse atrophy; and any other cause of chronic denervation. This problem is not seen if the injury is acute, but rather develops after 24-48 hours.
Recent literature suggests that the risk of adverse events when succinylcholine is used on known hyperkalemic patients (K > 5.5mEq/L) is lower than generally believed, with a maximum catastrophic event risk of 7.9%.30 Although this clearly is not a trivial risk, succinylcholine may still be the drug of choice when neuromuscular paralysis is required and suitable alternatives are not available.
Succinylcholine can be stored unrefrigerated for up to three months with only minimal degradation (10% loss) of its paralytic properties.18
Rapacuronium (Rapalon). Rapacuronium is designed as a competitor to succinylcholine in RSI. To date, this agent has the shortest onset of action and duration of any non-depolarizing paralytic. Unfortunately, rapacuronium recently was removed from the market due to a few cases of fatal bronchospasm attributed to its use.
Rocuronium (Zemuron). Rocuronium is slightly slower than succinylcholine in onset of paralysis, but it is faster than most other non-depolarizing agents. A recent meta-analysis reported that although rocuronium was inferior to succinylcholine in providing excellent intubating conditions, it was comparable to succinylcholine in inducing clinically acceptable intubating conditions.32 A recent report looked at rocuronium and found it to be an effective agent for RSI when succinylcholine was contraindicated.33
Pass the Tube. The goal of RSI is to get to this very point with the least possible difficulty. Here, the ET tube is passed through the cords via direct visualization. Prior to and during this process, cricoid pressure is maintained until the ET tube cuff is inflated where appropriate. A complete discussion of basic intubating techniques is beyond the scope of this text, so only a few tips will be presented. Many other techniques, tools, and tricks will be covered in the second part of this article.
One technique that has been described to facilitate direct visualization of a slightly anterior larynx is called "BURP" for "Backwards-Upwards-Rightwards-Pressure."34,35 The assistant applies pressure to the thyroid cartilage, first backward, then upward, and finally rightward. The adult larynx should be displaced about 2 cm to the right. Meanwhile, the intubator should attempt direct visualization of the larynx. Alternatively, the intubator can place his or her hands over the assistant’s hand and direct the pressure while attempting to visualize the glottis. When the cords are seen, pressure can be released by the intubator, and the assistant can continue to hold the optimal position.
A recent article described the use of a simple and effective technique called External Laryngeal Manipulation (ELM). ELM achieves the same backward, upward and rightward airway repositioning as does "BURP," however the pressure is applied by the intubator with his or her right hand.36,37 One of the most common pitfalls is failure to adequately sweep the tongue out of the way. By inserting the blade as far to the right as possible, the intubator more effectively can force the tongue to the left.
The laryngoscope blade can be placed as deep as possible into the oropharynx, allowing it to enter the esophagus. When the blade slowly is withdrawn, the first anatomical structure to be encountered is the larynx, followed by the epiglottis.
Prove Placement. The final step is to verify the correct placement of the ET tube into the trachea. Inadvertent placement of the ET tube into the esophagus is OK. Failure to immediately recognize and remedy this error is not.
After the tube is passed and the cuff is inflated (where appropriate), the chest should be auscultated to listen for breath sounds. The stethoscope need only be placed in three locations to properly auscultate: the left axilla, the right axilla, and over the epigastrum. Absent breath sounds and/or sounds of gastric insufflation means that the wrong tube has been accessed. Unequal breath sounds can imply that the tube is in the right (or sometimes the left) mainstem bronchus.
In all ORs, the standard of care is to use the detection of a CO2 waveform with formal capnography as confirmation of tracheal placement of an ET tube. The standard should be no less in the ED. Although quantitative capnography devices are beginning to appear in EDs, they are not yet commonplace. The use of inexpensive color-change CO2 detectors represents a practical alternative. The detection of CO2, indicated by a purple to yellow color change, is 100% specific for tracheal placement of the ET tube, whereas the failure to detect color change strongly suggests esophageal intubation.38 In cardiac arrest, the lack of lung perfusion can lead to the absence of CO2 and a lack of color change despite the correct placement of the ET tube in the trachea.
The esophageal intubation detector (EID) is a simple device that relies on negative pressure to detect misplacement of an ET tube. This device is a small bulb that is squeezed to evacuate the air and then placed on the end of the ET tube. When the bulb is released, it tries to reexpand. If the ET tube is in the esophagus, the esophageal walls, which are not rigid, will collapse around the end of the ET tube and prevent air from being sucked up the tube and thereby prevent bulb reinflation. In the rigid trachea, however, air can be sucked into the ET tube and the bulb will reinflate in fewer than two seconds. In clinical application, this device generally has been effective in detecting most esophageal intubations when direct visualization was not possible or capnography was not available.39-41 A recent report, however, documented cases in which the detector gave false positive results for tracheal intubation.42
A chest radiograph should be performed as soon as possible to confirm ET tube placement and document position.
Issues in the Pediatric Airway
A detailed discussion of all of the factors affecting the pediatric trauma airway is beyond the scope of this paper. Highlights of the anatomic and physiologic differences between the adult and pediatric patient as they pertain to airway management will be presented.43,44
- Large tongue in children;
- Anterior position of tracheal opening: younger than 2 years of age—high anterior tracheal opening; 2-8 years—transition; older than 8 years—airway is like small adult;
- Large occiput causing neck flexion;
- Large tonsils and adenoids;
- Small cricothyroid membrane—cricothyroidotomy contraindicated;
- Acute angle between epiglottis and laryngeal opening—difficult nasal intubation;
- Narrowest part of the airway is below the vocal cords at the cricoid ring.
- Shorter time to oxygen desaturation. As a result of increased basal metabolism and smaller functional residual capacity, pediatric patients can desaturate in 50% of the time that an adult patient does.
- Need for higher doses (2 mg/kg) of succinylcholine
- High tendency for vagal effects of succinylcholine—must use atropine to prevent bradycardia in patients younger than 10 years of age.
Implications for Airway Management. The above anatomic and physiologic differences have the following implications that warrant adjustment in standard intubating technique:
- Pay attention to adequate preoxygenation and expect rapid desaturation;
- Visualization of the anterior airway may be facilitated with a straight pediatric blade—if the airway is not easily visualized, try withdrawing a deeply placed blade slightly and watch the epiglottis fall into view;
- Do not hyperextend the neck. In a nontrauma patient, a towel roll can be placed behind the shoulders to raise the torso to match the position of the head;
- In-line spine immobilization during orotracheal intubation is recommended;
- Use uncuffed ET tubes until size 6.0 is required. Estimate ET tube size as (age in years + 16)/4;
- Pretreat patients with atropine (0.01 mg/kg with 0.1 mg minimum);
- Use 2 mg/kg succinylcholine;
- Do not perform surgical cricothyroidotomy in patients younger than 10 years of age;
- Use caution and expect difficulty with nasotracheal intubation;
- Do not push the ET tube too deep and intubate the right mainstem bronchus;
- Use Broselow tape to do dosages, diameters, and depths.
Implications for the Hypotensive Patient
In the injured patient who is hypotensive and requires definitive airway management, some modifications to the standard RSI protocol should be given consideration. Although almost all induction agents can produce hypotension and myocardial depression, the two agents etomidate and ketamine have the best hemodynamic profiles.27,45 Etomidate has little effect on cardiac contractility and respiratory rate, making it an excellent choice for induction in the trauma patient. Although etomidate is very cardiostable, in hypotensive or volume depleted patients, doses should be reduced to one half the usual induction dose (from 0.3 mg/kg to 0.15 mg/kg).46
Ketamine releases endogenous catecholamines. In patients who are not catecholamine-depleted by prolonged maximal physiological stress, ketamine will accelerate heart rate and raise blood pressure. In patients with significant head injury, ketamine remains relatively contraindicated due to its possible adverse effects on intracranial pressure.45,46
Barbiturates (thiopental and methohexital), propofol, and large doses of midazolam should not be used in hypotensive patients due to their propensity to significantly lower blood pressure.
Fortunately, the most commonly employed paralytic agent, succinylcholine, does not produce hypotension. Bradycardia, which most often is seen in children who receive succinylcholine, can be abolished with small doses of atropine (0.02mg/kg). If succinylcholine must be redosed in adults, atropine (1-2 mg IV) should be given prior to the second dose to prevent enhanced vagal tone.
1. Walls RM. Rapid sequence intubation in head trauma. Ann Emerg Med 1993;22:1008-1013.
2. Wilson ME. Predicting difficult intubation. Br J Anaesthesia 1988;61:311.
3. American Society of Anesthesiology. Practice guidelines for management of the difficult airway—A report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology 1993;78:597-602.
4. Walls RM. Management of the difficult airway in the trauma patient. Contemporary Issues in Trauma. Emerg Med Clin North Am 1998; 16:1, 45-61.
5. Langeron O, Masso E, Huraux C, et al. Prediction of difficult mask ventilation. Anesthesiology 2000;92:1229-1236.
6. Kaide C. Invasive and non-invasive ventilation. In: Hoskstra JW, ed. Handbook of Cardiovascular Emergencies. 2nd ed. Philadelphia; Lippincott Williams & Wilkins:2001.
7. Danzel DF, Pozos RS, Hamlet MP. Accidental hypothermia. In: Auerbach PS, ed. Wilderness Medicine. 3rd ed. St. Louis; Mosby:1995.
8. American College of Emergency Physicians. Rapid-sequence intubation [practice guidelines]. Ann Emerg Med 1997;29:573.
9. Roppolo LP, Vilke GM, Chan TC, et al. Nasotracheal intubation in the emergency department, revisited. J Emerg Med 1999;17:791-799.
10. Li J, Murphy-Lavoie H, Bugas C, et al. Complications of emergency intubation with and without paralysis. Am J Emerg Med 1999;17: 141-143.
11. Tayal VS, Riggs RW, Marx JA, et al. Rapid-sequence intubation at an emergency medicine residency: Success rate and adverse events during a two-year period. Acad Emerg Med 1999;6:31-37.
12. Sakles JC, Laurin EG, Rantapaa AA, et al. Airway management in the emergency department: A one-year study of 610 tracheal intubations. Ann Emerg Med 1998;31:325-332.
13. Walls RM. Rapid-sequence intubation comes of age. Ann Emerg Med 1996;28:79-81.
14. Gerardi MJ, Sacchetti AD, Cantor RM. Rapid-sequence intubation of the pediatric patient—Pediatric Emergency Medicine Committee of the American College of Emergency Physicians. Ann Emerg Med 1996;28:55-74.
15. Tobias JD. Airway management for pediatric emergencies. Pediatric Annals 1996;25:317-328.
16. Dimitriou V. Flexible lightwand-guided tracheal intubation with the intubating laryngeal mask Fastrach in adults after unpredicted failed laryngoscope-guided tracheal intubation. Anesthesiology 2002; 96: 296-299.
17. Appendix 1. In: Walls RM, Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management. 1st ed. Philadelphia; Lippincott Williams & Wilkins: 2000.
18. Schneider RE. Sedatives and induction agents. In: Walls RM, Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management. 1st ed. Philadelphia; Lippincott Williams & Wilkins: 2000.
19. Zink BJ, Snyder HS, Raccio-Robak N. Lack of a hyperkalemic response in emergency department patients receiving succinylcholine. Acad Emerg Med 1995;11:974-978.
20. Baraka AS, Taha SK, Aouad MT, et al. Preoxygenation: Comparison of maximal breathing and tidal volume breathing techniques. Anesthesiology 1999;91:3, 612-616.
21. Nimmagadda U. Efficacy of pre-oxygenation with tidal volume breathing. Anesthesiology 2000;93:693-698.
22. Lev R, Rosen P. Prophylactic lidocaine use preintubation: A review. J Emerg Med 1994;12:4, 499-506.
23. Samaha T, Ravussin P, Claquin C, et al. Prevention of increase of blood pressure during endotracheal intubation in neurosurgery: Esmolol versus lidocaine. Ann Fr Anesth Reanim 1996;15:36-40.
24. Lanoix R, Gupta R, Leak L, et al. C-spine injury associated with gunshot wounds to the head: Retrospective study and literature review. J Trauma 2000;49:860-863.
25. Adachi Y, Satomoto M, Higuchi H, et al. Fentanyl attenuates the hemodynamic response to endotracheal intubation more than the response to laryngoscopy. Anesth Analg 2002;95:233-237.
26. Walls RM. The emergency airway algorithms. In: Walls RM, Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management. 1st ed. Philadelphia; Lippincott Williams & Wilkins:2000.
27. Smith DC, Bergen JM, Smithline H, et al. A trial of etomidate for rapid sequence intubation in the emergency department. J Emerg Med 2000;18:13-16.
28. Stockham RJ, Stanley TH, Pace NL, et al. Fentanyl pretreatment modifies anaesthetic induction with etomidate. Anaesthesia Intensive Care 1988;16:171-176.
29. Schenarts CL, Burton JH, Riker RR. Adrenocortical dysfunction following etomidate induction in emergency department patients. Acad Emerg Med 2001;8:1-7.
30. Schow AJ, Lubarsky DA, Olson RP, et al. Can succinylcholine be used safely in hyperkalemic patients? Anesth Analg 2002;95:119-122.
31. Gronert GA. Cardiac arrest after succinylcholine: Mortality greater with rhabdomyolysis than receptor upregulation. Anesthesiology 2001;94:523-529.
32. Perry JJ. Are intubating conditions using rocuronium equivalent to those using succinylcholine? Acad Emerg Med 2002;9:813-823.
33. Sakles JC, Laurin EG, Rantapaa AA, et al. Rocuronium for rapid sequence intubation of emergency department patients. J Emerg Med 1999;17:611-616.
34. Knill RL. Difficult laryngoscopy made easy with a "BURP." Can J Anaesth 1993;40:279-282.
35. Takahata O, Kubota M, Mamiya K, et al. The efficacy of the "BURP" maneuver during a difficult laryngoscopy. Anesth Analg 1997;84:419.
36. Knopp RK. External laryngeal manipulation: A simple intervention for difficult intubations. Ann Emerg Med 2002;40:38-40.
37. Levitan RM, Mickler T, Hollander JE. Bimanual laryngoscopy: A videographic study of external laryngeal manipulation by novice intubators. Ann Emerg Med 2002;40:30-37.
38. Walls RM. Confirmation of endotracheal tube placement. In: Walls RM, Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management 1st ed. Philadelphia; Lippincott Williams & Wilkins: 2000.
39. Bozeman WP, Hexter D, Liang HK, et al. Esophageal detector device versus detection of end-tidal carbon dioxide level in emergency intubation. Ann Emerg Med 1996;27:95.
40. Kasper CL, Deem S. The self-inflating bulb to detect esophageal intubation during emergency airway management. Anesthesiology 1998; 88:898-902.
41. Zaleski L, Abello D, Gold M. The esophageal detector device: Does it work? Anesthesiology 1993;79:244-247.
42. Ardagh M, Moodie K. The esopheagal detector device can give false positives for tracheal intubation. J Emerg Med 1998;16:747-749.
43. Luten RC. The pediatric patient. In: Walls RM, Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management. 1st ed. Philadelphia; Lippincott Williams & Wilkins:2000.
44. Yamamoto LG. Emergency airway management—Rapid sequence intubation. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 4th ed. Philadelphia; Lippincott Williams & Wilkins:2000.
45. Springhouse Physician’s Drug Handbook, 8th ed. Springhouse, PA; Springhouse Publishing Co.:1999.
46. Schneider RE. Muscle relaxants. In: Walls RM, Luten RC, Murphy MF, et al, eds. Manual of Emergency Airway Management. 1st ed. Philadelphia; Lippincott Williams & Wilkins:2000.