The prominence of the occiput, the small neck, and the narrow thorax mean that positioning the child to avoid airway obstruction is different than for an adult. The child may need a pad or folded sheet under the small of the back, to lift the chest and compensate for the large occiput. This will allow the neck to assume a neutral position. Hyperextension of the neck may occlude the child’s airway. The child’s larger tongue may require a jaw thrust or chin lift in order to open the airway.
Oral airways in children can maintain a patent airway or eliminate pharyngeal obstruction by the tongue. This airway must be properly measured before use — one that is too large can cause pharyngeal and glottic trauma. An airway that is too small can push the tongue down and actually worsen the occlusion. Nasal trumpets are useful for older children and adolescents. They are not available for small children and infants. Insertion techniques, complications, and contraindications are no different from those in adults.
Bag-valve-mask ventilation is unchanged from that used in adults. In children, the size of the mask is critical. The mask must fit over the nose, cheeks, and chin. Using too small a bag will result in inadequate ventilation. Smallvolume, self-inflating bags do not deliver an adequate tidal volume to the infant with poorly compliant lungs. Child-size and adult-size self-inflating bags may be used for the entire age range of infants and children without fear of overinflation or barotrauma.12 All bag-valve-mask systems require a reservoir to ensure that 100% oxygen is delivered.
Pediatric bag-valve-mask devices are usually fitted with pop-off valves set at about 30-35 cm H2O pressure. This pressure cutoff was based on an experimental study involving newborn lungs and cannot be well extrapolated to the clinical picture. In the clinical model, increased airway resistance and decreased lung compliance may require ventilatory pressures well in excess of 30 cm H2O.13 Activation of the pop-off valve may lead to inadequate delivery of needed volume, particularly in the presence of reduced lung compliance or increased airway resistance.14
When using the BVM to ventilate the patient, it is important to ensure that the child has a clear airway and that the chest rises while using the bag. Effective ventilation will move the child’s chest about the same amount as when a child takes a deep breath. If there is no chest movement, there is no ventilation. If the ventilation is ineffective, both the airway and the ventilation efforts need to be promptly reassessed. The optimal position for the operator is usually behind the patient’s head. Cricoid pressure should be used when the child is at risk for aspiration or vomiting.
Mouth-to-mask resuscitation is effective in children and infants and may be more effective than BVM. Inverting the Laerdal Pocket Mask™ may fit a child’s airway better.
Although in-hospital intubation has a much lower incidence of complications than intubation of the pediatric patient in the field, about 25% of pediatric in-hospital endotracheal intubations do have complications, and about 30% of these are serious.15 These serious complications include the inability to intubate, mainstem intubation, aspiration, dislodgement of the tube, esophageal intubation, airway trauma, and barotrauma. These complications were markedly reduced with appropriate sedation in this and other studies.16,17
Multiple clinical studies have demonstrated that RSI, for pediatric patients, can be performed safely and effectively in the field by properly trained providers.18 These reports encompass patients with a wide range of ages and clinical presentations. The key to success is proper training and skill retention.
Assess the Risks
Ensure that, at a minimum, the AMPLE (allergies, medications, past medical history, last meal, events leading to the need for intubation) history is available, if at all possible. The intubating clinician should personally examine the neck, face, head, nose, throat, and chest, even when a fullteam approach is used for resuscitation. (See Table 3 for contraindications to RSI).
Get Equipment Ready
In many EDs, equipment for pediatric emergency intubation is not always kept in the same working area where it will be needed. The operator should ensure that all necessary equipment is opened, laid out, and fully functional before any medications are given to the patient.
Generally, a straight blade is used for pediatric intubation, particularly for infants under a year old. The more anterior airway and the floppy epiglottis of the child and infant may make the straight blade more appropriate for the child from 12 months to 6 years of age. For a child older than 6-8 years of age, both Macintosh and straight blades are commonly used.
Equipment for an alternative airway should always be readily available in the proposed intubation room. For the field EMS provider, this means that the airway control kit can always rescue the airway. For the pediatric population, this should include both cricothyrotomy and jet ventilation equipment. Depending on the experience of the operator, an appropriately sized laryngeal mask airway could also be used.
Choosing a Pediatric Tube Size
There are many charts and tables to aid in tube size and selection, but these are rarely available when needed. An excellent and often readily available written aid to tube size and doses of resuscitation drugs is the Broselow® tape. This body tape converts body length into appropriate sizes for tubes, blades, length of tube to be inserted, size of laryngoscope blades to be used, and doses of drugs.
Remember in the child that you must not only select the proper size tube, you must put it into the larynx to the proper depth. Usually the depth of the tube in centimeters can be calculated as 3 times the size of the tube. A lighted endotracheal tube can be visualized in the child’s neck, giving an appropriate depth. Alternatively, the Broselow® tape also gives the proper depth of insertion.
Cuffed vs Uncuffed Tubes
Most major emergency medicine, pediatric ICU, and pediatric anesthesia textbooks instruct that the tube should not have a cuff if the child is under 8 years of age. This dictum was promulgated prior to the development of low-pressure, high-volume cuffs in appropriate sizes for children and infants, and this is now open to question.
In children, cuffed tubes are believed to add little to prevention of aspiration, and the smaller size of the cuffed tube will decrease the available airflow.19 There are 3 arguments against the use of cuffed endotracheal tubes:
- The presence of a leak ensures that the tube is not compressing the tracheal mucosae against the child’s nondistensible cricoid ring. Cuffed tubes increase the risk of mucosal injury in the airway. An uncuffed tube that is too large will also cause mucosal ulceration, tracheal swelling, and postextubation croup.
- Adding a cuff necessitates using a smaller tube, which increases the airway resistance and work of breathing. 19 Infants ventilated through small endotracheal tubes will have prolonged inspiration and expiration, leading to smaller delivered tidal volumes and a positive end-expiratory pressure during ventilatory support.19
- Cuffs are not necessary, because the appropriately sized tube seals well at the cricoid ring. The narrowest part of the pediatric airway is in the subglottic area, rather than at the cords (as in adults).
An uncuffed tube should be large enough to fit the subglottic area and leak at about 25-30 mm Hg of inspiratory pressure. If the tube is so large that it does not leak at all, then the child should be reintubated with the next smaller size tube. A tube that is too small will allow aspiration and make positive pressure ventilation more difficult. A tube that leaks may invalidate tidal volume measurement accuracy in mechanically ventilated children with some mechanical ventilators.20
The development of low-pressure, high-volume cuffs in appropriate sizes for children and infants means that a cuffed tube that allows complete protection against aspiration is now available. The modern low-pressure, high-volume cuff has much greater volume and requires a lower inflation pressure to produce a seal. Because the fit of the cuffed tube can be adjusted, the need for repeat intubation attempts to replace an ill-fitting tube is eliminated.
Since the inflated cuff must now go through the cords, inadvertant extubation with patient movement should be markedly decreased over the uncuffed tube. The seal of the cuff will improve the reliability of end-tidal gas monitoring and measurement of respiratory mechanics and markedly reduce the risk of aspiration.20
Recent research from large studies has shown that these tubes are safe for long-term use in children.21,22 Current pediatric intubation recommendations may be outdated and certainly deserve further scrutiny, in view of these findings.
Monitor the Patient
Cardiorespiratory monitoring is essential for all patients who are ill enough to require intubation — children being no exception. Heart monitoring, pulse oximetry, and automated blood pressure monitoring should be readily available in every ED. These basic monitors should be used routinely in every patient for whom intubation is even contemplated.
Cardiac monitoring may alert the operator to bradycardia, tachycardia, or dysrhythmia in apneic patients. Pulse oximetry is the best means of demonstrating the development of hypoxia during an intubation attempt. Unsuspected hypotension may be revealed with automated blood pressure monitoring.
After intubation in an ED, the proper endotracheal tube position must be confirmed by physical examination, chest x-ray, and a nonauscultatory procedure.
Preoxygenate the Patient
Preoxygenation replaces the patient’s functional residual capacity of the lung with oxygen. If the patient is placed on 100% oxygen as soon as intubation is considered, then they have already been preoxygenated.
In adults, preoxygenation will allow as much as 3-4 minutes of apnea before hypoxia develops. The child may not be able to tolerate apnea of this duration, due to smaller functional residual capacity and higher basal oxygen consumption. This translates to a quite limited measure of security while the pediatric patient is apneic during the RSI sequence.
A rise of the PaCO2 in apnea is usually not of significant concern, unless the patient has a head injury or the airway is severely compromised prior to the intubation. PaCO2 will rise at about 3 mm Hg/min, when the patient is apneic.
Ordinarily, a bag and mask should not be used to artificially ventilate the patient, when RSI is contemplated and the patient is spontaneously breathing. The risk of gastric insufflation and subsequent regurgitation is reduced if bagging is not used. Ventilations may be assisted in synchrony with natural respirations while the patient is still breathing. If bagging is necessary, because of a failed intubation or respiratory compromise, then cricoid pressure (as described below) should be continued at all times.
Sellick’s maneuver (cricoid pressure) will decrease the chances of regurgitation by pressing the cricoid cartilage firmly against the esophagus.23-25 (The latter study shows the positive effects of Sellick’s maneuver in children aged 2 weeks to 8 years.) When pressure is properly applied, the soft, yielding esophagus will be compressed between the cricoid cartilage and the vertebral column. (Figure 1)
Sellick’s maneuver should always be used when the patient is ventilated with a bag-valve mask prior to intubation. The operator should not release cricoid cartilage pressure, until they are certain that the tube is in the trachea. Since Sellick’s maneuver is not a guarantee against regurgitation, inflate the cuff of the tube as soon as possible for older children, and start positive pressure breathing for younger children and infants.
Medicate the Patient
The first medications given in RSI should reduce the physiologic responses of the patient to the forthcoming intubation. These responses include bradycardia, tachycardia, hypertension, hypoxia, increased intracranial pressure, increased intraocular pressure, and cough and gag
Infants and young children can develop profound bradycardia during intubation from medication effects, vagal stimulation, and hypoxia. Vagal stimulation and subsequent bradycardia may occur from stimulation of the oropharynx by the laryngoscope blade.26-29 Succinylcholine can also produce bradycardia in all age groups, although the mechanism of this is not clear.30,31 Hypoxia, of course, can lead rapidly to profound bradycardia.
Atropine blocks the reflex bradycardia that is associated with the use of succinylcholine and laryngoscopy. In children under the age of 5, this reflex is more pronounced. In the literature, pretreating these pediatric patients with atropine is often advocated, in order to minimize vagal effects.32,33 The appropriate dose is 0.02 mg/kg to a maximum of 0.5 mg in the child and 1 mg in the adolescent. A minimum dose of atropine should be 0.1 mg. For effect at the time of intubation, atropine should be administered at least 2 minutes prior to intubation.
Use of atropine in the pretreatment of pediatric patients prior to use of succinylcholine has been examined by Fleming et al in the Canadian Journal of Emergency Medicine.34 These authors reviewed both prospective studies and surveys, and found that no pretreatment with atropine was needed.35-38 It should be noted that the authors of the 2 prospective studies also felt that atropine was unnecessary and should be reserved for children with persistent bradycardia.35,36 Many of the studies that have supported the use of atropine were conducted in the operating room and involved the use of multiple drugs, including anesthetic agents, which may have confounded any relationship between succinylcholine and bradycardia.39 More than 80% of surveyed anesthesiologists believed that neonates, infants, and children should be premedicated with atropine, when repeated doses of succinylcholine were used.
Atropine prior to single-dose succinylcholine during pediatric intubation increases the likelihood of ventricular dysrhythmias and masks the bradycardia that can result from hypoxia. The use of atropine when more than 1 dose of succinylcholine is required may be appropriate, but the patient needs to be carefully evaluated for hypoxia before, during, and after the second dose of succinylcholine. Lidocaine has been shown to attenuate the rise in intracranial pressure (ICP) associated with intubation, although the clinical importance of this rise is somewhat controversial.33 It also decreases the cough reflex and may decrease the incidence of postlaryngoscopy hypertension and tachycardia.40
Lidocaine may be ineffective in blunting the hypertension or tachycardia associated with intubation. The recommended dose of lidocaine is 1.5 to 3 mg/kg intravenously. As with atropine, when used, lidocaine must be given at least 2 minutes prior to intubation in order to be effective. Alternatively, lidocaine may be sprayed into the posterior pharynx and trachea. Again, this is somewhat controversial, as spraying lidocaine into the trachea may require almost as much manipulation as intubation itself.
Beta-blockers, such as esmolol 1.5 mg/kg over 30 seconds or labetalol 0.25 mg/kg, may also be used in the stable patient to blunt the rise in ICP associated with intubation.41 Use of beta-blocking agents is dangerous in the patient with cardiovascular instability or the asthmatic patient.
Attenuation of adverse cardiovascular and ICP responses is optional in moribund and desperate situations. In these cases, the intubator should proceed directly to paralytic and sedation agents.
Multiple agents have been used for sedation during the process of intubation in children, among them barbiturates, benzodiazepines, opiates, nonbarbiturate sedatives, and dissociative agents. Each of these agents has their proponents and detractors, relative indications and contraindications. The ideal sedative should induce rapid unconsciousness in the child with a short duration and little or no cardiovascular side effects. Unfortunately, the ideal agent does not exist.
The sedative of choice should always be given prior to the paralytic agent. Although sedatives and paralytics can be given at the same time, paralysis is such a frightening event that sedation should be assured prior to the onset of paralysis.
Table 4 lists commonly used sedatives for RSI in both adults and children. Any of these sedating agents will produce acceptable results in RSI when used at the recommended dose. The choice of sedative is based on the clinical state of the patient and the effects and side effects of the medication.
Fentanyl is a rapid-acting and very potent opiate of relatively short duration. It produces analgesia within 90 seconds, with an effective duration of about 30 minutes. In addition to its profound sedative and analgesic effects, fentanyl may decrease the tachycardia and hypertension associated with intubation. It appears to be well tolerated hemodynamically, with little hypotension in most children. Fentanyl is indicated when hemodynamic control of the patient is critical. Fentanyl may be easily reversed with narcotic antagonists, such as naloxone.
The usual recommended dose of fentanyl is 2 to 3 μg/ kg, given 1 to 3 minutes prior to intubation. A higher dose of 5 to 7 μg/kg is indicated to block hypertension and tachycardia, and some authorities suggest as much as 15 μg/kg. Neonates appear to be more sensitive to fentanyl, and decreased doses should be used for them.
All opiates, fentanyl included, cause respiratory depression in a dose-dependent response. Fentanyl may also cause seizures, chest wall rigidity, and skeletal muscle movements. There are some reports of increased ICP associated with fentanyl, particularly in children. It should be used with caution when ICP is a major factor. An alternative narcotic agent with similar properties to fentanyl is alfentanil, 20-30 μg/kg. Morphine is not recommended for use in RSI in children.
Barbiturates and Other Hypnotic Agents
Thiopental (2-5 mg/kg IV) is a short-acting barbiturate with an onset of 10 to 20 seconds and duration of 5-10 minutes. There is abundant emergency and anesthesiology experience with thiopental for all ages. Although thiopental is a sedative, there is no analgesic effect. It causes a decrease in intracranial pressure, intracerebral blood flow, and cerebral oxygen consumption. It is most useful in patients with increased ICP (eg, head trauma, meningitis). Thiopental is not normally recommended for intubation sedation in children in other situations.
Thiopental may cause profound hypotension by vasodilation and myocardial depression. It should not be used in the hypotensive or hypovolemic patient of any age. Like all sedatives, thiopental causes respiratory depression. Thiopental should not be used for patients with asthma, as it may cause additional bronchospasm by release of histamine.
Methohexital (1-1.5 mg/kg IV) is a short-acting barbiturate with an onset of less than 1 minute and a duration of about 5-7 minutes. Methohexital is quite similar to thiopental in action and contraindications. It also causes respiratory depression and may cause seizures in high doses. It has no advantages over thiopental in children. Etomidate (0.2 - 0.4 mg/kg IV) is an ultrashort-acting, nonbarbiturate hypnotic agent that has been used as an induction agent for anesthesia for years in both children and adults.42 Etomidate has minimal hemodynamic effects and may be the drug of choice in a hypotensive or trauma patient.43 It causes less cardiovascular depression than either the barbiturates or propofol. Etomidate has also been shown to decrease intracranial pressure, cerebral blood flow, and cerebral oxygen metabolism.
Propofol (1-3 mg/kg IV) is a relatively new anesthetic induction and sedative agent. It has an extremely rapid onset, within 10 to 20 seconds, and a short duration of action of 10 to 15 minutes. Propofol should not be used in patients with known allergies to soy and eggs. Propofol decreases intracranial pressure and cerebral metabolism. It may cause significant hypotension, which limits usefulness in trauma patients. Lower doses can be used for patients with unstable blood pressure. Unlike other agents, propofol can be used as a drip for continued sedation after the intubation. The continued sedation dose is 0.075 to 0.15 mg/kg/minute.
Diazepam (0.2-1.0 mg/kg IV) is a moderately long-acting benzodiazepine (30 to 90 minutes) with slow onset (2-4 minutes). It causes less cardiovascular and respiratory depression than the barbiturates. If alcohol is present, the respiratory depression of diazepam is augmented. Diazepam must be titrated, as the effective induction dose is quite variable. It is more useful as a long-term sedative agent for the intubated patient after the procedure. Diazepam has significant amnestic effects.
Diazepam is irritating to veins and may cause localized thrombosis. This is a particularly important side effect in children who may have difficult venous access. Diazepam is not recommended for use in children for this reason alone. Do not use diazepam in patients with glaucoma.
Lorazepam (0.1-0.4 mg/kg) is a long-acting benzodiazepine, and it is most useful for long-term sedation of the intubated pediatric patient. It may be used as an anticonvulsant and sedative for the child with status epilepticus. It has no other place in RSI.
Midazolam (0.1-0.4 mg/kg IV) is a rapid-onset, short-acting benzodiazepine (30-60 minutes) with potent amnestic effects. It is slower in onset than the hypnotic agents and should be administered 2 full minutes before intubation is attempted. Midazolam may require 3 to 5 minutes for complete effect. The typical RSI dose is much higher than the dose used for sedation, and it still may not be reliably effective in a 0.3-mg/kg dose. Midazolam is faster in onset, shorter in action, and has a narrower dose range than either lorazepam or diazepam. Midazolam causes respiratory and cardiovascular depression. It does not increase ICP and may provide some small decrease in cerebral blood flow.
The effects of the benzodiazepines are generally not as reliable for RSI as the hypnotic agents. Benzodiazepines are most useful as an adjunct, to provide retrograde amnesia of the procedure or as agents in the patient with ongoing seizures.
All of the benzodiazepines are reversible with flumazenil. There is a small but significant risk of seizures when using flumazenil. Benzodiazepines have little effect on the intracerebral pressure. All of the benzodiazepines are suitable for use in the patient with status epilepticus.44
The only neuroleptic agent that is useful for intubation is ketamine. Ketamine is often described as a dissociative anesthetic, where the patient may appear to be awake, but is amnestic and unresponsive to pain. In contrast to the other sedative agents, ketamine increases the cardiac output, pulse rate, blood pressure, myocardial oxygen consumption, cerebral blood flow, intracranial pressure, and intraocular pressure.45 Although ketamine has direct negative inotropic properties, it causes a release of endogenous catecholamines, resulting in the positive overall effects. Ketamine also increases salivary and bronchial secretions.46 Secretions can be decreased with atropine 0.01 mg/kg or glycopyrrolate 0.005 mg/kg.
Ketamine causes awakening hallucinations that many adults find unpleasant. These emergence reactions occur in up to 50% of adults, but are rare in children under 10 years of age.47 Ketamine is particularly useful in the asthmatic patient, as it is a bronchodilator. It is the sedative of
choice in the asthmatic child with respiratory failure.48,49
Ketamine is contraindicated in head injury (due to both the increased oxygen consumption and increased intracranial pressure associated with ketamine). It should be used with extreme caution in hypertensive patients (because it increases blood pressure) and those with open eye injuries and glaucoma (due to increased intraocular pressure). However, ketamine may be the drug of choice in the hypotensive, unstable patient.
The dose of ketamine for RSI in children is 1-2 mg/kg. At this dose, anesthesia occurs within 1 minute and lasts about 5 to 10 minutes. Some authorities feel that children who are sedated with ketamine should also be treated with atropine to reduce secretions, but this opinion is not universal.
Neuromuscular Blocking Agents
The perfect paralytic agent for the child would have an extremely rapid onset and a duration that is proportional to the dose used — it would also have sedative, analgesic, and amnestic properties, be safe for use in all ages, from birth to over 100 years, have minimal side effects, and not require any special storage. This agent also does not yet exist. Current neuromuscular blocking agents may be either a depolarizing agent, such as succinylcholine, or a nondepolarizing agent, such as pancuronium or curare. None of these have sedative properties.
Use of neuromuscular blocking agents (Table 5) is controversial, with anesthesiologists fearing increased morbidity and mortality when non-anesthesiologists use these agents. The largest study to date, in a community hospital with emergency physicians performing intubations with these agents, has not validated these concerns.50 The only absolute contraindication to use of a neuromuscular blocking agent would be an inability to manage the airway after making the patient apneic.
Succinylcholine is considered an ideal paralytic agent, because of the rapid onset of action (within 45 seconds) and the short duration of the drug (4-5 minutes). The intravenous dose of succinylcholine is 2 mg/kg for infants and small children; for older children and adolescents, the dose is 1 mg/kg. Although approved for IM use in infants and children, the IM route is not recommended in the emergency patient. Unfortunately, succinylcholine has significant side effects, largely related to the depolarization of the muscle cell. These side effects limit the use of succinylcholine in children.
Hyperkalemia: Perhaps the most clinically significant complication of succinylcholine is hyperkalemia. Although the effect has been documented for over 30 years, the precise mechanism of hyperkalemia is not yet known. It is currently thought to be due to an increased number of acetylcholine receptors in these patients. The acetylcholine receptors are found within the muscle membrane, not just at the neuromuscular junction. The increase in acetylcholine receptor sites occurs within 5 to 20 days after the development of the disease or injury. Succinylcholine can cause lethal hyperkalemia in patients with burns, crush injuries, abdominal infections, tetanus, muscle disorders, and denervating disorders.51-53 Succinylcholine can be used safely in massive trauma, burns, spinal cord injuries, etc, if used within this 5-day grace period. Obviously, patients with underlying hyperkalemia, such as patients with renal failure, should not be given succinylcholine.
Prolonged Paralysis: Succinylcholine can cause prolonged paralysis in those children who have a deficiency of pseudocholinesterase or an atypical pseudocholinesterase. 54 Several drugs have also been associated with prolonged paralysis, including magnesium, lithium, and quinidine.55 Patients who are intoxicated with cocaine may have prolonged paralysis when given succinylcholine, because cocaine is competitively metabolized by cholinesterase. The net effect of any disturbance in metabolism of succinylcholine is to prolong paralysis from 5-10 minutes to several hours. Although known pseudocholinesterase deficiency is a contraindication, the only complication would be prolongation of the paralysis.
Malignant Hyperthermia: Malignant hyperthermia is thought to occur from excessive calcium influx through open channels.56 It is associated with markedly increased temperatures, metabolic acidosis, rhabdomyolysis, and disseminated intravascular coagulopathy. Approximately 1 in every 15,000 patients given succinylcholine will develop malignant hyperthermia.57 This problem has prompted the FDA to limit the use of succinylcholine in infants and children, except in emergency situations.58
Increased Intraocular Pressure: Succinylcholine causes a transient rise in intraocular pressure. Theoretically, this increased intraocular pressure could cause expulsion of the vitreous in an open eye injury. There has never been a documented case of this complication, despite widespread use of succinylcholine in open eye surgery.59 The prudent practitioner will use a nondepolarizing agent in penetrating eye injuries, if one is readily available.
Increased Intracranial Pressure: The significance of the rise in intracranial pressure that accompanies succinylcholine use is controversial. The drug has been used widely and successfully in this setting. The transient rise in pressure may be due to a direct effect of fasciculations, increased cerebral blood flow, or sympathetic stimulation. Pretreatment with a nondepolarizing agent will blunt this response,60 though pretreatment may not be practical when intubation is urgent.
Muscle Fasciculations: Fasciculations are asynchronous contractions of every muscle fiber. These fasciculations occur until paralysis has been achieved. Diffuse muscle pain is a common complaint after the use of succinylcholine. During fasciculations, gastric pressure increases, enhancing the risk of aspiration.61 Fasciculations can be prevented by pretreatment with a small dose of a nondepolarizing agent, such as vecuronium, prior to the administration of succinylcholine.60 Many physicians do not use a pretreatment dose.
If intubation is not successful during the initial paralysis, a second dose of succinylcholine can be used in adolescents; however, a repeated dose in infants and small children may cause bradycardia and even asystole.62 Repeated doses of succinylcholine in children should not be used.
The nondepolarizing neuromuscular blocking agents bind in a competitive, nonstimulatory fashion to the α-subunit of the acetylcholine receptor. Because there is no muscle stimulation prior to paralysis, these agents do not produce fasciculations. There are 3 types of nondepolarizing drugs available: benzylisoquinoliniums, aminosteroids, and quaternary amines. Of these, only the benzylisoquinoliniums and aminosteroids are used in RSI.
Although usually not needed in the ED, nondepolarizing agents can be reversed by use of an anticholinesterase agent, such as edrophonium or neostigmine. Reversal may take several minutes and cannot be used as a “safety net” for a failed intubation.
The newer nondepolarizing agents (vecuronium, rocuronium, and mivacurium) can induce intubating paralysis in a time frame comparable with succinylcholine. Unfortunately, the shortest-duration nondepolarizing agent has a duration twice that of succinylcholine. Onset time of paralysis for nondepolarizing agents is inversely related to the potency of the agent.
Some patients have a significant release of histamine associated with use of the nondepolarizing muscle relaxants.63 These symptoms can be avoided with slower infusion of the agent, but this may not be an option during emergency intubation. None of the nondepolarizing agents should be used in patients with myasthenia gravis.
Vecuronium: Vecuronium is an aminosteroid nondepolarizing agent. It has an intermediate duration of action of 30-60 minutes, with an initial dose of about 0.1 mg/kg. It produces clinical effects in 30 seconds and intubation paralysis in 1-4 minutes. A priming dose of 0.01 mg/kg given 2 minutes before intubation will shorten the onset of vecuronium to about 30 seconds. Concerns over arrhythmiasin children associated with succinylcholine use have made high-dose vecuronium (0.28 mg/kg) a popular choice for emergent pediatric airways.64
Vecuronium has been associated with a myopathy of critical illness in children who have concomitantly received high doses of steroids. The exact mechanism of the myopathy is not known. It is associated with use of other aminosteroid neuromuscular blocking agents. It is unlikely that single use of these agents will be associated with this myopathy, but caution should be used in children receiving high doses of steroids.
Rocuronium: Rocuronium is an aminosteroid nondepolarizing agent that is similar to vecuronium and has a very rapid onset of action. A dose of 0.8 mg/kg will produce paralysis in infants and children in 30 seconds or less. Recovery time from paralysis is between 30 and 45 minutes. This agent may be used quite successfully as a replacement for succinylcholine, if the extended recovery time is tolerable.
Mivacurium: Mivacurium is a short-acting nondepolarizing benzylisoquinolinium muscle relaxant. It has a short onset of action (30-60 seconds), with intubation conditions achieved within 75-120 seconds. It lasts only 15 to 20 minutes. The typical RSI dose is about 0.15 to 0.3 mg/kg. Mivacurium is metabolized by plasma cholinesterase, and children recover from blockade much quicker than adults do.65 This effect may make mivacurium more useful in pediatric intubation.
Pancuronium: Pancuronium is another aminosteroid neuromuscular blocking agent that will provide acceptable conditions for intubation in 90-120 seconds, with paralysis that lasts from 45 to 90 minutes. It is classified as a long-acting agent with a slow onset. The slow onset limits usefulness in the ED setting. Pancuronium is primarily excreted in the urine, so reduced renal function or urinary output will increase the duration of effect. Pancuronium can cause severe histamine reactions.
Intubate the Patient
Intubation is performed after the airway muscles are fully relaxed, which usually occurs about 45 seconds after the administration of succinylcholine. Cricoid pressure should be maintained until the cuff is inflated and the tube position verified.
The conventional wisdom is that the most experienced person present at an intubation should be the one doing the intubation, because the patient is paralyzed and sedated. This is an unacceptable policy for a training institution. If this caveat were always followed, newer physicians would remain untrained. Until a resident is completely comfortable, in the judgment of the attending, then the attending emergency physician should be within reach of the patient, until the patient is successfully intubated.
If intubation fails, cricoid pressure should be maintained, and the patient can be ventilated with a bag-valve mask. After the patient is reoxygenated, then either intubation should be reattempted, or an alternative airway technique employed.
After intubation, the tube must be confirmed to be in the trachea. This verification is more important than the intubation itself. The bedside clinical assessment consists of visualizing the endotracheal tube as it passes through the vocal cords. This is followed by listening over the epigastrium for bowel sounds and listening over each lung field for the presence and equality of breath sounds. Looking for condensation on the endotracheal tube with exhalation and watching for the chest to rise and fall with inspiration completes the clinical assessment.
The process of verification of tube placement is controversial. Each and every one of the clinical indicators of proper tube placement has been known to fail. The sequence of events that precipitates intubation in the child is often accompanied by one or more conditions that can cause these failures of verification. Unrecognized esophageal intubation is catastrophic for the patient. Further confirmation of tube placement can be by documentation of carbon dioxide from the lungs, documentation of stable or increasing oxygen saturation, and by x-ray of the chest for tube placement. The astute emergency physician will always verify the tube placement by using a combination of these and will always reverify tube placement in children when clinical conditions deteriorate or when the patient has been moved.
In the perfect intubation, the tube will be seen to pass through the child’s cords. Unfortunately, in the stress of an emergency intubation — with vomitus or blood, difficult anatomy or cervical immobilization — visualization of the tube’s passage through the cords is all too often merely a fond aspiration.66
Likewise, it is difficult to even look for expansion of the chest without any gastric distention in the immobilized patient with potential chest trauma (and in many other clinical situations). While it is nice to see, it cannot be relied upon as the only sign of a good intubation.
Ideally, the breath sounds will be heard equally when the tube is in appropriate position in the trachea. Air meeting water (or fluid) causes bubbling, the sound of which implies that the tube is in the esophagus or stomach. In the small child, normal breath sounds may be heard when listening over the stomach. If breath sounds (but no bubbling) are heard over the stomach, do not pull the tube, but complete the rest of the assessment. Listen 2 breaths on the right third intercostal space in the midaxillary line and compare to 2 breaths on the left side in the third interspace.
Pulse oximetry has long been a standard method of onitoring the patient with respiratory difficulties. If the oxygen saturation is rising, or stays at an acceptable level in a paralyzed patient, then the endotracheal tube is quite likely in the appropriate place (ie, there certainly is no esophageal intubation). Unfortunately, the pulse oximeter is not particularly useful in the patient with profound shock or cardiac arrest.
Carbon Dioxide Detectors
End-tidal carbon dioxide measurements or a disposable colorimetric device (CO2 detector) can be used in children. 67,68 These devices work by measurement (colorimetric or direct) of the carbon dioxide produced by the body and eliminated by the lungs.69 If the ET tube is placed in the esophagus, then there should be no carbon dioxide in the exhaled gas. The end-tidal CO2 detector works so well in the operating room that its use there is considered standard of care by anesthesiologists.70
A normal-looking waveform and a “digital read out” confirm that the endotracheal tube is in the trachea. (Figure 2) In low cardiac output states, such as shock, cardiac arrest, or inadequate chest compressions, ETCO2 may not be detected. If a patient has consumed carbonated beverages or if mouth-to-mouth ventilation has been attempted, CO2 may be detected after esophageal intubation (ie, a false positive).71 The ETCO2 should rapidly decrease to zero (within 3-6 breaths) in this situation, and also the waveform will not be “normal-looking.” Vukmir et al reported a sensitivity and specificity of 100% for endotracheal tube localization by capnography.72
The digital readout of ETCO2 can be displayed in mm Hg (partial pressure of CO2 in exhaled gas) or as a percentageof carbon dioxide in the exhaled gas. Most of the common devices use “infrared absorption of CO2” as their principle of operation. (Figure 3 and Figure 4) Another similar CO2 detection device is the MiniCAP III (MSA Catalyst Research, Owings Mills, Maryland). This device is a battery-operated capnometer that emits a flash and beep during each breath that contains CO2. An alarm sounds for each breath that does not contain CO2. It is small, relatively inexpensive, and reusable. Its reliability and sensitivity are comparable to the Easy Cap II.
In the colorimetric device (Figure 5), a pH-sensitive chemical indicator is enclosed in a plastic housing and is connected to the gas stream between the endotracheal tube and the bag-valve mask. This pH-sensitive indicator changes color when exposed to CO2. The color varies between expiration and inspiration, as the CO2 level increases or decreases. The color changes from purple (when exposed to room air or oxygen) to yellow (when exposed to about 4% CO2). The response time of the device is sufficiently fast to detect changes of CO2 breath-by-breath.
However, this device is not very sensitive when CO2 output is low, as it is during CPR. All colorimetric CO2 detectors have been shown to be falsely negative in the patient who has had a cardiac arrest and falsely positive in the patient who has recently consumed a carbonated beverage.73 In one prospective study, the sensitivity of this device in detecting proper endotracheal placement in the cardiac arrest patient was only 85%.74 This means that as many as 15% of properly placed endotracheal tubes (in cardiac arrest patients) would be inappropriately removed when this device is relied upon exclusively. These conditions occur far more frequently in emergency medicine practice than in the operating room. The waveform of a capnometer will not be normal in either of these conditions, and this should alert the operator to a potential problem.
Esophageal Detector Devices
Syringe aspiration esophageal detector devices (EDDs) have recently been used to confirm tube placement.75,76 These devices use the rapid refill of a bulb syringe or equivalent through the endotracheal tube as “proof” that the tube is in the airway, rather than the esophagus. In adults, there is high assurance that the ETT is not in the esophagus, but the EDD may misidentify endobronchial or mainstem intubation as esophageal. Marley et al showed that the esophageal detection device correctly identified 100% of esophageal intubations (but only 35 of 40 ET intubations).76 There is no study assuring that these devices will be effective in the deliberate air leak associated with uncuffed tubes used in a pediatric airway. EDDs are currently approved only for children older than 5 years or greater than 20 kg body weight.
Following confirmation by auscultation, inspection, esophageal detector devices, and/or CO2 measurement, a hest x-ray should always be obtained. A chest x-ray can also help with depth and placement of the tube. Ideally, the tip of the endotracheal tube should be in the middle third of the trachea, just proximal to the carina. The provider must realize that, although a radiograph is viewed as a gold standard, the portable anteroposterior radiograph can miss an esophageal intubation, if the trachea and esophagus are aligned during the film.
Although it is impractical to get a radiograph confirming tube placement in every elective intubation in the operating room or in the field, this is not true in emergency medicine. Despite the fact that the radiograph will be the gold standard by which the legal field judges our performance, a radiograph takes several minutes to obtain and process, and the patient needs appropriate and adequate ventilation in the meantime. The clinician must confirm tube placement prior to obtaining a radiograph and ensure that the tube does not move during this radiograph.
Secure the Tube
The risk of inadvertent dislodgement of the ETT or mainstem bronchus intubation is much higher in the small child, due to the shorter trachea and bronchus. The endotracheal tube must protrude only 3 to 4 cm past the cords, in order to avoid a right mainstem bronchus intubation. The tracheal length from larynx to carina is short (4-5 cm in a newborn and only 7-8 cm in an 18-month-old child), so dislodgement of the uncuffed endotracheal tube is a common complication. Since the child’s neck is much more flexible than the adult’s, and the tube most often does not have a cuff, motion of the neck can dislodge an ETT in a child.
Security of the tube includes sedation, ensuring that the child will not move and that the child’s head does not move during radiographs and other procedures postintubation. Following each such procedure, the oxygen saturation should be carefully monitored. A falling saturation or change in clinical status should prompt the astute clinician to reassess the placement of the endotracheal tube.