By Charles E. Stewart, MD, FACEP
There are few more important tasks in emergency medicine than airway management. 1-4 Whatever method is used must be effective, for the problem airway does not allow the luxury of waiting until the "physician" arrives, or until the problem has cured itself. Airway compromise is the most common cause of death and severe morbidity in the acutely ill or injured child.
Intubation of the adult larynx and trachea is taught in ACLS courses and is required of every paramedic. These courses often stress the skills of inserting an endotracheal tube, but do not discuss the decision-making that accompanies the procedure. It is assumed that the procedure will be limited to moribund patients.
In the past, when the paramedics arrived, the patient's condition could range from frankly moribund to simply "running out of steam." If the patient was combative or awake, the paramedic was forced to delay rather than attempt an intubation with the few tools available in the field. This delay was often to the patient's detriment. It is clear that many of these patients would benefit from an earlier intubation. The minimal morbidity associated with short-term intubation justifies the procedure in most critically ill patients.
Until recently paramedics were quite limited in the tools available to control movement and sedate the patient. The need to temporize (inappropriately) completely changed with the technique known as Rapid Sequence Intubation (RSI). This trend first started with air ambulance services, and was followed shortly by selected ground-based ambulance services.
RSI is defined as the rapid (nearly simultaneous) administration of both a neuro-muscular blocking agent and a potent sedative agent to facilitate intubation while decreasing the risks of aspiration, combativeness and potential damage to the patient. It is the ultimate in control, since, when properly done, the patient literally can no longer breathe without the clinician. There is ample evidence that both pediatric and adult patients emergently intubated with the principles of RSI have both lower complication rates and higher success rates than with all other techniques.
Unfortunately, the decision-making process associated with intubation of a far-from-moribund patient is not taught in most intubation curricula.
Paramedics should ask five questions when deciding whether to intubate a patient. Consideration of these questions will help guide the decision to intubate a conscious and breathing patient. If there are adequate means in the field to correct this problem without intubation, the procedure is not appropriate.
1. Can the patient maintain an airway?
2. Can the patient protect this airway?
3. Is the patient appropriately ventilated?
4. Is the patient appropriately oxygenated?
5. Must the patient be intubated for a specific therapy or for treatment of a specific condition?
Clinical evaluation of ventilation is often difficult without arterial blood gases. Careful serial evaluation of the depth and rate of respiration can approximate it, but this is only an approximation. Evaluating oxygenation will require pulse oximetry. Paramedics must consider intubation in each patient where the answer to the first four questions is no.
After the patient is evaluated and it is determined that he is unable to maintain an airway, protect it, and ensure both oxygenation and ventilation, the question is, "What is the simplest way to correct this problem?" If the airway can be established by positioning the patient, insertion of an oral or nasal airway and intubation are not yet needed. If the patient is not ventilating because of an overdose of opiates, appropriate therapy is not intubation, but judicious use of a narcotic antagonist.
Likewise, if the patient must get therapy or has a condition that will benefit from intubation, then intubation will be appropriate. For example, if the patient must be sedated for air transport, he will likely require intubation. Because intubation in an air ambulance is much more difficult than in either an ED or field ambulance, early intubation is indicated. Sedation is unlikely to help the patient's airway status.
The paramedic must constantly reassess the patient's status. If the patient's condition changes, this change may mandate emergent intubation.
Rapid-sequence induction is a similar technique used by our anesthesiology colleagues to rapidly deliver general anesthesia in similar unprepared patients at risk for aspiration of stomach contents. The anesthesia emphasis is on continued sedation and induction of general anesthesia once intubation is accomplished. Emergency medicine focuses on the procedure of intubation and maintenance of an airway, and removes much of the sedation immediately following intubation. There is a significant difference in the use of paralytics and sedation to facilitate intubation and using them as the first steps in anesthesia.
There is no advantage to using RSI in the deeply comatose patient or the patient who has cardiac arrest. In every other patient, RSI is faster and safer than any alternative technique.5-8 RSI should be considered in every nonarrested patient requiring emergency intubation.
In the patient with potentially increased intracranial pressure (ICP), RSI blunts further ICP increases due to laryngoscopy, coughing or struggling during the intubation.
There are three major assumptions inherent in RSI. Every paramedic must realize that these assumptions are an integral part of the technique and drive the actual technique of RSI:
1. The patient has a full stomach.
Since emergency patients rarely present with an empty stomach, a major precept of RSI is that the patient is about to vomit. Furthermore, the majority of these same patients present after receiving bag-valve-mask oxygen therapy with subsequent gastric distention. Since unconscious patients have decreased laryngeal closure reflexes and decreased lower esophageal sphincter tone, this further predisposes the patient to regurgitation and aspiration.9 The mortality of regurgitation and subsequent aspiration is between 30% and 70%.10,11 For those who don't die, the hospital stay is about 3 weeks, most of which is in the ICU. The technique of RSI is designed to prevent this major problem. While apnea can be managed by a period of bag-valve-mask ventilation and failure to intubate can be managed by a surgical airway, the risk of aspiration cannot be ignored.
2. The operator can secure an airway.
Some form of airway can be secured even if the initial attempt(s) at intubation are not successful.
Failure is not an option!
If the operator can't guarantee an airway, it will be fatal to the patient.
Intrinsic to this assumption is the secondary postulate that the operator knows all of the available equipment, has it immediately available, and can both size it and employ it rapidly.
3. The operator can resuscitate the patient.
See above. If you don't have the equipment and knowledge to fully resuscitate the patient, you shouldn't be taking away critical survival drives.
· Spontaneous breathing with adequate ventilation and oxygenation.
· Operator concern that both intubation and mask ventilation may not be successful due to: major laryngeal trauma; upper airway obstruction; distorted facial or airway anatomy.
· Operator unfamiliarity with the medications used.
In these cases, the paramedic should not paralyze the patient. If necessary, a surgical airway would be appropriate.
Ensure that at least the AMPLE history is available, if possible (Allergies, Medications, Past medical history, Last meal, Existing circumstances). The intubating paramedic should personally examine the neck, face, head, nose, throat and chest, even when a full surgical team approach is used for resuscitation.
Conditions that can lead to problems with intubation include cervical immobilization, limited mouth opening, big tongue, high arched palate, buck teeth, receding chin, thick neck and, of course, the disrupted airway from blunt trauma to the face and neck. Distorted anatomy or requirement of a specific position to maintain upper airway patency may cause significant problems with rapid sequence intubation, particularly in patients who are dependent on upper airway muscle tone or specific positioning to maintain the patency of the airway. These patients may be better intubated in the emergency department or with surgical airway techniques.
The operator should ensure that all needed equipment is opened, laid out and fully functional before any medications are given to the patient. Minimum immediately available equipment includes:
o Appropriately sized bag-valve-mask with reservoir
o Suction (fully hooked up and working)
o Oxygen (hooked up to a bag-valve mask)
o Laryngoscope with appropriate sized blades and functioning lights
o Appropriately sized endotracheal tubes (have immediately available at least one size above and below the predicted size)
o Stylet for the endotracheal tube
o All pharmaceutical agents to be used in the procedure
o Alternative airway equipment at the operator's side.
Equipment for an alternative airway should always be readily available in the immediate vicinity of the intubator. For an adult, this would mean that a cricothyrotomy kit is kept in the intubation kit. In the pediatric population, this should include both cricothyrotomy equipment for older children and jet ventilation equipment. Depending on the experience of the operator, an appropriately sized laryngeal mask airway could also be used.
Cardiorespiratory monitoring is essential for all patients who are ill enough to need intubation. Children should not be an exception. Heart monitoring, pulse oximetry and blood pressure monitoring should be readily available for every responder who contemplates RSI. These monitors should be used as a routine measure in every patient where intubation is even considered as a possible procedure.
Cardiac monitoring may alert the operator to bradycardia, tachycardia or dysrhythmia in apneic patients. Pulse oximetry is the best monitoring to detect hypoxia during an intubation attempt. Unsuspected hypotension may be revealed with automated blood pressure monitoring.
After intubation, the proper endotracheal tube position must be confirmed with clinical examination and a non-auscultatory procedure.
Pre-oxygenation replaces the patient's functional residual capacity of the lung with oxygen. This gives a limited time of security if the patient is apneic during the RSI sequence. If the patient is placed on 100% oxygen (assisted respiration with bag-valve-mask or non-rebreathing high- flow mask) as soon as intubation is considered, the patient has already been preoxygenated prior to the intubation.
In adults, preoxygenation will permit as much as 3-4 minutes of apnea before hypoxia develops. A child may not be able to tolerate apnea as long, due to smaller functional residual capacity and the higher basal oxygen consumption of children.
Rise of the PaCO2 in apnea is not usually a significant concern unless the patient has a head injury or is severely compromised prior to the intubation. PaCO2 rises at about 3 mmHg/min when the patient is apneic.
Ordinarily, a bag and mask should not be used to artificially ventilate the patient. Ventilations may be assisted in synchrony with natural respirations. When the patient is adequately preoxygenated, there is no need for forcible ventilation just prior to intubation. This habit markedly increases the risk of gastric insufflation and subsequent regurgitation. If bagging is necessary because of a failed intubation, cricoid pressure should be continued at all times.
The first medications given should reduce the patient's physiologic responses to the subsequent intubation. These responses include bradycardia, tachycardia, hypertension, hypoxia, increased intracranial pressure, increased intraocular pressure, and cough and gag reflexes.
Although there is good rationale for using these medications, the final decision is the medical director's. Protocols for RSI should be prepared in advance with specific medications for each situation discussed with and approved by the medical director and the receiving emergency physicians.
Infants and young children can develop profound bradycardia during intubation from medication effects, vagal stimulation and hypoxia. Vagal stimulation may occur from stimulation of the oropharynx by the laryngoscope blade. Succinylcholine can also produce profound bradycardia in infants. Hypoxia, of course, can rapidly cause profound bradycardia in both the infant and child.
Atropine blocks the reflex bradycardia that is associated with the use of succinylcholine and laryngoscopy. In children under age 5, this reflex is more pronounced, and pretreating these pediatric patients with atropine can minimize vagal effects.12,13 The appropriate dose is 0.02 mg/kg to a maximum of 1 mg. To be effective, atropine should be administered at least 2 minutes prior to intubation.
Lidocaine has been shown to blunt the rise in ICP associated with intubation, although this is somewhat controversial.14 It also decreases the cough reflex and may decrease the incidence of post-laryngoscopy hypertension and tachycardia. Lidocaine may be ineffective in blunting hypertension or tachycardia associated with intubation. The recommended dose of lidocaine is 1.5 to 3 mg/kg intravenously. As with atropine, 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.
Attenuation of adverse CV and ICP responses is optional in moribund and desperate situations.
Multiple agents have been used for sedation during the process of intubation, including barbiturates, benzodiazepines, opiates, non-barbiturate sedatives and dissociative agents. Each of these agents has its proponents, relative indications, contraindications and detractors. The ideal sedative should induce rapid unconsciousness with short duration and little or no cardiovascular side effects. The ideal agent does not yet exist.
The sedative agent 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. The choice of sedative agent is based on clinical state of the patient and effects of medication.
Fentanyl is a rapid-acting and very potent opiate of relatively short duration (see Table I). 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 tachycardia and hypertension associated with intubation. It appears to be well tolerated hemodynamically with little hypotension in most patients. 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 2-3 micrograms/kg, given 1-3 minutes prior to intubation. A higher dose of 5-7 mcg/kg is indicated to block hypertension and tachycardia, and some authorities suggest as much as 15 mcg/kg. Neonates appear to be more sensitive to fentanyl, and smaller doses should be used.
Like all opiates, fentanyl causes 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.
Morphine in a dose of 0.1-0.2 mg/kg has also been used as sedation for RSI. Morphine has both a longer duration of action and a longer onset time than fentanyl. It takes as much as 3-5 minutes for morphine to adequately sedate a patient. In addition, morphine may not blunt the rise in ICP, tachycardia or hypertension as well as fentanyl. Morphine is not recommended for RSI in the field because of the longer onset time and the failure to blunt tachycardia or hypertension.
Thiopental (2-5 mg/kg IV) is a short acting barbiturate with an onset of 10-20 seconds and a duration of 5-10 minutes. There is abundant emergency and anesthesiology experience with thiopental. Although thio-pental 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 the patient with increased ICP (head trauma, meningitis).
Thiopental should not be used for patients with asthma, as it may cause additional bronchospasm by releasing histamine. Thiopental may cause hypotension by vasodilation and myocardial depression. It should not be used in the hypotensive or hypovolemic patient. Like all sedatives, thiopental causes respiratory depression.
The side effects of hypotension and bronchospasm limit the usefulness of barbiturates in the prehospital arena. These agents should probably be reserved for ED intubation.
Methohexital (1-1.5 mg/kg IV) is a short-acting barbiturate with onset in under 1 minute and duration of about 5-7 minutes. Methohexital is quite similar to thiopental in action and contraindications. It definitely causes respiratory depression and may cause seizures in high doses. The side effects of methohexital and thiopental limit their usefulness in prehospital care.
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.16
Etomidate has minimal hemodynamic effects and may be the drug of choice in a hypotensive or trauma patient.17 It causes less cardiovascular depression than either the barbiturates or propofol. Etomidate has been shown to decrease intracranial pressure, cerebral blood flow and cerebral oxygen metabolism. For these reasons, etomidate is probably the sedative drug of choice for prehospital RSI. Etomidate may decrease cortisol synthesis with one dose. In appropriate patients, steroid replacement may be used to offset this action.
Propofol (1-3 mg/kg IV) is a relatively new anesthetic induction and sedative agent. It has an extremely rapid induction time, within 10-20 seconds, and a short duration of action at 10-15 minutes. Although RSI is well described with this agent, it is unlikely that propofol will be carried by most EMS services.
Propofol decreases intracranial pressure and cerebral metabolism, and 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 procedure. The continued sedation dose is 0.75-0.15 mg/kg/minute.
Diazepam (0.2-1.0 mg/kg IV) is a moderately long-acting benzodiazepine (30-90 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. Diazepam is more useful as a long-term sedative agent for the intubated patient after the procedure. Diazepam has significant amnestic effects. It is irritating to veins and may cause localized thrombosis. Do not use for patients with glaucoma.
Lorazepam (0.1-0.4 mg/kg) is a long-acting benzodiazepine. It is most useful for long-term sedation of the intubated patient.
Midazolam (0.1-0.4 mg/kg IV) is a 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 3-5 minutes for complete effect. The typical RSI dose is much higher than a dose used for sedation and 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. It causes respiratory and cardiovascular depression. It does not increase ICP and may provide some small decrease in cerebral blood flow.
The effects of 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 in the previously awake patient or as agents in the patient with ongoing seizures. Benzodiazepines have little effect on intracerebral pressure. All of the benzodiazepines are reversible with flumazenil.
Benzodiazepines should not be used for EMS intubation, as the effects are both relatively unpredictable and better agents can be found. Benzodiazepines may be effectively used in field RSI for their amnestic effects.
The only neuroleptic agent that is useful in 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 other sedative agents, ketamine increases cardiac output, pulse rate, blood pressure, myocardial oxygen consumption, cerebral blood flow, intracranial pressure and intraocular pressure.18 Although ketamine has direct negative inotropic properties, it causes a release of endogenous catecholamines resulting in positive overall effects. Ketamine also increases salivary and bronchial secretions.19 Secretions can be decreased with atropine 0.01 mg/kg or glycopyrrolate 0.005 mg/kg.
Ketamine may cause 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.20
Ketamine is particularly useful in asthmatic patients, as it is a bronchodilator. It is the sedative of choice in the asthmatic patient with respiratory failure.21,22 It should be readily available for EMS providers.
It is contraindicated in head injury (due to both increased oxygen consumption and increased intracranial pressure associated with ketamine). It should be used with extreme caution in hypertensive patients (increases blood pressure) and those with open eye injuries and glaucoma (due to increased intraocular pressure). Ketamine may be the drug of choice in the hypotensive unstable patient, however.
The dose of ketamine for RSI in children is 2 mg/kg. At this dose, anesthesia occurs within one minute and lasts about 5-10 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.
The perfect paralytic agent would have an extremely rapid onset, a duration that is proportional to the dose used, have sedative, analgesic and amnestic properties, be safe from age 1 hour to over 100 years, have minimal side effects, and not require any special storage. This agent does not yet exist. Current neuromuscular blocking agents may be either a depolarizing agent such as succinylcholine, or nondepolarizing agents like pancuronium or curare, none of which have sedative properties.
Use of neuromuscular blocking agents is controversial, with anesthesiologists fearing increased morbidity and mortality when used by nonanesthesiologists. The largest study to date in a community hospital with emergency physicians intubating with these agents has not validated these concerns.23 The only absolute contraindication to using a neuromuscular blocking agent would be 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 drug's short duration (4-5 minutes). Succinylcholine binds to acetylcholine receptors at the neuromuscular junction and stimulates depolarization of the muscle cell. Unlike acetylcholine, succinylcholine produces continuous stimulation of the muscle cell, which is unable to return to its resting state and paralysis occurs. Paralysis will wane when the succinylcholine is hydrolyzed by pseudocholinesterase. Unfortunately, succinylcholine has significant side effects, largely related to the depolarization of the muscle cell.
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 5-20 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.24-26 (Table VI lists contraindications to succinylcholine use.) Succinylcholine can be safely used in massive trauma, burns, spinal cord injuries, etc., if used within this 5-day grace period. Obviously, patients with underlying hyperkalemia, such as renal failure patients, should not be given succinylcholine.
Prolonged paralysis: Succinylcholine can cause prolonged paralysis in patients who have a deficiency of pseudocho-linesterase or an atypical pseudocho-linesterase.27 Several drugs have also been associated with prolonged paralysis, including magnesium, lithium and quinidine.28 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.29 It is associated with markedly increased temperatures, metabolic acidosis, rhabdomyolysis, and disseminated intravascular coagulopathy. It is thought to occur once in every 15,000 patients given succinylcholine.30 This problem has prompted the FDA to ban the use of succinylcholine in infants and children except in emergency situations.31
Increased intraocular pressure: Succinylcholine causes a transient rise in intraocular pressure, which, theoretically, could cause expulsion of the vitreous in an open eye injury. There has never been a documented case of this complication despite widespread use in open eye surgery.32 The prudent practitioner will use a nondepolarizing agent in penetrating eye injuries if readily available.
Increased intracranial pressure: The significance of the rise in intracranial pressure that accompanies succinylcholine 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.33 Pretreatment may not be practical when intubation is urgent.
Muscle fasciculations: Fasciculations are asynchronous contractions of every muscle fiber. These fasciculations are present until paralysis occurs. Diffu...
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