Emergency Medical Service (EMS) presents with a 26-year-old male who is agitated and combative, in severe respiratory distress. Per EMS report, he has a history of asthma, and bystanders found him in severe respiratory distress after using crack cocaine. He has been intubated in the past for his asthma, often triggered by cocaine use, most recently 2 months ago during which he spent a week in the intensive care unit (ICU). He arrives at the emergency department (ED) after an EMS transport of 15 minutes during which he has been receiving continuous aerosolized albuterol via a nebulizer. He required restraints en route, is screaming in one- to two-word sentences on arrival, and is thrashing around the bed.

He is 5′ 2″ (157 cm) tall and weighs 165 lb, with a BMI 30.5 kg·m⁻². His vital signs are: respiratory rate 24 breaths per minute, heart rate 134 beats per minute, and blood pressure 110/60 mm Hg. He is diaphoretic and using his accessory muscles. His oxygen saturation is 89% on 15 L·min⁻¹ of oxygen via a non-rebreather and he is quickly becoming fatigued. You notice he has a scar on his neck from a prior cricothyrotomy and a steroid body habitus with an edematous face and short neck.

What Are This Patient’s Vital Organ System Reserves?

CNS reserve: There is nothing to indicate that this patient will respond abnormally to standard doses of induction agents, keeping in mind that he is obese and should be dosed accordingly. The patient is agitated and confused on arrival, which may be a consequence of crack cocaine use as well as carbon dioxide retention, in which case sensitivity to sedative hypnotic induction agents ought to be anticipated.

Cardiovascular reserve: This is a young patient who should theoretically have adequate cardiac reserve and normal systolic and diastolic cardiac function. Cocaine may stun the myocardium in high doses and cause sodium channel blockade. Respiratory acidosis can potentiate myocardial depression associated with anesthesia induction agents. Depending on the length of time he has been acutely ill and how adequate his oral fluid intake has been, he could also be relatively volume depleted. In combination with a decrease in venous return secondary to air trapping and auto-PEEP (positive end-expiratory pressure) seen with acute asthma, the presence of hypovolemia can precipitate a significant hypotension, particularly if induction agents are used to facilitate intubation.¹ The patient has been receiving a large amount of albuterol, a medication with significant β₂-agonist properties. β₂-agonists cause intracellular shifting of potassium, which may lead to hypokalemia and arrhythmias.² The combination of stress, respiratory acidosis, and large amounts of albuterol use can increase this patient’s risk of arrhythmias. When choosing induction agents, it is important to keep in mind that they all have negative inotropic properties for this patient.

Respiratory reserve: Patients with severe asthma have prolonged expiratory phases and air trapping.³ Peak flow and forced expiratory volume in 1 second (FEV₁) may be used to assess the degree of airway obstruction and to monitor improvement with treatment. Tidal volumes are limited, with minimal or no respiratory reserve. Substantial ventilation–perfusion mismatch is present, which limits the ability to oxygenate and denitrogenate the lungs prior to induction. Ventilation support may be necessary in severe asthma as these patients become significantly fatigued and unable to maintain gas exchange on their own. Ventilation support may be provide mechanically, requiring intubation or noninvasively by mask using noninvasive positive pressure ventilation (NPPV). These patients are at risk for rapid oxygen desaturation and worsening hypercapnea as apnea ensues as part of a rapid sequence intubation (RSI). But, the real challenge in managing the severe asthmatics occurs in the post-intubation phase.

Employing the Mnemonics Suggested in Chapter 1, Does This Patient Have a Difficult Airway?

Yes! Facial and neck edema from chronic steroid dependence may make bag-mask-ventilation (BMV) difficult. In addition, this patient is obese and in status asthmaticus, both of which are associated with very high airway pressures that can be difficult or impossible to overcome with a positive pressure BMV. Other than these factors, there appear to be no other predictors of a difficult BMV when applying the mnemonics MOANS (see section “Difficult BMV: MOANS” in Chapter 1).

While the LEMON mnemonic (see section “Difficult DL Intubation: LEMON” in Chapter 1) suggests that neck and face edema may make direct laryngoscopy difficult, there are no predictors of difficult use of video-laryngoscopes (CRANE, see section “Difficult VL intubation: CRANE” in Chapter 1). Subglottic stenosis is important to consider in this patient as he has experienced many tracheal intubations in the past, in conjunction with corticosteroid use and mechanical ventilation. However, the geometry of his upper airway appears normal, and he has a Mallampati Class II airway. His neck appears to be freely mobile.

Another mnemonic to assist the assessment of the feasibility of using an extraglottic device (EGD) is RODS (see section “Difficult Use of an EGD: RODS” in Chapter 1). Restricted mouth opening is not an issue in this patient and upper airway obstruction is only a possibility. However, he has severe obstructive lung disease and his compromised pulmonary compliance, the “stiffness of the lungs,” will seriously limit usefulness of an EGD just as BMV may be difficult.

There are several indicators of a potentially difficult airway in this patient, and he may not be an optimal candidate for an RSI. A failed intubation in a hypoxemic person with very poor lung compliance would be a very dangerous situation. A surgical airway may be difficult in this patient since he has a history of a cricothyrotomy and redundant neck tissue (SHORT, see section “Difficult Cricothyrotomy: SHORT” in Chapter 1). The decision to perform RSI should be in the context of the experience of the practitioner as well as the device(s) being used and availability of backup. For instance, the use of RSI may be very different if the practitioner is using a video-laryngoscope versus a standard laryngoscope.

What Other Airway Concerns That You Have for This Patient?

This patient has no respiratory reserves, rapid oxygen desaturation, hypotension, and possible subglottic stenosis. The insertion of a tracheal tube in a person who is already in bronchospasm may exacerbate his condition.

Have We Medically Optimized His Treatment Prior to Tracheal Intubation?

Patients should receive continuous supplemental oxygen to keep O₂ saturations above 90%. Short-acting β₂-agonists are the mainstay of treatment in asthma, via a nebulizer or metered dose inhaler.⁴ Long-acting β₂-agonists have a longer onset of action of at least 20 minutes and are not an effective rescue medication. This patient has already been on continuous bronchodilators for the 15-minute transport and is receiving supplemental oxygen via a non-rebreather. The addition of corticosteroid is recommended for patients with an acute moderate to severe exacerbation of asthma,⁵ although the delayed onset of action for corticosteroids (onset within a few hours, peak effect around 24 hours) will not be helpful in avoiding intubation in the immediate/emergency period. Since there is no evidence to suggest that IV steroid has an advantage over the oral route, oral steroids should be administered unless the patient is not tolerating the oral route. For reasons already outlined, avoiding intubation would be the best option if possible.

What Additional Medical Therapeutic Options Are Available to This Patient?

Anticholinergics: Meta-analysis suggests that there is a modest benefit in adding this therapy to β-agonists.⁶ Antagonizing cholinergic effects at muscarinic receptors can reduce smooth muscle contraction and the release of secretion at large airways. The use of anticholinergics such as ipratroprium bromide reduces hospital admission rates (30%–60%, NNT 5–11).⁷

Magnesium: Two meta-analysis have been performed analyzing the effect of IV magnesium on patients with asthma.^8,9 Seven trials were identified and the investigators conclude that magnesium has no confirmed role in the management of mild or moderate asthma. In severe asthma, there is evidence that magnesium improves pulmonary function and decreases hospitalization rates, although there is no good evidence that magnesium decreases the need for intubation in patients with severe asthma. Magnesium is unlikely to cause harm. However administration should not delay intubation or any other therapy.

Noninvasive ventilatory support (NIVS): One randomized trial and several small uncontrolled trials support the use of NIVS in acute asthma.^10–14 NIVS has been demonstrated to improve expiratory flow rates and reduce the need for hospitalization, although a recent meta-analysis by Ram et al.¹⁵ concluded that routine use of NIVS in severe acute asthma could not be recommended. Patients who have an alert mental status and intact airway reflexes may be good candidates to trial NIVS before considering intubation. The patient in this case is uncooperative and combative so we need to consider intubation instead.

What Are the Possible Options Regarding Airway Management in This Patient?

A trial of NIPPV could be considered. This patient is very uncooperative and therefore would require sedation. A trial of ketamine at lower doses and NIPPV could be considered very carefully. In one study, this was used to denitrogenate patients but it was found that a few patients were able to tolerate NIPPV after the low-dose ketamine and intubation was averted.¹⁶ In this particular group of patients, and despite the reservations that have been mentioned, RSI by a skilled practitioner is probably the best choice. Planning ahead is crucial, as is deciding on a Plan B and C in the event Plan A should fail. While recognizing the limitations of denitrogenation prior to tracheal intubation (described above), the practitioner should administer as high an oxygen concentration as possible to the patient, employing a bag-mask unit if the patient can tolerate its use. Use of nasal cannula during the apneic phase has been shown to delay desaturation.^16,17 This should be applied prior to induction and left on during the peri-intubation phase. As an added advantage, the practitioner can provide gentle assisted ventilation to the patient if he is able to tolerate it, taking care not to cause insufflation of the stomach, vomiting, or gagging. Rapid sequence induction drugs chosen should be administered to the patient while he remains in a comfortable position, in this patient most commonly sitting upright. Once the patient loses consciousness, the patient can be placed in the supine position for laryngoscopy and intubation. A large, 8.0-mm ID or larger, endotracheal tube (ETT) is preferred in order to reduce resistance and facilitate aggressive pulmonary toilet. However, given patient’s prior history of multiple intubations and cricothyrotomy, a series of smaller sized ET tubes should be available in anticipation of potential airway stenosis.

Lidocaine dosed at 1.5 mg·kg⁻¹ has been used to attenuate the reflex bronchospasm in response to airway manipulation and to decrease arrhythmias during intubation.^18–20 However, the effectiveness of lidocaine has varied among studies.²¹ The recommendation to use IV lidocaine in RSI protocols for the severe asthmatic is extrapolated from the results of studies employing healthy volunteers with a history of bronchospastic disease.^21–24 However, in a prospective, randomized, double-blind, placebo-controlled trial of 60 patients, lidocaine and placebo groups did not have significantly different transpulmonary pressure and airflow immediately after intubation and at 5-minute intervals.²⁵ Given that there is no established evidence that lidocaine improves long-term outcomes, its use is provider dependent.

Ketamine is generally considered to be the induction agent of choice in the asthmatic patient because it increases circulating catecholamines and inhibits vagal outflow. In addition, it is a direct smooth muscle dilator that does not cause histamine release.²⁶ While case reports of dramatic improvement in pulmonary function with ketamine have driven its popularity,^27,28 no randomized studies have been performed to demonstrate ketamine’s superiority over other induction agents. In a case series, 19 of 22 asthmatic patients with active wheezing had a decrease in bronchospasm during ketamine-induced anesthesia.²⁹ In one prospective, placebo-controlled, double-blind trial of 14 mechanically ventilated patients with bronchospasm, the seven patients treated with 1.0 mg·kg⁻¹ ketamine had a significant improvement in oxygenation but no improvement in PCO₂ or lung compliance. In addition, the outcome (discharge from the ICU) was the same in both groups. The study population was heterogeneous, making valid conclusions of the benefit of ketamine difficult.³⁰ A randomized, double-blind, placebo-controlled trial of low-dose IV ketamine, 0.2 mg·kg⁻¹ bolus followed by an infusion of 0.5 mg·kg⁻¹·h⁻¹, in non-intubated patients with acute asthma failed to demonstrate a benefit in IV ketamine.³¹ Although evidence is limited, at the present time, based on its mechanism of action and safety profile, ketamine appears to be the best agent available for RSI in the asthmatic. Intravenous ketamine 1.5 mg·kg⁻¹ should be given immediately before the administration of 1.5 mg·kg⁻¹ of succinylcholine. Ketamine may have central sympathomimetic effects and this should be carefully considered in patients with cardiac ischemic, intracranial injury, or elevated intraocular pressures. In these patients, etomidate may safely be used as an alternative induction agent.

Delayed sequence intubation (DSI) can also be considered. In contrast to RSI, DSI allows for the administration of sedatives and denitrogenation before the administration of a paralytic agent and intubation. One prospective observational case series studied DSI in patients who were spontaneously breathing and did not tolerate denitrogenation. The patients in this study were given an initial dose of ketamine at 1 mg·kg⁻¹ followed by 0.5 mg·kg⁻¹ boluses until patients were dissociated. The study concluded that DSI allowed denitrogenation and significant improvement in oxygen saturation in patients who did not tolerate oxygenation with traditional methods (BVM, NIPV, etc.). In agitated patients similar to the one in the case above, DSI may provide an opportunity for sedation and oxygenation that might eliminate the need for intubation if the patient improves or simply increase oxygenation prior to intubation.

How Would You Intubate the Trachea of This Patient?

1. 
   

   Pre-Procedure Preparations:

   
   

   The following difficult airway devices should be ready if available:

   
   
   
   
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     an Eschmann Tracheal Introducer (also known as gum-elastic bougie)

     
     
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     a fiberoptic or video-laryngoscope if available

     
     
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     a cricothyrotomy kit

     
     
   • 
     

     an EGD, or an intubating LMA™

     
     

     The following drugs should be available:

     
     
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     ketamine at 1 to 2 mg·kg⁻¹

     
     
   • 
     

     succinylcholine at 1.5 to 2 mg·kg⁻¹

     
     
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     Rocuronium 1.2 mg·kg⁻¹

     
     
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     sedation and paralytic agents for post-intubation management

   
   
   
   
2. 
   

   Cardiac monitors are applied along with pulse oximetry. Denitrogenation is achieved using high-flow oxygen with the patient sitting.

   
   
3. 
   

   Ketamine is administered IV and the patient is observed until unconscious. This should take 1 to 2 minutes.

   
   
4. 
   

   Succinylcholine (or rocuronium if there are contraindications to succinylcholine use) is administered. The patient is placed supine with the head and neck placed in a “sniffing” position. Cricoid pressure may be applied by an assistant. The patient is observed for fasciculations.

   
   
5. 
   

   Laryngoscopy is performed. The cords are visualized easily and the ETT is passed and secured.

   
   
6. 
   

   Capnography is used to confirmed correct tracheal placement.

   
   
7. 
   

   Post-intubation drugs are administered for sedation and paralysis.