How to rescue a crashing asthmatic patient in a remote emergency department: Ketamine and non-invasive ventilation

INTRODUCTION Management of the patient in a severe asthma exacerbation (SAE) can be incredibly challenging. These patients are at risk of developing respiratory failure and arrest and may require intubation and invasive mechanical ventilation. The risks of intubating and ventilating these patients include laryngospasm, worsening bronchospasm, gas trapping, barotrauma and cardiac arrest.1 When performing rapid-sequence intubation of a patient in SAE, ketamine is often the induction drug of choice.2 Ketamine is a dissociative anaesthetic which can provide sedation while maintaining cardiorespiratory reflexes. The risks of hypotension and respiratory depression from ketamine are low. Ketamine is also a bronchodilator, which is an additional benefit to using this drug in patients with obstructive lung disease.3 Because of these unique properties, ketamine can also be used to perform delayed-sequence intubation, where the drug facilitates pre-oxygenation of an agitated patient in respiratory failure prior to administering a paralytic and performing a controlled intubation.2 Ketamine has also been found to improve the respiratory status of intubated patients in SAE despite 24 h of conventional therapy and mechanical ventilation.4 There is emerging evidence that ketamine sedation can also facilitate non-invasive positive pressure ventilation (NIPPV) in agitated patients with respiratory failure, avoiding intubation altogether. A retrospective study published in 2024 found ketamine to improve NIPPV tolerance in agitated patients with severe exacerbations of heart failure, chronic obstructive pulmonary disease (COPD) and asthma.5 In a case similar to ours, a 36-year-old male in respiratory failure due to SAE failed conventional medical treatment and did not tolerate NIPPV due to agitation.6 He received six bolus doses of ketamine 50 mg intravenous (IV) over a 40-min period which allowed him to tolerate NIPPV and improve his respiratory acidosis. The patient continued to improve after ketamine was discontinued and was discharged from hospital 48 h after his ED presentation. In this article, we describe a scenario in which a patient presented in SAE to a small remote hospital that was not equipped with an intensive care unit (ICU). We were able to manage our patient with ketamine sedation and non-invasive ventilation, avoiding the risks of intubation and invasive ventilation in our resource-limited setting. Our patient had a highly positive outcome, and we suggest this strategy be considered as definitive management for status asthmaticus in both resource-limited and resource-rich settings. CASE REPORT A 51-year-old female presented to our remote emergency department in Happy Valley-Goose Bay, Newfoundland and Labrador, in March 2019 complaining of shortness of breath and a non-productive cough. She had a past medical history of asthma and a 25 pack-year smoking history. She had been treated in our emergency room several times over the preceding 3 months for asthma exacerbations. On initial examination, she had mildly increased work of breathing, a respiratory rate of 24, oxygen saturation of 96% on room air, heart rate of 110 and blood pressure of 150/90. Expiratory wheezes were heard on auscultation of her bilateral lung fields. A venous blood gas showed a pH of 7.4 and pCO2 of 47 mmHg. She was treated promptly with nebulized salbutamol and ipratropium and prednisone 50 mg orally. She remained in our ER for observation. Several hours later, the patient rapidly deteriorated. Her oxygen saturation decreased to 90% and she developed severe increased work of breathing with subcostal retractions and a respiratory rate of 40. Her chest was silent. Her mental status changed and she became agitated. She was placed on nasal prong oxygen which was titrated up to 8 L/min. She was treated with continuous nebulized salbutamol and ipatropium, epinephrine 0.3 mg intramuscular, magnesium sulphate 2G IV and methylprednisolone 100 mg IV. A portable chest X-ray was normal. We attempted to start NIPPV, but she became increasingly agitated and did not tolerate this. An arterial blood gas revealed a pH of 7.2 and a PaCO2 of 65 mmHg. At this point, the patient was evidently in hypercarbic respiratory failure and at risk of respiratory arrest. Our 25-bed health centre was staffed by family physicians with limited specialist backup. Our community had a single anaesthesiologist on-call year-round, supported by two local respiratory therapists. We did not have any local internal medicine specialists. We had a special care unit in which we offered cardiac monitoring and NIPPV. Our established practice was to transfer patients requiring higher levels of care to St. John’s, NL. Due to the remote location of our community, air ambulance transfer was required for all transfers to St. John’s. The flight time was typically 2 h. In our case, intubation and invasive mechanical ventilation would have certainly been required prior to air transfer. Wary of the risks of intubating and ventilating a patient in a SAE in our resource-limited setting, we decided to try ketamine for its bronchodilating and sedating properties. Our hope was to decrease the patient’s agitation to help her tolerate NIPPV. Immediately prior to giving ketamine, the patient’s respiratory rate was 40, heart rate was 130, blood pressure was 173/95 and her oxygen saturation was 94% on 8 L/min of nasal prong oxygen. We gave the patient 1 mg/kg of ketamine, administered intravenously over a slow push. Within minutes her work of breathing improved and her respiratory rate decreased to 24. She had improved air entry on auscultation of her lungs. Her heart rate and blood pressure increased slightly to 136 and 174/104. The ketamine achieved light sedation, decreased the patient’s agitation and allowed the patient to tolerate NIPPV. Thirty min following the first ketamine dose, the patient’s respiratory rate increased to 30 and she became slightly agitated again. We repeated a ketamine 1 mg/kg IV bolus and started a ketamine infusion of 0.5 mg/kg/h IV. This dose maintained light sedation and allowed for the continuation of NIPPV with an FiO2 of 35%, a peak end expiratory pressure of 5 cmH2O and a peak inspiratory pressure of 13 cmH2O. She maintained a spontaneous respiratory rate of 24. Continuous nebulised salbutamol was given while she was on NIPPV. Ceftriaxone 2G IV and azithromycin 500 mg IV were also given. Normal saline maintenance fluid was started at 100 cc/h. Following 4 h of the ketamine infusion and NIPPV, the patient’s work of breathing and air entry was greatly improved. The ketamine infusion was stopped and the patient quickly returned to a normal mental status with a Glasgow Coma Scale of 15. She was not agitated and was able to tolerate the NIPPV for several hours without sedation. Serial arterial blood gasses showed improvement in her pH to 7.4 and her PaCO2-33 mmHg. NIPPV was then discontinued and she was admitted to the inpatient unit of our hospital on 2 L of nasal prong oxygen. Methylprednisolone 100 mg IV was continued every 6 h and salbutamol nebules were continued every 4 h. The following morning, the patient was alert and oriented, sitting up and eating breakfast. She was able to speak in full sentences and reported feeling much better. Her oxygen was 94% on room air, respiratory rate was 24, heart rate was 112 and blood pressure was 142/82. She had an unexpected finding of excessive urinary output of 500 cc/h for a 10 h period on day 3 of admission. She was moderately hypernatremic and hyperchloremic with a serum sodium of 154 and chloride of 117. All other electrolytes were normal. Her kidney function was normal. We suspected she had urea osmotic diuresis secondary to steroid-induced tissue catabolism.7 We changed her maintenance fluid to dextrose 5% in 0.45% saline and began weaning down her steroid doses. Within 24 h, her urine output and electrolytes normalised. Four days following her emergency room presentation, the patient felt well, had normal vital signs and was discharged from the hospital. DISCUSSION Our case demonstrates the successful use of ketamine and NIPPV as definitive management of a patient in respiratory failure secondary to SAE. This strategy prevented intubation, invasive mechanical ventilation and an air-ambulance transfer to a tertiary care centre. Our dose regimen of ketamine 1 mg/kg IV boluses followed by 0.5 mg/kg/h IV infusion was effective in achieving light sedation that allowed the patient to tolerate NIPPV with spontaneous respiration and a return to her baseline mental status once the infusion was stopped. Ketamine has known risks of hypertension, tachycardia, vomiting, apnoea and laryngospasm.8 The only adverse effects observed in our case were mild and short-term increases in heart rate and blood pressure. The patient’s length of stay in hospital was much shorter than would be expected if she had been intubated. We suspect her electrolyte abnormalities and excessive diuresis were the complications of excessive IV steroids rather than ketamine. A limitation of our study is the absence of pulmonary function testing to distinguish if this patient had any asthma-COPD overlap, which may have affected her treatment response. An additional limitation is that we are unable to ascertain whether the patient’s positive outcome was primarily due to the bronchodilating effects of ketamine, or due to the sedating effect of ketamine that allowed her to tolerate NIPPV. We suspect she benefitted from both properties. Future randomised controlled trials comparing NIPPV with ketamine versus alternative sedating agents or placebo would be helpful to further understand the unique benefits and risks of ketamine treatment in patients with respiratory failure. We conclude that a ketamine infusion combined with NIPPV is a promising treatment strategy to manage patients with SAE, especially when agitation is limiting the effectiveness of NIPPV alone. This treatment approach can prevent intubation and invasive mechanical ventilation, which may be particularly helpful to clinicians working in remote facilities without access to an ICU. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest.

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