Sedation challenges in patients with E-cigarette, or vaping, product use-associated lung injury (EVALI)

Background

E-cigarette, or vaping, product use-associated lung injury (EVALI) has become a recent epidemic affecting patients across USA. There is an increasing concern given that it disproportionately affects young and otherwise healthy patients. Recently, over 2100 cases have been reported in 49 states that have resulted in at least 42 deaths.1 2 Health agencies have released warnings on the use of E-cigarettes, especially those containing the psychoactive ingredient THC.1–7 Studies have analysed the physiological effects on cannabis users in regard to cardiovascular, cerebrovascular and respiratory associations.8 9 Patients using these products, whether for medical or non-medical reasons, may be at increased risk of adverse events. We present a case of THC-related EVALI in a young, healthy patient who rapidly progressed to acute respiratory failure with a focus on the challenges encountered regarding sedation and analgesia during mechanical ventilation.

Case presentation

A 23-year-old woman with no reported medical history or prescription medication use presented with myalgias, subjective fevers, dyspnoea, cough and intermittent confusion for 6 days. On examination, the patient was well-nourished, uncomfortable appearing, tachypneic but able to speak in full sentences. Other than tachypnea, pulmonary auscultation was without abnormalities. Body mass index noted 25.87 (70.83 kg). Physical examination was otherwise unremarkable.

On admission to the general medical ward, a workup revealed mild leucocytosis with normal urinalysis. The patient had a fever with T_max was 101.7°F and remained tachycardic despite appropriate intravenous fluids. Chest X-ray was unremarkable (figure 1). CT angiography revealed non-specific bilateral subpleural ground-glass opacities concerning for atypical infection versus acute pneumonitis (figures 2 and 3). A thorough social history revealed no alcohol or prescription drug abuse. The patient did endorse extensive vaping, up to several times an hour, using a combination of Juul nicotine cartridges, prefilled cartridges obtained both online and from a friend known to contain an unknown concentration of THC, as well as ‘Dank Vapes’ in the month leading up to admission. A urine drug screen was consistent for THC in the patient’s system.

Figure 1

Chest X-ray on admission non-specific peripheral infiltrates without effusions or hilar abnormalities.

Figure 2

Coronal CT thorax with contrast patchy subpleural ground-glass opacities with sparing of majority of central parenchyma. No effusions noted.

Figure 3

Axial CT thorax with contrast bilateral lower lobe ground-glass opacities in a posterior distribution. No honeycombing or bronchiectasis noted.

On the third day of admission, the patient was transferred to the intensive care unit (ICU) for worsening hypoxia. She was in apparent respiratory distress, tachypneic to a rate of 42/min and only able to speak in two to three word sentences. Pulmonary auscultation revealed diffuse rhonchi with bibasilar crackles. The remainder of her haemodynamics were as follows: BP: 137/56; mean arterial pressure: 83 mm Hg; temperature 101.8°F (38.8°C); volume status: euvolemic. Immediately on transfer to the ICU, the patient developed worsening respiratory distress with intermittent hypoxia and SpO₂ measurements to 50%–60% via pulse oximetry while on 100% high flow nasal cannula (Optiflow at 60 L/min). Each episode of hypoxia resolved, with the return of SpO₂ into the 90 s. The patient was prepared for immediate intubation with procedural consent for intubation able to be obtained from both patient and her mother. The patient and her mother reported no prior intubations or a known history of first degree relatives with reactions to anaesthesia. Given the emergent nature to proceed with intubation, a blood gas was not obtained prior to intubation.

The medical team prepared for rapid sequence intubation (RSI) with standard dosing of propofol 1.5 mg/kg and rocuronium 1 mg/kg. Patient was preoxygenated via high flow nasal cannula (Optiflow) 60 L/min at 100% FiO₂ and a time-out completed. RSI was administered while patient maintained oxygenation via high flow nasal cannula during the procedure. After 45 s, patient was noted to have respiratory effort and a clenched jaw, however, no other muscle rigidity noted. An additional 0.5 mg/kg propofol was administered with notable relaxation of her jaw and; patient was no longer initiating her own breaths and a prompt desaturation to 50% measured via pulse oximetry was noted. She was successfully and quickly intubated with the return of oxygen saturation to >95%. No muscle rigidity was noted postintubation and patient remained afebrile with continuous temperature monitoring.

Differential diagnosis

Given the patient’s presentation, imaging findings and acute progressive decompensation, a broadened differential including infectious, auto-immune and toxin-mediated lung injuries were considered. Bronchoscopy was conducted with transbronchial biopsies of the left lower lobe revealing diffuse alveolar damage consistent with a toxin-induced lung injury (figure 4A–C) and together with her CT findings, a potential diagnosis of EVALI.7 10 Infectious workup remained negative, and bronchial alveolar lavage (BAL) were unremarkable.

Figure 4

(A–C) Pathology slides from transbronchial biopsies. A: 100×; B: 200×; C: 400× features show severe acute lung injury consistent with diffuse alveolar damage. The interstitium is mildly expanded by oedema and there are a moderate number of eosinophilic hyaline membranes in alveolar spaces constituting diffuse alveolar damage. There are no eosinophils, evidence of haemorrhage, granulomas or giant cells. Grocott’s methenamine silver (GMS) stains did exclude the possibility of pneumocystis or fungal infection. Additional hematoxylin and eosin (H&E) stains did not reveal any additional features.

Treatment

Initially, to cover for the potential etiologies that could create the specific CT findings, broad-spectrum antibiotics for respiratory pathogens were initiated. After her BAL findings, antibiotics were discontinued and she was initiated on intravenous methylprednisolone for 3 days given high suspicion for EVALI.3 7 10 Appropriate sedation and anxiolysis monitored by the Richmond Agitation-Sedation Scale (RASS) goal of 0 was very difficult; the patient required continuous infusions of fentanyl, propofol, dexmedetomidine and midazolam.

Outcome and follow-up

After 4 days the patient was extubated, steroids were discontinued, and she was ultimately discharged on 2 L/min supplemental oxygen for residual hypoxia. The patient returned 1 week later with dyspnoea and chest discomfort. Imaging revealed pneumothorax and pneumomediastinum with a left-sided apical bullous lesion and subcutaneous emphysema in the background of pan-lobar fibrosis, likely related to her previous inflammatory lung insult (figure 5). She only required supportive measures with nasal cannula oxygen and pain management until discharge. Follow-up in pulmonary clinic revealed no recurrent events after cessation from vaping.

Figure 5

Chest X-ray on two different admissions (A) First admission (2 days into admission): patchy bilateral subpleural ground glass opacities. (B) Second admission (7 days post discharge): diffuse subcutaneous emphysema with pneumomediastinum and large left apical blebbing in the background of diffuse fibrotic parenchymal lung changes.