Case of e-cigarette or vaping product use-associated lung injury (EVALI) in London, UK

Background

The health consequences of cigarette smoking are widely known among the general population and as a result of this, up to 70% of all smokers want to stop.1 Electronic cigarettes or vaping devices reached the market in 2007 and has since become increasingly popular with 3.6 million people now vaping in the UK. This is about half of the number of cigarette smokers.2 Public Health England concluded vaping is 95% less harmful than smoking cigarettes.3 Although, admittedly, this figure is based on a review in 2013 and does not account for the changes to e-cigarette devices and their liquids since then. By 2018, 52.8% of vape users had started as an aid to stopping smoking, as it has the ability to deliver the addictive nicotine without the harmful tobacco.2

Despite being considered safer than smoking, there have been a number of cases of patients developing e-cigarette or vaping product-use associated lung injury (EVALI). As of January 2020, the USA reported 2668 cases with 60 deaths as a result of EVALI.4 The outbreak of EVALI in the USA has caused a number of different lung diseases including organising pneumonia, diffuse alveolar damage and hypersensitivity pneumonitis. Tetrahydrocannabinol (THC), a potent, illegal, high-inducing cannabinoid and increasingly popular addition to vaping liquid has been present in 82% of EVALI cases in the USA.5 Of all THC associated EVALI cases, 78% of patients source it informally, that is, from friends, relatives, online or dealers.5 A recent case–control study found vitamin E acetate (VEA) in the bronchoalveolar lavage (BAL) fluid of 94% of 51 patients with EVALI and none in 99 healthy controls in the comparator group.6

Although believed to be safer than smoking, vaping still poses significant health risks. The perception of its safety has led to many non-smokers starting vaping, particularly among the younger population. However, as vaping has only been around since 2007, the long-term health consequences need to be further explored. EVALI cases in the UK have so far been less frequent than the epidemic in the USA. Here we present a probable case of vaping product use-associated lung injury in the attempt to raise awareness of the dangers associated with vaping.

Case presentation

A 38-year-old man initially presented to ambulatory care clinic with a 9-day history of headaches. No abnormality was identified on examination or CT of his head and he was subsequently discharged with a diagnosis of a migraine.

The patient then presented to the accident and emergency department 1 week later with a 3-day history of headaches and coughing. Within the previous 24 hours he had developed frank haemoptysis, approximately two tablespoons in volume, and worsening shortness of breath. The patient had no personal history of respiratory conditions, had no relevant travel history and no significant risk factors for tuberculosis infection.

On examination, the patient was hypoxic, requiring 2 L oxygen via nasal cannulae to maintain saturations of 99% with an increased respiratory rate of 22. Respiratory examination revealed bilateral coarse crackles worse on the right-hand side.

The patient was a current smoker reporting smoking approximately 8–10 cigarettes per day, along with daily cannabis for the last 28 years. Six weeks prior to admission, the patient had taken up vaping in an attempt to reduce cigarette consumption and admitted to still smoking 3–4 cigarettes a day alongside use of a vaping device. On further questioning, the patient revealed that he had been using around 10 mL of blackcurrant flavoured ‘totally wicked red label’ vaping oil per week purchased from high street shops but had been adding approximately 2 mL of a cannabis oil to each batch. This cannabis oil was bought from a friend who, unbeknownst to the patient, had manufactured it himself.

Investigations

Admission bloods showed a White cell count of 13.5 ×10⁹/L and C-reactive protein of 70 mg/l. The patient underwent a chest X-ray which identified bilateral consolidation (figure 1A).

Figure 1

(A) Plain film chest X-ray from admission demonstrating bilateral consolidation. (B) Plain film chest X-ray 2 months after initial presentation demonstrating resolution of consolidation.

A CT of the thorax showed bilateral bronchocentric marked ground glass changes in-keeping with an inhalational injury with areas of haemorrhage (figure 2).

Figure 2

There is widespread ground-glass opacification with an upper lobe predominance. There are areas of ground-glass opacification with intralobular and interlobular septal thickening giving a crazy paving appearance. Ground-glass opacification is predominantly in a bronchocentric distribution but there are patchy areas of peripheral opacification.

A respiratory viral screen including influenza A virus RNA, influenza B virus RNA, human metapneumovirus RNA, parainfluenza virus type 1, 2 and 3 RNA, Respiratory syncytial virus subgroups A and B RNA, rhinovirus RNA and adenovirus RNA were all negative.

HIV and hepatitis B and C were not detected, blood cultures remained negative. Sputum culture showed normal respiratory flora and sputum analysis for acid-fast bacilli were both smear and culture negative. A connective tissue disease screen was negative. Anti-myeloperoxidase (MPO) antibodies and anti-proteinase (PR3) antibodies were <0.2. There were no monoclonal immunoglobulins detected. Anti-glomerular basement membrane antibodies were <0.8.

Coxiella burnetii complement fixation test (CFT), Chlamydia genus CFT and mycoplasma serology were <1:16.

A bronchoscopy was performed the day after discharge, the endobronchial appearances were normal throughout. BAL fluid showed a heavy growth of Escherichia coli which was resistant to amoxicillin and co-amoxiclav. It was sensitive to tazocin and ertapenem but at the time of washings the patient had already completed his course of antibiotics. Acid-fast bacilli were not seen and no fungi were isolated. Microscopy of the fluid showed it to contain squamous cells, ciliated respiratory epithelial cells, lymphocytes and macrophages with no malignant cells.

Unfortunately, a sample of the patients e-liquid was not obtained and therefore not screened for compounds such as VEA.

Differential diagnosis

Differential diagnoses included primarily inhalation injury, pulmonary vasculitis, tuberculosis and atypical infection.

Treatment

The patient was started on intravenous tazocin on admission but by day 3 reported no improvement in symptoms. He was then started on 30 mg of prednisolone once a day for 2 weeks followed by a reducing regime. He was discharged on day 6 of admission with tazocin having been stepped down after 72 hours to oral co-amoxiclav and clarithromycin to complete 7 days total of antibiotics. He attended the day after discharge for outpatient bronchoscopy.

Outcome and follow-up

The patient improved rapidly with steroid treatment and had no further episodes of haemoptysis. His oxygen saturations on discharge were 98% on room air. He remained without a fever throughout his admission.

In respiratory clinic 2 months after initial admission, the patient underwent a repeat chest X-ray which showed complete resolution of previous changes (figure 1B), however he still reported significant breathlessness particularly on exertion with an exercise tolerance of only 200 m.

The patient underwent a further CT of the thorax 3 months after his initial presentation which demonstrated complete resolution of the previously noted bronchocentric ground-glass opacification. He had not used the cannabis oil or his vaping device since his discharge from hospital nor had he used cannabis. He continued to smoke traditional cigarettes.