Lung injury from e-cigarette use: a foul and pestilent congregation of vapours

Abstract

A 62-year-old man presented with worsening dyspnoea, haemoptysis and reduced exercise tolerance. He was found to be hypoxaemic with bilateral basal opacification on chest imaging, but inflammatory markers, respiratory virus PCR and sputum culture demonstrated no signs of infection. The patient reported having initially mild, yet progressive, symptoms since he started vaping 14 months previously. He was treated with oxygen therapy, supportive care and cessation of vaping. Chest imaging at discharge showed marked improvement of previous bilateral opacification and the patient returned to baseline exercise tolerance, with no oxygen requirement. Vaping is becoming more common in the UK and this case demonstrates the importance of considering electronic vaping-associated lung injury in cases of non-infective lung injury.

Background

Electronic vaping-associated lung injuries (EVALIs) have been previously reported in the USA, with over 1000 cases reported since June 2019.¹ However, despite large amounts of people vaping regularly, cases have yet to be reported in the same number in the UK. As of 2018, an estimated 6.2% of adults were vaping in the UK,² and this figure is probably now higher. Lung injury associated with e-cigarette use has been predominantly associated with the use of liquids containing vitamin E acetate or tetrahydrocannabinol and not sourced from mainstream commercial vendors. EVALIs have been described based on a number of presentations, from spontaneous pneumothoraces to diffuse alveolar haemorrhage and organising pneumonia.^3–5 As a result, the diagnosis is difficult to make and the current management relies solely on injury severity, clinical judgement and empirical lung insult treatment.⁶

We report a case of a probable EVALI in a North London hospital where no other cause for the patient’s presentation was found and there was improvement following cessation of vaping.

Case presentation

A 62-year-old Caucasian man presented to the A&E department with dyspnoea, haemoptysis and reduced exercise tolerance in December 2019. He reported approximately 14 months of milder symptoms, but worsening over the preceding 3–4 weeks. On examination, he was found to be tachypnoeic, hypoxaemic and there were bibasal crepitations on auscultation but no wheeze. Cardiovascular and abdominal examination was unremarkable, and he was afebrile and normotensive. Clinical examination found no signs of peripheral oedema and he was deemed clinically euvolaemic. The patient reported that his weight was stable and no lymphadenopathy was felt on examination. He had no history of Tuberculosis (TB), no recent travel, no new pets or occupational exposure.

He started vaping using an e-cigarette device around 14 months previously, and also had a 30 pack-year history for tobacco. He denied smoking any illicit substances, including cannabis. There was no spirometry diagnosis of Chronic obstructive pulmonary disease (COPD) and the patient denied any asbestos exposure. The patient attended A&E for pleuritic pain and dyspnoea in November 2018, correlating to the time that he commenced vaping, but this was a short self-limiting episode and required only analgesia. The patient did not come to medical attention again until this more severe episode.

Investigations

On admission, routine bloods demonstrated no signs of acute infection, with a normal white cell count (6.98 total, eosinophil count 0.22) and C reactive protein level (1.3), and no evidence of blood dyscrasia or hepatorenal dysfunction.

Chest radiograph on admission (figure 1) demonstrated patchy, diffuse opacification in the lower zones. Importantly, the heart size was normal, no pleural effusion was seen. The patient then had a CT pulmonary angiogram (CT-PA) within 24 hours of admission, no embolism was demonstrated in the central or segmental vessels. This initial chest imaging showed a background of emphysematous change in both upper lobes with diffuse consolidative change in the left mid and lower zones and right lower zone (more pronounced posteriorly). No changes suggestive of fibrosis or bronchiectasis were seen on the CT chest imaging (figure 2).

Figure 1.

Posteroanterior chest radiograph on admission, showing widespread bilateral lung field opacification, worse at the bases.

Figure 2.

Axial CT image through the lower chest showing widespread bilateral consolidation, consistent with acute lung injury. Note the underlying emphysematous change.

The patient also had his sputum cultured for bacterial growth and a swab sent for respiratory virus PCR, both of which were negative. An autoimmune screen was also performed and returned negative.

As the patient recovered on the ward, his condition was monitored with interval chest radiographs. These images demonstrated clear improvement over his 14-day admission. The patchy consolidation in the left middle zone markedly improved to complete resolution at discharge (figure 3), and that in the left and right lower zone also significantly improved. In addition, lung function testing at discharge produced a normal transfer factor result, making pulmonary haemorrhage unlikely.

Figure 3.

Posteroanterior chest radiograph at discharge showing almost complete resolution of previous radiographic changes seen on admission chest X-ray (figure 1).

Differential diagnosis

As previously mentioned, EVALI is largely a diagnosis of exclusion and therefore initial differential diagnosis represented a long list of pulmonary conditions. The severe hypoxaemia on admission meant that pulmonary embolism was considered, but a clinically significant embolism was ruled out by CT-PA. Additionally, common diagnoses such as viral and bacterial pneumonias had to be ruled out early in the admission. The patient presented with normal blood test results, negative cultures and negative viral throat swab PCR: making a bacterial or viral infective driver unlikely. An autoimmune screen was also negative.

The significant smoking history of the patient (30 pack-year) meant that pulmonary malignancy was a potential diagnosis, ruled out by chest imaging and improvement of symptoms. Similarly, the smoking history and emphysematous change are suggestive of undiagnosed COPD, and thus this presentation may have represented an acute exacerbation of that condition. However, the lack of an infective component, the patchy opacification on chest radiograph and physical examination findings makes this diagnosis unlikely.

The final diagnosis was that of EVALI, an acute non-infective lung injury related to vaping, and which appears to improve quickly after cessation of vaping. At this point, all other diagnoses had been effectively excluded, and with the patient’s presentation correlating with his e-cigarette usage and his improvement having ceased vaping, this diagnosis was thought to be the most likely explanation for the presentation.

The pathophysiology of EVALI is not clearly understood, but non-cardiogenic pulmonary oedema has been observed in some cases. Diuretic treatment was not prescribed for this patient as there were no clinical or radiological signs of fluid overload, and therefore it is unlikely that pulmonary oedema was the mechanism of lung injury in this case. It is more likely that this patient’s EVALI was a form of acute hypersensitivity pneumonitis, with vaping being the provoking factor. The radiological appearances (diffuse middle and lower zone consolidation), clinical presentation (hypoxaemia, dyspnoea) and rapid improvement with vaping cessation are suggestive of such.

Treatment

The patient received largely supportive management, including supplemental oxygen and chest physiotherapy. He also received a 5-day course of Doxycycline, initiated on admission; however, there was no rise in his inflammatory markers at any time during the admission. As the patient was improving, eosinophil count was normal and his oxygen requirement was falling gradually, it was felt that steroids were not required in this case.

The core treatment for EVALI is considered to be the cessation of vaping, removing the insult and allowing the lungs to recover. In this case, the patient stopped vaping on admission, after 14 months of increasing usage. His improvement over his admission and since discharge has almost definitely been due to this crucial intervention alone.

Outcome and follow-up

The patient was discharged from hospital after 14 days. He reported feeling back to his baseline and his symptoms of dyspnoea and reduced exercise tolerance had resolved. He was followed up in the ambulatory care unit 7 days later to confirm ongoing improvement and to undergo a contrast-enhanced CT chest scan to assess resolution. Overall, the outcome was that of clinical and radiological resolution of the lung injury in the context of sustained abstinence from vaping. It was reiterated to the patient that he should abstain from vaping for life and advice was given to return to medical attention if his symptoms return. No long-term medication changes were made, and as the patient was clinically well with further radiological improvement on repeat cross-sectional imaging, he was discharged from further follow-up for his probable EVALI.

Discussion

EVALI is a potentially serious public health issue, especially among younger people.⁷ EVALIs are generally diagnosed largely on the basis of symptom onset being correlated with vaping and improvement after vaping cessation.⁸ Therefore, diagnosing and treating the condition is problematic in current practice, largely due to the lack of clear understanding of EVALI and guidance available for its treatment.

Currently, the pathophysiology of EVALI is not clearly understood meaning diagnostic tests and tailored treatments are currently unavailable. Early research has shown that e-cigarette vapour is linked to an altered, possibly hypersensitive, immune response,⁹ and an increase in pneumococcal adherence to airways.¹⁰

Both of these findings potentially demonstrate that EVALI may be a process that increases pulmonary susceptibility to more common lung injuries. Thus, treatment of EVALI in its own right may remain the cessation of vaping and treatment of the symptomatic lung injury, as is current practice in the USA.⁶ Further research is needed to clarify the extent of the effect that vaping has on airway immunity, epithelial utility and alveolar integrity and function.

At present, the only EVALI management algorithm available is published by the Center for Disease Control (CDC) and focuses on supportive management with empirical treatment for infection if any signs suggest.¹¹ No such guidance exists for UK physicians, meaning no framework exists for its diagnosis or treatment. Therefore, EVALI in the UK is possibly underdiagnosed and consequently undertreated. National Health Service (NHS) sources are still promoting the use of vapes as a tool to aid in quitting smoking,¹² the risk−benefit ratio of which should be carefully considered.

This case report highlights the need for a clear framework for the diagnosis and management of EVALI within the NHS, both in primary and secondary care. EVALI also requires further medical research to allow for a firm understanding of its pathogenesis and to elucidate potentially diagnostic biomarkers and treatment targets. Moreover, the case also demonstrates that the diagnosis of EVALI should be suspected in all patients with acute lung injuries who vape regularly and vape cessation advice should be considered. The inclusion of EVALI into a differential diagnosis may be encouraged by the advent of an EVALI reporting system, which would also allow for a better estimation of the EVALI disease burden in the UK.

Learning points.

• Electronic vaping-associated lung injury (EVALI) should be considered in all patients using vapes, e-cigarettes or associated products who present with acute lung injury.

• Clear algorithms are required for diagnosing and managing cases of EVALI.

• Further research is required to understand the pathophysiology of EVALI, and the true health implications of vaping.