Vaping’s popularity has grown exponentially since its introduction to the US market in 2003. Its use has sky-rocketed since the unveiling of the vaping pods in 2017 which may account for the advent of the vaping related illnesses we are now seeing. Substances such as nicotine solution, tetrahydrocannabinol (THC) oil, cannabidiol (CBD) oil, and butane hash oil (BHC) packaged in cartridges available in various flavors and concentrations are aerosolized by the heating of metal coils in the e-cigarette/vaping devices. Cases from all over the country have recently been coming to light in which vaping has led to severe acute pulmonary disease or vaping-associated-pulmonary-injury (VAPI). A vast majority of the presenting patients in the reported cases have required hospitalization and intensive care, needing supplemental oxygen and even endotracheal intubation and mechanical ventilation. 98% of patients present with respiratory symptoms (dyspnea, hypoxia, chest pain, cough, hemoptysis), 81% of patients have gastrointestinal symptoms (nausea, vomiting, diarrhea, and abdominal pain), and 100% of patients have constitutional symptoms such as fever, chills, and fatigue/malaise on presentation. Although based on history and clinical presentation it is reasonable to have a high suspicion for VAPI, diagnostic workup to rule out alternative underlying causes such as infection, malignancy, or autoimmune process should be performed before establishing the diagnosis. Computed Tomography (CT) scans of the chest have predominantly shown ground-glass opacity in the lungs, often with areas of lobular or subpleural sparing. Although lung biopsies have been performed on a relatively low number of cases, lung injury patterns so far have shown acute fibrinous pneumonitis, diffuse alveolar hemorrhage, or organizing pneumonia, usually bronchiolocentric, and accompanied by bronchiolitis. Treatment plans that have led to clinical improvement in the reported cases center around high-dose systemic steroids, although there are a lack of data regarding the best regimen and the absolute need for corticosteroids. The role of antibiotics appears to be limited once infection has definitively been ruled out. We present the case of a young male who vaped THC oil and developed severe acute pulmonary injury requiring mechanical ventilation and showed a remarkable response to high dose steroid therapy with improvement in clinical symptoms and resolution of diffuse ground glass opacity on repeat HRCT scan.
An electronic cigarette or “e-cigarette” is a battery-powered device that vaporizes (hence the term “vaping”) a liquid solution in order to simulate smoking without burning the tobacco. Since its introduction in the market in 2003, its use and popularity has grown exponentially. When activated, usually by pressing a button, the metal coil in the device heats and vaporizes the liquid nicotine, emitting steam which is orally inhaled. Water vapor mixed with chemical byproducts are then exhaled. Apart from nicotine, other substances such as tetrahydrocannabinol (THC), cannabidiol (CBD), and butane hash oil (BHC) can also be inhaled using an e-cigarette device. There is an increasing concern surrounding the practice of vaping as well as an existing knowledge gap regarding vaping-induced-pulmonary-injury (VAPI), its precise mechanism of pathogenesis, and the best course of management in VAPI cases. Our case aims to contribute to this growing literature to help others further understand this relatively new syndrome.
A twenty-year-old male with no significant past medical history presented to our ER with fever, nonbloody vomiting of gastric content, and epigastric abdominal pain. Symptoms began four days prior to this presentation along with worsening dyspnea, a nonproductive cough, and one episode of submassive hemoptysis. He was recently seen one day prior at an urgent care center, during which a 2-view chest X-ray showed left perihilar and right basilar interstitial prominence. At that time, he was assessed to have community-acquired pneumonia and sent home on 250 mg of oral Azithromycin. Despite taking azithromycin for one day, his dyspnea worsened and he began to cough up yellow-brown sputum. He denied any previous similar symptoms and denied previous hospital admission for pneumonia. He denied any recent sick contacts or recent travel. Family history and past surgical history was negative. Social history was significant for marijuana use and occasional drinking with friends. He informed us that he has been vaping THC oil cartridges for 3-4 years. He denied smoking cigarettes or vaping nicotine.
At rest, his respiratory rate was 22/min, heart rate 118/min, blood pressure 135/75 mmHg, temperature 39.3°C, and oxygen saturation 94% on room air. Basic labs were significant for mild leukocytosis of 11.6TH/UL with a neutrophil predominance (92%) and no eosinophils, procalcitonin 0.39, ESR 69, CRP 32, and cannabinoid in urine drug screen. A complete metabolic panel was within normal limits. Blood cultures and respiratory viral PCR were negative. A portable chest X-ray in the ER on this admission showed interval increasing bibasilar infiltrates and persistent left perihilar interstitial prominence (Figure
(a) Portable chest X-ray done in the ER on presentation showing bibasilar infiltrates and interstitial prominence. (b) Portable chest X-ray on hospital day 4 prior to discharge with improvement in aeration of the lungs, especially the right lung medially and left lingula. There continues to be minimal interstitial infiltrates present.
(a) CT scan of the chest without contrast done prior to steroids demonstrating bilateral, multilobar diffuse interstitial and mixed infiltrates evident as “honey combing” and “ground glass” appearance, with well-defined fissure line showing that the infiltrate do no cross between lobes. (b) HRCT scan of the chest post steroid therapy showing resolution of the previously evident diffuse opacity. The scans are 5 weeks apart.
However, chest X-rays on the patient’s first and second day in the hospital showed no interval improvement of bibasilar infiltrates, and neither did the patient demonstrate any clinical improvement. All the tests ordered to detect infectious and rheumatological causes came back within normal limits (Table
Infectious and autoimmune labs tested.
Significant lab | Patient’s lab results | Lab reference range |
---|---|---|
IGE | 1900 IU/ml | 0–100 IU/ml |
IGG | 666 mg/dl | 700–1600 mg/dl |
IGM | 143 mg/dl | 40–230 mg/dl |
IGA | 180 mg/dl | 70–400 mg/dl |
CRP | 26.2 mg/dl | <0.3 mg/dl |
ESR | 69 mm/hr | 0–10 mm/hr |
Procalcitonin | 0.30 ng/ml | <0.05 ng/ml |
Lactate dehydrogenase | 234 IU/L | 87–241 IU/ml |
Urine cannabinoids | Positive | Threshold 50 ng/ml |
ANA screen | Negative | — |
Scl-70 | <1.0 AI | — |
C3 | 125 mg/dl | 90–180 mg/dl |
C4 | 26.6 mg/dl | 10–40 mg/dl |
RA | <10 IU/dl | =<15 IU/dl |
Cyclic citrullinated peptide | 16 | Weak positive: 20–39 |
ANCA | Negative p-anca, c-anca, atypical anca | — |
Cryoglobulins | None detected | — |
Glom basement Membrane IGG | <1.0 AI | — |
AFB culture and smear | Negative | — |
Fungus culture and smear | Negative | — |
Legionella culture | Negative | — |
Pneumocystis smear | Negative | — |
Lower respiratory culture | Negative | — |
|
Negative | — |
Urine culture | Negative | — |
Influenza A/B antigen | Negative | — |
RP panel | Negative | — |
HIV Ab/Ag, 4th gen | Nonreactive | — |
On hospital day 3, he became increasingly dyspneic, requiring 50 L oxygen via heated high flow nasal cannula. The patient was given another four doses of methylprednisolone 40 mg on this day. On hospital day 4, the patient’s dyspnea improved. The chest X-ray taken this day showed improvement in aeration of the lungs, especially the medial right lung and left lingula, along with continued minimal interstitial infiltrates. Antibiotics were discontinued, and he was given another 80 mg of intravenous methylprednisolone prior to hospital discharge on hospital day 4. He was discharged to his home on nine days of tapering prednisone starting at 60 mg daily.
Five weeks after his hospital admission, the patient presented to our pulmonary clinic for a follow-up. He reported feeling “90% back to normal” and said he has been able to help his uncle move some furniture without feeling exhausted or short of breath in doing so. He had felt short of breath with a mild dry cough for the first few days post-hospital discharge; however, he reported that these symptoms have greatly improved. His oxygen saturation was 98% on room air with a respiratory rate of 18/min at rest. His physical exam with respiratory focus was benign. High-resolution chest CT on this day did not convey any findings of acute or active pulmonary parenchymal disease (Figure
There is an increasing prevalence of cannabis use in e-cigarettes among the US youth. A study that examined data from about 20,000 middle and high school students regarding the use of e-cigarette devices with a substance other than nicotine reported cannabis use in e-cigarettes by 8.9% of all students and 30.6% of those who ever used e-cigarettes [
The proposed reason explaining why vaping THC oil damages the lung tissue is largely debated and may be the direct impact of cannabinoid vapors or the inflammation from the flavoring and diluting additives in the cartridges. There are growing reports of illegal contamination of TCH cartridges with vitamin-E acetate oil as a diluting agent. Vitamin-E oil, which is otherwise harmless on topical application, is known to cause severe inflammatory reaction in the pulmonary parenchyma when inhaled [
A large case series with a cluster of 53 cases of severe pulmonary disease associated with vaping, reported to the Wisconsin Department of Health Services and the Illinois Department of Public Health, described 98% of patients as having respiratory symptoms (dyspnea, hypoxia, chest pain, cough, and hemoptysis), 81% of patients as having gastrointestinal symptoms (nausea, vomiting, diarrhea and abdominal pain), and 100% of patients as having constitutional symptoms like fever, chills, and fatigue/malaise on presentation. Possibly due to the symptom profile resembling community-acquired pneumonia, patients often end up receiving empiric antibiotics in the ER without much improvement in their condition [
Although based on history and clinical presentation it is reasonable to have a high suspicion for VAPI, a diagnostic workup to rule out infection, malignancy, or autoimmune processes as the underlying cause should be performed before establishing the diagnosis. CT chest scans on several reported cases of VAPI have predominantly shown ground-glass opacity, often with areas of lobular or subpleural sparing. Cases of vaping-associated acute lipoid pneumonia may additionally demonstrate nodular tree-in-bud opacities [
Treatment plans that have led to clinical improvement in the reported cases center around respiratory support and high-dose systemic steroids, although there is a lack of data regarding the best regimen and the absolute need for corticosteroids. The role of antibiotics appears to be limited once infection has definitively been ruled out. Many centers tend to empirically cover for community-acquired pneumonia. However, clinical improvement has largely been noted, mostly after administering high-dose steroids [
In summary, our case adds to the growing body of literature on VAPI, for which suspicion should be high in patients who use e-cigarettes and present with acute respiratory symptoms. It also goes on to highlight that high dose steroid therapy can be lifesaving. Bilateral ground-glass opacity in the lungs on CT; negative blood, sputum, and BAL culture for infection; and negative rheumatological markers in such a setting are highly suggestive of this diagnosis. The decision to do flexible bronchoscopy with biopsy and BAL specimen cytology should be tailored on a case-by-case basis, but doing so would expand our knowledge of this newly-emerging syndrome.
The authors declare that they have no conflicts of interest.