Severe Respiratory Disease Associated with Vaping: A Case Report

Evan Denis Schmitz MD

La Jolla, CA USA

Abstract

A case of severe respiratory disease associated with vaping cannabinoid oil is reported in a 38-year-old woman. She presented with shortness of breath and nonproductive cough. Chest x-ray and CT scan showed diffuse ground glass opacities and consolidation. Bronchoscopy showed diffuse bronchial erythema and bronchoalveolar lavage contained an increased percentage of eosinophils (59%). She was treated with high dose corticosteroids and rapidly improved.

Case Report

History of Present Illness

A 38-year-old woman complained of worsening shortness of breath and nonproductive cough for four weeks. She used to be able to climb three flights of stairs but now can barely walk ten feet. She had been treated with various forms of antibiotics, inhalers and steroids and was taking 20 mg of prednisone a day on the day of hospitalization. She also received opiates to help control her cough. She denied any hemoptysis, fever, chills, or sputum production. Because of her progressive symptoms she was hospitalized for further evaluation and management.

Past Medical History, Social History and Family History

She has a history of obesity and fibromyalgia. She has a prior history of smoking one to two packs a day for five years quitting approximately 15 years ago. Because of a family crisis she tried vaping cannabidiol (CBD) oil approximately one month prior to admission. She also resumed smoking tobacco one half a pack per day. Her family history was unremarkable.

Medications

She was taking prednisone 20 mg/day and cyclobenzaprine (Flexeril®) for her fibromyalgia. She was also taking codeine cough syrup.

Review of Symptoms

She did have some chest pain associated with her shortness of breath as well as chronic muscle aches and intermittent lower extremity edema. Her review of systems was otherwise unremarkable.

Physical Examination

Vital Signs: BP 137/72 mm Hg, Pulse 84 beats/min, temperature 98.8 °F, respirations 22 breaths/min, height 5’0, weight 231 lbs, SpO2 96%

General: She was morbidly obese and only able to speak in short sentences.

Mouth: Moist. Mallampati 3.

Pulmonary: Faint expiratory crackles. No wheezing.

Cardiovascular: Normal rate, regular rhythm, normal heart sounds and intact distal pulses. Exam reveals no gallop and no friction rub. No murmur heard.

Abdominal: Soft, bowel sounds normal. No distension, mass or tenderness. No rebound or guarding. Centripetal obesity.

Extremities: Normal range of motion. No edema or tenderness.

Lymphatics: No cervical or supraclavicular adenopathy.

Neurological: Alert and oriented to person, place and time.

Skin: Warm and dry. No rash, erythema or pallor. Not diaphoretic. Capillary refill within normal limits. No skin tenting.

Psychiatric: Depressed mood.

Laboratory

Pertinent findings are on her laboratory evaluation include an elevated white blood cell count of 16,850 cells/µL with an increased number of neutrophils. Her electrolytes, liver enzymes, creatinine, blood urea nitrogen and urinalysis were within normal limits.

Radiology

Her admission chest x-ray is shown in Figure 1.

Figure 1. The admission portable chest x-ray showed bilateral patchy pulmonary infiltrates.

To better define the areas of consolidation, a thoracic CT scan was performed (Figure 2).

Figure 2. Representative images in lung windows from contrast enhanced thoracic CT scan showing nonspecific patchy areas of ground glass and alveolar opacities with septal thickening involving both lungs.

Hospital Course

Echocardiography was unremarkable. Bronchoscopy with bronchoalveolar lavage was performed. She had diffuse upper and lower airway erythema and considerable coughing during the procedure. The cell differential revealed an increase in eosinophils (59%) and multiple foamy macrophages. Smears and cultures of the lavage fluid were negative for pathogens. She was treated with high dose corticosteroids (methylprednisolone 1000 mg/day). She rapidly improved over four days with her cough and shortness of breath resolving. A chest x-ray at discharge revealed improvement of the pulmonary infiltrates (Figure 3).

Figure 3. Chest x-ray on the morning of discharge showing near resolution of her pulmonary infiltrates.

Discussion

At the time of this writing (9/21/19) there have been 530 cases of lung injury associated with e-cigarette product use or vaping reported with seven deaths (1).  Nearly three fourths (72%) of cases have been male with two thirds (67%) 18 to 34 years old. Most patients have reported a history of using e-cigarette products containing tetrahydrocannabinol (THC). Many patients have reported using THC and nicotine. Some have reported the use of e-cigarette products containing only nicotine.

At present no specific e-cigarette or vaping product (devices, liquids, refill pods, and/or cartridges) or substance has been linked to all cases. It seems likely that there may be different mechanisms of lung injury from different substances. In support of this concept, the present case had high numbers of eosinophils in the bronchoalveolar lavage while other cases have shown an increase in neutrophils (2). Our patient was treated with high dose corticosteroids and did improve while on the corticosteroids. However, the time course does not establish a definite relationship between corticosteroid treatment and her improvement.

At present the CDC recommends refraining from using e-cigarette or vaping products (1). Anyone who uses an e-cigarette or vaping product should not buy these products (e.g., e-cigarette or vaping products with THC or CBD oils) off the street, and should not modify or add any substances to these products that are not intended by the manufacturer.

References

1. CDC. Outbreak of lung injury associated with e-cigarette use, or vaping. September 19, 2019. Available at: https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html (accessed 9/21/19).
2. Arizona Thoracic Society. September 2019 Arizona thoracic society notes. Southwest J Pulm Crit Care. 2019;19(3):99-100. [CrossRef]

Cite as: Schmitz ED. Severe respiratory disease associated with vaping: a case report. Southwest J Pulm Crit Care. 2019;19(3):105-9. doi: https://doi.org/10.13175/swjpcc062-19 PDF 

June 2017 Pulmonary Case of the Month

Robert Horsley, MD

Lewis J. Wesselius, MD 

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ USA

History of Present Illness

A 61-year-old woman presented to the emergency department for 3 days of fevers up to 102º F, malaise, and progressive shortness of breath. Her symptoms started immediately after he last naltrexone injection for alcohol use disorder.

Past Medical History, Social History and Family History

• Alcohol use disorder
• Treated with monthly naltrexone injections, received 3 doses total, and gabapentin
• No other previous medical issues
• Nonsmoker

Physical Examination

• Vital signs: Pulse 100, BP 108/90, respiratory rate 34, SpO2 93% 10L non-rebreathing mask
• Cyanotic on room air
• Lungs clear

Radiography

A portable chest x-ray was performed in the emergency department (Figure 1).

Figure 1. AP chest radiograph taken in the emergency department.

A thoracic CT scan was performed (Figure 2).

Figure 2. Representative images from thoracic CT in lung windows.

Laboratory

• CBC showed a white blood cell count of 12,000 cells/mcL.
• The differential showed a left shift.
• Lactate was 5.2 mmol/L

Which of the following is (are) true? (Click on the correct answer to proceed to the second of five pages)

1. A lactate level of 5.2 can be a normal finding in a critically ill patient
2. Her symptoms are likely an allergic reaction to naltrexone
3. The most likely diagnosis is an atypical pneumonia
4. 1 and 3
5. All of the above

Cite as: Horsley R, Wesselius LJ. June 2107 pulmonary case of the month. Southwest J Pulm Crit Care. 2017;14(6):255-61. doi: https://doi.org/10.13175/swjpcc063-17 PDF

June 2013 Pulmonary Case of the Month: Diagnosis Makes a Difference

Lewis J. Wesselius, MD¹

Henry D. Tazelaar, MD²

Departments of Pulmonary Medicine¹ and Laboratory Medicine and Pathology²

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 64 year old man from Southern Arizona was referred for a second opinion on a diagnosis of chronic eosinophilic pneumonia that was poorly responsive to corticosteroid therapy. The patient first became ill February 2012 with cough and congestion.  His wife was ill at the same time. Both were treated with antibiotics. His wife improved but he never fully recovered with ongoing symptoms of cough and some dyspnea.

He was admitted to another hospital in August 2012 due to worsening shortness of breath and pulmonary infiltrates on chest x-ray. During this admission he underwent bronchoscopy with bronchoalveolar lavage (BAL) that demonstrated 78% eosinophils. A video-assisted thorascopic (VATs) lung biopsy was done and the patient was diagnosed with chronic eosinophilic pneumonia. He was begun on therapy with high dose prednisone (80 mg/day) but had only slight improvement in symptoms.

He was followed by a pulmonologist and continued on prednisone who questioned the possible development of pulmonary fibrosis. Earlier this year he was started on mycophenolate mofetil and the dose was increased to 1000 mg bid while the prednisone was tapered to 5 mg every other day. He was also being treated with fluticasone/salmeterol 250/50 twice a day. The patient continues to have dyspnea with limited activity. His last pulmonary function testing was done in December 2012. At that time his forced vital capacity (FVC) was 51% of predicted and his diffusing capacity for carbon monoxide (DLco) was 40% of predicted.

PMH, SH, FH

He had a history of obstructive sleep apnea (OSA) and had undergone an uvulopharyngoplasty (UPPP). There was also a history of gastroesophageal reflux disease (GERD) and he had a prior Nissen fundoplication. He had a history of osteoarthritis and had undergone a right shoulder replacement.

He had a remote smoking history, a history of modest alcohol use, but no history of using recreational drugs.  He worked as an airline pilot.

His present medications included mycophenolate mofetil 1000 mg twice a day, prednisone 5 mg every other day, voriconazole 200 mg daily (started after BAL showed a few colonies of Aspergillus), and fluticasone/salmeterol 250/50 twice a day.

Physical Examination

Blood pressure 134/88 mm Hg.  Resting oxygen saturation 96%.

Chest:  bibasilar crackles but no wheezes.

Cardiovascular: the heart had a regular rhythm but no murmur.

Extremities: no clubbing or edema.

The remainder of the physical examination was unremarkable.

Chest Radiography

His chest x-ray is shown in figure 1.

Figure 1. Initial chest x-ray.

Which of the following diseases has/have been associated with increased eosinophils in bronchoalveolar lavage fluid?

1. Interstitial lung diseases
2. Acquired immunodeficiency syndrome (AIDS)-associated pneumonia
3. Idiopathic eosinophilic pneumonia
4. Drug-induced lung disease
5. All of the above

Reference as: Wesselius WJ, Tazelaar HD. June 2013 pulmonary case of the month: diagnosis makes a difference. Southwest J Pulm Crit Care. 2013;6(6):247-54. PDF 

Treatment of Coccidioidomycosis-associated Eosinophilic Pneumonia with Corticosteroids

Joshua Malo, MD

Yuval Raz, MD 

Linda Snyder, MD

Kenneth Knox, MD

University of Arizona Medical Center

Department of Medicine

Section of Pulmonary, Allergy, Critical Care, and Sleep Medicine

Tucson, AZ 85724

Abstract

Pulmonary coccidioidomycosis is a common cause of community-acquired pneumonia in endemic areas of the southwestern United States. The clinical spectrum of this disease ranges from an asymptomatic presentation to severe disease with ARDS and hypoxemic respiratory failure. Despite evidence supporting the use of corticosteroids for severe pulmonary disease in other fungal infections, there is currently no established role for this therapy in coccidioidomycosis infections. Peripheral eosinophilia is a common feature of coccidioidomycosis; however, pulmonary eosinophilia is rarely reported. In the setting of pulmonary eosinophilia of other etiologies, corticosteroid therapy has been demonstrated to have a role in reducing the inflammatory response and leading to a more rapid resolution of hypoxemic respiratory failure. We report a case of a patient with primary pulmonary coccidioidomycosis complicated by severe pulmonary eosinophilia that demonstrated rapid improvement after the initiation of corticosteroid therapy.

Case Report

A 71-year-old man presented to the emergency room in Tucson, Arizona with a one-week history of fever, cough, and malaise. The patient’s symptoms began while returning from a trip to northern California. A chest radiograph ordered by the primary care physician demonstrated a right upper lobe consolidation (Figure 1) and azithromycin was prescribed. Fevers persisted along with worsening cough over the next three days, and the patient presented for further evaluation.

Figure 1. Admission radiograph demonstrating right upper lobe airspace disease

Medical history was remarkable for viral cardiomyopathy requiring placement of an ICD after an episode of sudden cardiac death in 2006. An episode of S. bovis bacteremia occurred 4 months prior to the current presentation and was treated with a course of cefazolin. There is no known personal or family history of atopic disease. There is no history of tobacco use or significant occupational exposures. The patient had been living in Arizona during the preceding year and had no other recent travel history, dust, or environmental exposures.

On physical exam, temperature was 38.8°C and pulse oximetry saturation was 90 percent on room air. The patient was in moderate respiratory distress with rales auscultated in the right upper lung zone. Subsequent laboratory examination revealed a PaO2 of 69 mmHg on 4 liters-per-minute of oxygen via nasal cannula. A metabolic panel showed elevated transaminases and his initial leukocyte count was 11.8 x 10³/mL with differential including 5% eosinophils.

The patient was admitted to the medical ward and treated with vancomycin, cefepime, and moxifloxacin for pneumonia caused by a potentially resistant organism. Fluconazole was started on the third hospital day for empiric treatment of primary pulmonary coccidioidomycosis. A CT angiogram of the chest showed bilateral multilobar pneumonia (Figure 2).

Figure 2. CT angiogram of the chest demonstrating multilobar consolidation of the right lung

The patient deteriorated and required intubation for severe hypoxemia two days later. A bronchoalveolar lavage revealed Coccidioides spherules on cytological examination. Liposomal amphotericin B was initiated, which led to the development of oliguric renal failure necessitating hemodialysis. Initial Coccidioides serology was negative, however sputum and BAL cultures demonstrated C. immitis. Despite antifungal therapy his pulmonary status worsened with progressive bilateral pulmonary infiltrates and worsening hypoxemic respiratory failure (Figure 3).

Figure 3. CXR demonstrating progressive bilateral alveolar opacities consistent with ARDS.

In addition, he had a steadily increasing peripheral eosinophilia reaching a maximum of 40 percent with a leukocyte count of 14.8 x 10³/mL despite the absence of any signs of disseminated coccidioidomycosis. A repeat BAL again showed Coccidioides spherules and eosinophils of 40 and 56 percent from the right middle lobe and lingula, respectively. Methylprednisolone 40mg IV three times daily was started with a decline in blood eosinophils to one percent within 24 hours. Chest radiographs and A-a gradient rapidly improved over the next 3 days leading to successful extubation. The patient was transitioned to oral fluconazole and prednisone and discharged from the hospital in good condition two weeks later.

At the follow-up six weeks after initial presentation, he remains on fluconazole and prednisone 15mg daily with no signs of disseminated coccidioidomycosis and is continuing a gradual reduction of prednisone dosage.

Discussion

Coccidioidomycosis is caused by either of 2 species of the dimorphic fungus Coccidioides. Endemic regions are present in North and South America, with the majority of cases within the United States arising in Arizona and California. Although peripheral eosinophilia is a commonly reported finding (1), pulmonary eosinophilia has rarely been described.

Acute eosinophilic pneumonias may be idiopathic or a secondary inflammatory response to various infections or environmental exposures. In regions where endemic fungal infections are common, differentiating between eosinophilic pneumonias of idiopathic versus infectious etiology is vital in order to avoid inappropriate therapy and its adverse consequences. A review of the literature concerning pulmonary coccidioidomycosis and concurrent pulmonary eosinophilia demonstrates only 9 prior case reports. Corticosteroid therapy was used for treatment of the pulmonary eosinophilia in only 3 of these cases, 2 of which resulted in death from disseminated coccidioidal infection (1-3). One case ended in spontaneous resolution of disease without antifungals or corticosteroids leading the authors to suggest a conservative approach with corticosteroids due to the risk for dissemination (4).

In our case, there was progressive clinical deterioration despite ten days of treatment with appropriate antifungal regimen, leading to our decision to treat with corticosteroids. The immediate decrease in peripheral eosinophilia in conjunction with the rapid clinical improvement leads us to the conclusion that corticosteroids were beneficial in the resolution of his acute respiratory failure. The clinical response observed is similar to that expected in idiopathic acute eosinophilic pneumonia which supports the notion that the eosinophilic response, as opposed to the primary infection, was primarily responsible for our patient’s severe hypoxemia.

There remains a risk for disseminated disease. In the cases cited in which patients died of dissemination, antifungal therapy preceding corticosteroid therapy was not described. Due to the risk of underlying pulmonary coccidioidomycosis in endemic regions, corticosteroid therapy for eosinophilic pneumonia should only be considered in the setting of severe hypoxemic respiratory failure and once adequate antifungal therapy has been initiated.

According to recent guidelines there is no role for corticosteroid therapy in the treatment of coccidioidomycosis due to a lack of convincing data for efficacy and safety (5). There is precedent for treating severe pulmonary disease caused by other fungal infections, such as histoplasmosis and blastomycosis, with corticosteroids. We suggest that there is a role for the use of corticosteroid therapy in the setting of progressive respiratory failure due to coccidioidomycosis with associated pulmonary eosinophilia that has failed conventional antifungal therapy.

References

1. Echols RM, Palmer DL, Long GW. Tissue eosinophilia in human coccidioidomycosis. Rev Infect Dis 1982;4:656–664.
2. Lombard CM, Tazelaar HD, Krasne DL. Pulmonary eosinophilia in coccidioidal infections. Chest 1987;5:734–736
3. Swartz J, Stoller JK. Acute Eosinophilic Pneumonia Complicating Coccidioides immitis Pneumonia: A Case Report and Literature Review. Respiration 2009;77:102–106
4. Whitlock WL, Dietrich RA, Tenholder MF. Acute eosinophilic pneumonia (letter). N Engl J Med 1990;322:635
5. Limper AH, Knox KS, Sarosi GA, et al. Treatment of fungal infections in adult pulmonary and critical care patients. Am J Respir Crit Care Med 2011;183:96–128

The authors report no conflicts of interest

Address correspondence to:     Joshua Malo, MD

                                             University of Arizona Medical Center

                                             Department of Medicine    

                                             Section of Pulmonary, Allergy, Critical

                                             Care and Sleep Medicine

                                             Tucson, AZ 85724

                                             E-mail: jmalo@deptofmed.arizona.edu

Reference as: Malo J, Raz Y, Snyder L, Knox K. Treatment of coccidioidomycosis-associated eosinophilic pneumonia with corticosteroids. Southwest J Pulm Crit Care 2012;4:61-66. (Click here for a PDF version of the manuscript)