Dust in the Wind

Eosinophilic infiltration may lead to fibrosis, as was found on the lung biopsy. She should be counseled to avoid “fine dust exposure” in the future. Follow-up lung imaging and pulmonary function tests (PFTs) should be performed once her acute illness resolves. She should be strongly urged not to smoke tobacco. Interestingly, there are reports that ex-smokers who restart smoking have an increased risk of eosinophilic pneumonia, but in this case dust exposure is the more likely etiology.

She was diagnosed with acute eosinophilic pneumonia (AEP). Antibiotics were discontinued, and oral prednisone was initiated at 40 mg daily, with a brisk response and resolution of her dyspnea. She was discharged with a 6-week prednisone taper. She had no cough, dyspnea, chest pain, or fevers at her follow-up 14 days after discharge. On a 6-week, postdischarge phone call, she continued to report no symptoms, and she maintained abstinence from cigarette smoking.

This case highlights that the very best test in any medical situation is a thorough, detailed history and physical examination. A comprehensive history with physical examination is noninvasive, safe, and cheap. Had the history of fine-dust exposure been known, it is likely that a great deal of testing and money would have been saved. The patient would have been diagnosed and treated earlier, and suffered less.

First described in 1989,^1,2 AEP is an uncommon cause of acute respiratory failure. Cases have been reported throughout the world, including in the United States, Belgium, Japan, and Iraq.^2,3 AEP is an acute febrile illness with cough, chest pain, and dyspnea for fewer than 7 days, diffuse pulmonary infiltrates on chest radiograph, hypoxemia, no history of asthma or atopic disease, no infection, and greater than 25% eosinophils on a BAL.^1,3 Physical examination typically reveals fever, tachypnea, and crackles on auscultation.¹ Peripheral blood eosinophilia is inconsistently seen at presentation but generally observed as the disease progresses.¹ Peripheral eosinophilia at presentation is positively correlated with a milder course of AEP, including higher oxygen saturation and fewer intensive care admissions.⁴ Acute respiratory failure in AEP progresses rapidly, often within hours.¹ Delayed recognition of AEP may lead to respiratory failure, requiring intubation, and even to death.¹

Reticular markings with Kerley-B lines, mixed reticular and alveolar infiltrates, and pleural effusions are usually found on chest radiography.¹ Bilateral areas of ground-glass attenuation, interlobular septal thickening, bronchovascular bundle thickening, and pleural effusions are seen on chest CT.⁵ Marked eosinophilic infiltration of the interstitium and alveolar spaces, as well as diffuse alveolar damage with hyaline membrane fibroblast proliferation and inflammatory cells, are present on lung biopsy.¹ Restriction with impaired diffusion capacity is found on PFTs. However, PFTs return to normal after recovery.¹

AEP is distinguished from other pulmonary diseases by BAL, lung biopsy, symptoms, symptom course, and/or radiographically. AEP is often misdiagnosed as severe community-acquired pneumonia and/or acute respiratory distress syndrome, as AEP tends to occur in previously healthy individuals who have diffuse infiltrates on chest radiograph, fevers, and acute, often severe, respiratory symptoms.^1-3 Other eosinophilic lung diseases to rule out include simple pulmonary eosinophilia, chronic eosinophilic pneumonia, eosinophilic granulomatosis with polyangitis (Churg-Strauss), idiopathic hypereosinophilic syndrome, infection, and drug reactions.^1,3,5 Simple eosinophilic pneumonia is characterized by no symptoms or very mild pulmonary symptoms and transient patchy infiltrates on radiography.^3,5 Patients with simple pulmonary eosinophilia do not have interlobular septal thickening, thickening of the bronchovascular bundles, or pleural effusions radiographically, as seen with AEP.⁵ Chronic eosinophilic pneumonia is subacute, with respiratory symptoms of more than 3 months in duration, in contrast with the 7 days of respiratory symptoms for AEP, and is also not associated with interlobular septal thickening, thickening of the bronchovascular bundles, or pleural effusions on radiography.^3,5 Unlike AEP, chronic eosinophilic pneumonia often recurs after the course of steroids has ended.³ In contrast with AEP, eosinophilic granulomatosis with polyangitis is associated with concomitant asthma and the involvement of nonpulmonary organs.³ Idiopathic hypereosinophilic syndrome is characterized by extremely high peripheral eosinophilia and by eosinophilic involvement of multiple organs, and it requires chronic steroid use.³ Patients with allergic bronchopulmonary aspergillosis (ABPA), in contrast with AEP, typically have steroid-dependent asthma and chronic respiratory symptoms.³ ABPA also differs from AEP in that radiographic infiltrates are localized and transient, and the syndrome may relapse after steroid treatment.³ Other infectious etiologies that may present similarly to AEP include invasive pulmonary aspergillosis, pulmonary coccidiodomycosis, Pneumocystis jioveri pneumonia, pulmonary toxocariasis, pulmonary filariasis, paragonimiasis, and Loeffler syndrome (pneumonia due to Strongyloides, Ascaris, or hookworms), highlighting the importance of a thorough travel and exposure history.^1,3 Several drugs may cause eosinophilic lung disease, including nitrofurantoin, tetracyclines, phenytoin, L-tryptophan, acetaminophen, ampicillin, heroin, and cocaine, which necessitates a thorough review of medication and illegal drug use.³

Steroids and supportive care are the treatment of choice for AEP, although spontaneous resolution has been seen.^1,3 Significant clinical improvement occurs within 24 to 48 hours of steroid initiation.^1,3 Optimal dose and duration of therapy have not been determined; however, methylprednisolone 125 mg intravenously every 6 hours until improvement is an often-used option.¹ Tapers vary from 2 to 12 weeks with no difference in outcome.^1-3 AEP does not recur after appropriate treatment with steroids.^1,3

Little is known about the etiology of AEP. It usually occurs in young, healthy individuals and is presumed to be an unusual, acute hypersensitivity reaction to an inhaled allergen.¹ A report of 18 US soldiers deployed in or near Iraq proposed dust exposure and cigarette or cigar smoking as a cause of AEP.² Similar to our patient’s fine-dust exposure and recent onset of cigarette smoking, the soldiers were exposed to the dusty, arid environment for at least 1 day and had been smoking for at least 1 month.² The authors proposed that small dust particles irritate alveoli, stimulating eosinophils, which are exacerbated by the onset of smoking. Alternatively, cigarette smoke may prime the lung such that dust triggers an inflammatory cascade, resulting in AEP.² Because of the potential for the rapid progression of respiratory failure, it is critical that clinicians recognize that AEP may be caused by relatively new cigarette smoking and dust in the wind.