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Idiopathic acute eosinophilic pneumonia

Idiopathic acute eosinophilic pneumonia
Literature review current through: Jan 2024.
This topic last updated: Aug 01, 2023.

INTRODUCTION — Idiopathic acute eosinophilic pneumonia (AEP) was first described as a cause of acute respiratory failure in 1989 [1,2]. Subsequently, cases of AEP have been reported worldwide [3-6]. Although both AEP and chronic eosinophilic pneumonia (CEP) are characterized by eosinophilic infiltration of the pulmonary parenchyma, these disorders are clinically distinct [7].

The clinical features and management of idiopathic acute eosinophilic pneumonia will be reviewed here. Other conditions associated with pulmonary eosinophilia are presented separately (table 1).

(See "Overview of pulmonary eosinophilia".)

(See "Chronic eosinophilic pneumonia".)

(See "Pleural fluid eosinophilia".)

(See "Epidemiology, pathogenesis, and pathology of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)".)

(See "Clinical features and diagnosis of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)".)

(See "Eosinophilic granulomatosis with polyangiitis (Churg-Strauss): Treatment and prognosis".)

Other etiologies of acute diffuse parenchymal lung infiltrates are likewise discussed elsewhere:

(See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults".)

(See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".)

(See "Acute interstitial pneumonia (Hamman-Rich syndrome)".)

(See "The diffuse alveolar hemorrhage syndromes".)

(See "Cryptogenic organizing pneumonia".)

ETIOLOGY — The cause of acute eosinophilic pneumonia (AEP) remains unknown. Some investigators have suggested that AEP is an acute hypersensitivity reaction to an unidentified inhaled antigen in an otherwise healthy individual [1]. The following observations are consistent with this hypothesis:

In several reports, patients have been involved in unusual outdoor activities just prior to the onset of their illness [1,8-10]. As an example, AEP developed in at least one firefighter following the collapse of the World Trade Center towers in 2001 [10]. Another case developed in a young male smoker after he inhaled smoke from fireworks for three consecutive nights [11].

A temporal relationship has been described in a number of patients between the development of AEP and the recent onset of cigarette smoking (for the first time or following a period of smoking cessation) [8,12-24]. In one patient, a cigarette-smoking challenge test led to recurrence of eosinophilic pneumonia [13]. In contrast, the process resolved in another patient despite continued cigarette smoking [25]. An association between passive smoking and AEP has also been reported [26].

AEP has been described in water pipe users who smoke tobacco or marijuana [27,28]. Water pipe smoking increases the volume of smoke inhaled and the concentration of ultrafine particles, compared with cigarettes. Electronic cigarettes and "heat-not-burn" devices have been associated with AEP in separate reports [29-36]. AEP has also been associated with aromatherapy following fragrance oil inhalation [37,38]. (See "Patterns of tobacco use", section on 'Other forms of tobacco' and "Vaping and e-cigarettes".)

Eighteen cases of AEP were described among over 180,000 military personnel deployed in or near Iraq from March 2003 to March 2004 and treated at Landstuhl Regional Medical Center (LRMC) [15]. All patients smoked, and the onset of smoking was recent in 14. All but one patient had significant exposure to fine airborne sand or dust; no other common source exposure could be identified. A retrospective chart review of 43 total cases of AEP in military personnel treated at LRMC from 2003 to 2010 found that 91 percent were cigarette smokers and 77 percent had recently started or increased their smoking [39].

The possible role of environmental factors in the home was addressed in a study in which provocation challenges were performed in the homes of stable patients with a recent history of AEP [40]. The challenge resulted in the development of a similar illness with fever, cough, fatigue, and dyspnea. Inspiratory crackles became audible and hypoxemia developed in all cases. Similar challenges at the patients' workplaces were negative. After moving out of their homes, the patients engaged in their usual work and experienced no recurrent episodes.

Isolated cases of AEP have been described in HIV-infected patients, and following inhalation of cocaine or heroin [41-43]. The pathogenesis of these possible associations is not known.

Several cases of AEP presumably triggered by SARS-CoV-2 infection have been described [44-46].

PATHOLOGY — Few patients with acute eosinophilic pneumonia (AEP) have undergone lung biopsy other than by transbronchial biopsy [47,48]. One series described nine open and thoracoscopic lung biopsies from the consultation and teaching files of the Mayo Clinic [47,48]. Key histopathologic features included:

Severe extent of disease, with abnormalities in over 75 percent of the surface area of the lung sampled.

Acute and organizing diffuse alveolar damage (DAD) was common. Hyaline membranes and interstitial widening (due to a combination of edema, fibroblast proliferation, and inflammatory cells characteristic of the organizing phase of DAD) were each seen in 78 percent of cases. (See "Acute interstitial pneumonia (Hamman-Rich syndrome)".)

Marked numbers of interstitial and lesser numbers of alveolar eosinophils were found in all samples (picture 1).

Other features included: type II pneumocyte hyperplasia (55 percent of cases), interstitial lymphocytes (100 percent of cases), an organizing intraalveolar fibrinous exudate (100 percent of cases), and perivascular and intramural inflammation without necrosis (33 percent of cases) (picture 2).

Granulomas and alveolar hemorrhage were absent.

CLINICAL FEATURES — Acute eosinophilic pneumonia (AEP) is a rare disease, and the clinical studies that are available have been retrospective in nature [8,18,24,49]. AEP can occur at any age, even in previously healthy children, though most patients are between 20 and 40 years of age [50,51]. Men are affected approximately twice as frequently as women [1,2,9,52-55]. A minority have a history of allergic disease [19].

Clinical presentation – Patients present with an acute illness of less than four weeks duration; in most cases the duration of symptoms is less than seven days. Nonproductive cough (95 percent), dyspnea (92 percent), and fever (88 percent) are present in almost every patient [19]. Associated symptoms and signs can include malaise, myalgias, night sweats, chills, and pleuritic chest pain [19].

Physical examination shows fever (often high) and tachypnea. Bibasilar inspiratory crackles and occasionally rhonchi on forced exhalation are heard upon auscultation of the chest [19,55,56]. Clubbing and signs of cor pulmonale have not been reported.

Hypoxemic respiratory insufficiency is frequently identified at presentation and often requires mechanical ventilation. In one series, 14 of 22 patients (63 percent) developed respiratory failure and required mechanical ventilation [8]. Hyperdynamic shock has been reported, but is unusual [57].

Laboratory features – Patients generally present with an initial neutrophilic leukocytosis [8,12,19]. In most cases, the eosinophil fraction is not elevated initially, but may become markedly elevated during the subsequent course [8,54,56,58]. The erythrocyte sedimentation rate and C-reactive protein are elevated, and the IgE level has been high in a majority of the patients in whom it was measured [40,52-55].

EVALUATION — Acute eosinophilic pneumonia (AEP) is typically suspected in a patient with progressive dyspnea less than a month in duration and a chest radiograph showing diffuse parenchymal opacities. Among the first steps in the evaluation is to ask the patient about medication usage, particularly any drugs associated with pulmonary eosinophilia (eg, cocaine, daptomycin, gemcitabine, infliximab, ranitidine, sulfasalazine/mesalamine, venlafaxine), previous irradiation of the chest, or travel or residence in an area with an increased likelihood of exposure to endemic parasites or fungi (table 1) [59-69].

Laboratory studies — No laboratory studies are specific for AEP. However, in the evaluation of patients with dyspnea, cough, fever, and radiographic pulmonary opacities, the usual laboratory tests include a complete blood count and differential, blood urea nitrogen, creatinine, hepatic function tests, urinalysis, and blood cultures. As noted above, patients do not typically have peripheral blood eosinophilia at the time of presentation [2,70].

Certain laboratory tests are helpful to evaluate for diseases in the differential diagnosis of AEP:

An antineutrophil cytoplasmic antibody (ANCA) test for granulomatosis with polyangiitis (GPA) or eosinophilic granulomatosis with polyangiitis (EGPA, Churg Strauss). However, ANCA is only positive in 40 to 60 percent of patients with EGPA, so a negative test doesn’t exclude the diagnosis. (See "Granulomatosis with polyangiitis and microscopic polyangiitis: Respiratory tract involvement", section on 'Laboratory tests' and "Clinical features and diagnosis of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)", section on 'Antineutrophil cytoplasmic antibodies'.)

Enzyme-linked immunoassays for IgM and IgG specific for Coccidioides. (See "Coccidioidomycosis: Laboratory diagnosis and screening".)

Enzyme-linked immunosorbent assay (ELISA) or other serologic test for Strongyloides or Paragonimiasis, depending on likelihood of exposure. (See "Strongyloidiasis", section on 'Serology'.)  

In a small series, the expectorated sputum showed eosinophilia in six of nine patients, but the sensitivity and specificity of sputum cell counts have not been formally evaluated [54].

If an adequate amount of pleural fluid is present, thoracentesis is generally indicated. Pleural fluid may demonstrate a marked eosinophilia (10 to 50 percent) [6-9,20,55,71].

Imaging — At the onset of AEP, the chest radiograph may show only subtle reticular or ground glass opacities, often with Kerley B lines [71,72]. As the disease progresses, bilateral diffuse mixed ground glass and reticular opacities develop [1,2,9,52-55,72] (image 1A-B). Isolated ground glass (approximately 25 percent of cases) or reticular (approximately 25 percent of cases) opacities may also be seen on presentation. The distribution of opacities in AEP is diffuse, unlike chronic eosinophilic pneumonia, in which the opacities are typically localized to the lung periphery. (See "Evaluation of diffuse lung disease by conventional chest radiography".)

Small pleural effusions are common (noted in up to 70 percent of patients) and are frequently bilateral [8,58,61].

High-resolution computed tomography (HRCT) scans are not essential to the diagnosis but can help characterize the distribution of opacities and guide selection of an area of involvement for bronchoalveolar lavage. The HRCT is always abnormal in patients with AEP and is characterized by bilateral, random, and patchy ground-glass or reticular opacities (image 2) [19,73]. Centrilobular nodules and air-space consolidation are seen in approximately 50 and 40 percent, respectively [19]. In mild cases, the lesions are sparse or localized [54,74]. At the height of the disease process, HRCT reveals ground-glass opacities along the bronchovascular bundles. Pleural effusions, usually bilateral, are present in almost 90 percent. (See "High resolution computed tomography of the lungs".)

Pulmonary function tests — Due to the acute presentation, it is often not possible to obtain pulmonary function tests. When performed, a restrictive process may be noted (reduced forced vital capacity [FVC] and total lung capacity with a normal forced expiratory volume in one second [FEV1]/FVC); diffusing capacity for carbon monoxide (DLCO) is commonly reduced [7,9,55].

Oxygenation is typically monitored by pulse oximetry.

DIAGNOSIS — The diagnosis of acute eosinophilic pneumonia (AEP) is typically based upon clinical criteria that include bronchoalveolar lavage (BAL) eosinophilia with exclusion of known causes of pulmonary eosinophilia (table 1). Lung biopsy is rarely necessary.

Diagnostic criteria — A confident diagnosis of AEP can usually be made without a lung biopsy in patients who meet the following criteria [7,8,71,75]:

A febrile illness of short duration (one month or less, but often less than one week)

Hypoxemic respiratory failure (eg, pulse oxygen saturation [SpO2] <90 percent on room air or arterial oxygen tension [PaO2] <60 mmHg)

Diffuse pulmonary opacities on chest radiograph

BAL differential cell count showing eosinophilia >25 percent

Absence of known causes of eosinophilic pneumonia, including drugs, infections, asthma, or atopic disease (table 1) (see "Overview of pulmonary eosinophilia")

Bronchoscopy with bronchoalveolar lavage — BAL is performed in the majority of patients to quantitate eosinophilia and to exclude infection, hemorrhage, or malignancy (eg, germ cell tumor, leukemia). The BAL is performed using a sequential instillation and recovery of 50 to 60 mL aliquots (to evaluate for hemorrhage) in an area of radiographic opacity. Samples are sent for cell count, microbiologic studies, and cytology. (See "Role of bronchoalveolar lavage in diagnosis of interstitial lung disease" and "Role of lung biopsy in the diagnosis of interstitial lung disease".)

In AEP, the BAL fluid typically shows a very high proportion (>25 percent) and total number of eosinophils [8,9,39,49,54,55]. While data on other cell counts are limited, the proportion of BAL lymphocytes is approximately 10 to 30 percent and the proportion of BAL neutrophils is 1 to 16 percent [9,14,19,26]. The level of eosinophilia returns to normal when the illness resolves [9,54,55].

Lung biopsy — Lung biopsy is rarely necessary to make a diagnosis of AEP in immunocompetent patients with a compatible history and prominent BAL eosinophilia in the absence of infection or another known precipitant [7,8,75]. Indications for lung biopsy would include concern about an infectious etiology that could not be quickly excluded by BAL or failure to respond to systemic glucocorticoids.

DIFFERENTIAL DIAGNOSIS — For patients with acute, fulminant respiratory failure, diffuse radiographic opacities, and bronchoalveolar lavage (BAL) eosinophilia, the differential diagnosis includes:

Eosinophilic granulomatosis with polyangiitis – Eosinophilic granulomatosis with polyangiitis (EGPA, Churg Strauss), like acute eosinophilic pneumonia (AEP), can present with progressive respiratory insufficiency, fever, radiographic pulmonary opacities, and BAL eosinophilia. However, peripheral blood eosinophilia >10 percent is characteristic of EGPA and uncommon at presentation in AEP. In addition, the multisystemic involvement typically seen in EGPA would be absent in AEP. (See "Clinical features and diagnosis of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)", section on 'Diagnostic criteria'.)

Fungal infection – Infections due to Coccidioides immitis and Trichosporon species can cause acute eosinophilic pneumonia [76-79]. For Coccidioides, a history of travel or residence in an endemic area should alert the clinician to the possibility. The cases of acute eosinophilic pneumonia associated with Trichosporon have all been reported from Japan, and there may be a degree of overlap with summer-type hypersensitivity pneumonitis [79]. In one case report, AEP was caused by the inhalation of a large amount of vapor released by a household composter [80]. Aspergillus fumigatus was cultured from the composter soil and the bronchoalveolar lavage fluid. (See "Overview of pulmonary eosinophilia", section on 'Fungal and mycobacterial infections' and "Primary pulmonary coccidioidal infection", section on 'Diagnosis'.)

In another case report, invasive aspergillosis mimicked AEP in a patient with previously undiagnosed chronic granulomatous disease (caused by defects in phagocyte nicotinamide adenine dinucleotide phosphate [NADPH] oxidase) [81]. (See "Chronic granulomatous disease: Pathogenesis, clinical manifestations, and diagnosis".)

Parasitic infection – Infections due to Ascaris, Paragonimus, Strongyloides, and Toxocara can present with diffuse pulmonary opacities and peripheral blood and BAL eosinophilia. Often, a history of travel or residence in an endemic area will alert the clinician to the possibility. (See "Overview of pulmonary eosinophilia", section on 'Helminth infections'.)

Eosinophilic pneumonia due to drugs, toxins, and lung irradiation – Eosinophilic pneumonia can be caused by drugs, toxins, and lung irradiation; these possibilities are best investigated by a careful history (table 1) [26]. (See "Overview of pulmonary eosinophilia", section on 'Medications and toxins'.)

Other processes that might have a similar clinical presentation, but without BAL eosinophilia include acute respiratory distress syndrome (ARDS), acute interstitial pneumonia, fulminant cryptogenic organizing pneumonia (COP), diffuse alveolar hemorrhage (DAH), and granulomatosis with polyangiitis (GPA). (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Diagnosis' and "Acute interstitial pneumonia (Hamman-Rich syndrome)", section on 'Diagnosis' and "The diffuse alveolar hemorrhage syndromes" and "Granulomatosis with polyangiitis and microscopic polyangiitis: Respiratory tract involvement", section on 'Bronchoscopy' and "Cryptogenic organizing pneumonia", section on 'Diagnosis'.)

TREATMENT — Initial management of acute eosinophilic pneumonia (AEP) usually includes supportive care with supplemental oxygen and possibly mechanical ventilation, empiric antibiotics until culture results are available, and systemic glucocorticoid therapy. While clinical trial data are lacking, most patients with AEP experience progressive respiratory failure without systemic glucocorticoid therapy, but improve rapidly (within 12 to 48 hours) in response to intravenous or oral glucocorticoid therapy [8,19,54-56]. Occasional patients with milder initial disease have experienced spontaneous improvement following smoking cessation and without glucocorticoid therapy [8,19,24,54,55]. Thus, we recommend treatment with systemic glucocorticoids for almost all patients with AEP (after exclusion of infectious causes), except those with clear evidence of an improving course [82].

The optimal dose or length of glucocorticoid treatment is not known, and initial therapy often varies based upon the severity of disease:

In the presence of severe hypoxemia or respiratory failure requiring mechanical ventilation, methylprednisolone (60 to 125 mg every six hours) is given until respiratory failure resolves (usually within one to three days).

In the absence of respiratory failure (eg, pulse oxygen saturation >92 percent on low-flow supplemental oxygen), initial treatment with oral prednisone (40 to 60 mg daily) is reasonable.

Oral prednisone in a dose of 40 to 60 mg per day is then continued for two weeks beyond the complete resolution of symptoms and abnormalities on the chest radiograph [19,71]. At that time, the dose can be reduced by 5 mg every seven days until complete cessation of therapy [2,9,19,82]. If the patient shows clinical stabilization with rapid resolution of all symptoms, then earlier glucocorticoid tapering (over 7 to 14 days) may be an acceptable treatment strategy especially for AEP patients who present with initial eosinophilia [83].

A longer treatment course (up to four weeks) with tapering and discontinuing of prednisone over the subsequent two to four weeks may occasionally be required in patients who experienced severe respiratory failure with delayed resolution of symptoms and radiographic abnormalities.

If a patient fails to respond to glucocorticoids, an alternative diagnosis should be entertained. There are no data on treatments other than glucocorticoids.

OUTCOMES — Symptomatic and radiographic improvement is usually rapid and progressive with complete radiographic clearing over one to two months after initiation of systemic glucocorticoids [8]. Similarly, pulmonary function tests return to normal after recovery from the illness [8].

Relapse is uncommon and is usually associated with resumption of cigarette smoking after initial cessation [14,18-20,24].

The pleural effusions may resolve more slowly than the pulmonary parenchymal opacities [9].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Interstitial lung disease".)

SUMMARY AND RECOMMENDATIONS

Presentation – Idiopathic acute eosinophilic pneumonia (AEP) typically presents with an acute febrile illness of less than four weeks duration (often less than seven days), a nonproductive cough, and progressively worsening dyspnea. Associated symptoms and signs may include malaise, myalgias, night sweats, and pleuritic chest pain. (See 'Introduction' above and 'Clinical features' above.)

Etiology – AEP has been associated most often with new onset or resumption of cigarette smoking. Heavy inhalational exposure to smoke, fine sand, and dust has also been associated with AEP. (See 'Etiology' above.)

Pathology – Lung histopathology obtained in a small number of patients reveals extensive abnormality with marked eosinophilic infiltration in the interstitium and alveolar spaces, acute and/or organizing diffuse alveolar damage, and absence of granulomas or hemorrhage. (See 'Pathology' above.)

Evaluation

Laboratory studies – At presentation, the peripheral blood count usually shows a neutrophilic leukocytosis without eosinophilia, although peripheral blood eosinophilia may develop over the course of the disease. (See 'Laboratory studies' above.)

Imaging – The initial chest radiograph may show only subtle reticular or ground glass opacities, often with Kerley B lines. As the disease progresses, bilateral diffuse mixed ground glass and reticular opacities develop. Typical findings on high-resolution computed tomography (HRCT) scans include bilateral, random, and patchy ground-glass or reticular opacities and also small bilateral pleural effusions. (See 'Imaging' above.)

Diagnosis – A confident diagnosis of AEP can usually be made on the basis of the combination of an acute febrile illness of short duration (one month or less), hypoxemic respiratory failure, diffuse pulmonary opacities on chest radiograph, and bronchoalveolar lavage eosinophilia (>25 percent), after exclusion of infection, vasculitis, or other known precipitants (eg, drugs, irradiation) (table 1). (See 'Diagnosis' above and "Overview of pulmonary eosinophilia".)

Initial treatment – For the majority of patients with AEP, we recommend treatment with systemic glucocorticoids after exclusion of infection (Grade 1B). This recommendation is due to the severity and progressive nature of respiratory impairment and the dramatic response to glucocorticoids. The optimal dose of glucocorticoids is not known, but a reasonable course is to select the dose based upon the severity of respiratory impairment. (See 'Treatment' above.)

In the presence of severe hypoxemia or respiratory failure requiring mechanical ventilation, methylprednisolone (60 to 125 mg every six hours) is given until respiratory failure resolves (usually within one to three days).

In the absence of respiratory failure (eg, pulse oxygen saturation >92 percent on room air), initial treatment with oral prednisone (40 to 60 mg daily) is reasonable.

Tapering therapy – Oral prednisone is continued at a dose of 40 to 60 mg per day for two weeks beyond the complete resolution of symptoms and conventional chest radiograph abnormalities. Prednisone is then tapered over approximately four weeks and discontinued. (See 'Treatment' above.)

Exposure avoidance – As cigarette smoking initiation or increase in amount are often associated with AEP and as relapses have been associated with resumption of smoking, complete smoking cessation should be strongly encouraged. Relapses have not been well-documented in other cases of acute exposures, but avoidance is prudent when an etiology can be identified. (See 'Treatment' above.)

Prognosis – Symptomatic and radiographic improvement is usually rapid and progressive with complete radiographic clearing over one to two months. Relapse is uncommon and is usually attributable to resumption of cigarette smoking after initial cessation. (See 'Outcomes' above.)

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Topic 4374 Version 30.0

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