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Absence of Peripheral Eosinophilia on Initial Clinical Presentation Does Not Rule Out the Diagnosis of Acute Eosinophilic Pneumonia

2015; Elsevier BV; Volume: 3; Issue: 4 Linguagem: Inglês

10.1016/j.jaip.2015.01.008

2213-2201

Becky Buelow, Brian T. Kelly, Heidi Zafra, Kevin J. Kelly,

Asthma and respiratory diseases

A previously healthy 17-year-old white male presented emergently with a 3-day history of fever, dry cough, and progressive dyspnea. He had initiated tobacco smoking 3 months ago, but quit 1 week before presentation. He denied other recreational drug use and was not taking any prescribed or over-the-counter medications. He had recently traveled to the desert in Texas. His family history was noncontributory. On initial physical examination, he was febrile to 38.9°C as well as tachypneic and hypoxic (O2 saturation of 86% on room air). He had diffuse coarse breath sounds with conversational dyspnea. His initial white blood cell count demonstrated a leukocytosis of 16,000 cells/μL (normal, 4,000-10,500 cells/μL) with an elevated absolute neutrophil count of 14,560 cells/μL (normal, 1440-7560 cells/μL) and a normal absolute eosinophil count of 480 cells/μL (normal, 0-500 cells/μL). His hemoglobin and platelets were normal. The initial chest x-ray demonstrated diffuse bilateral interstitial pulmonary opacities with a right-sided pleural effusion but without cardiomegaly (Figure 1). His clinical status worsened quickly on the day of admission, and he required intubation with mechanical ventilation, right-sided chest tube placement, and vasopressor support. With the acute nature of the pneumonia and critical condition of the patient, critical care physicians initially believed that performing a bronchoalveolar lavage (BAL) would add risk without additional benefit. After consultation with allergists who had working knowledge of acute eosinophilic pneumonia's (AEP's) disease process, an emergent bronchoscopy was performed. It revealed 23% eosinophils, 45% neutrophils, 10% lymphocytes, 4% monocytes, and 18% alveolar macrophages in the BAL. Infectious studies of common viruses, bacteria, and fungi were all negative. Precipitins for molds and pigeon serum were all negative. A drug screen was negative. Anti-neutrophil cytoplasmic antibody associated vasculitis was a less likely etiology given the patient had no history of asthma, no evidence of upper airway disease, and no evidence of renal or nervous system disease. Thus, anti-neutrophil cytoplasmic antibody testing was not performed. With exclusion of other likely etiologies of pulmonary eosinophilia, the diagnosis of AEP was made. The patient was urgently started on high-dose parenteral corticosteroids (1 g/d). The patient improved rapidly with removal of his chest tube and weaning of his vasopressor support. He was extubated to room air after only 3 days of high-dose corticosteroids. His medication was then converted to 60 mg of prednisone daily. On day 8 of his hospitalization, he developed a profound peripheral eosinophilia with an absolute eosinophil count of 1995 cells/μL (normal, 0-500 cells/μL). By this time, he had returned to clinical and radiologic baseline (Figure 1). He was discharged home on a 2-week oral prednisone wean, but was lost to follow-up. The diagnostic criteria for AEP, also known as the Pneumonia of Allen, are outlined in Table I.1Uchiyama H. Suda T. Nakamura Y. Shirai M. Gemma H. Shirai T. et al.Alterations in smoking habits are associated with acute eosinophilic pneumonia.Chest. 2008; 133: 1174-1180Crossref PubMed Scopus (112) Google Scholar, 2Park H.N. Chung B.H. Pyun J.E. Lee K.C. Choung J.T. Lim C.H. et al.Idiopathic acute eosinophilic pneumonia in a 14-month-old girl.Korean J Pediatr. 2013; 56: 37-41Crossref PubMed Scopus (9) Google Scholar, 3Cottin V. Cordier J.F. Eosinophilic lung diseases.Immunol Allergy Clin N Am. 2012; 32: 557-586Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar AEP does not have a clear etiology, but risk factors for disease development do exist (Table I).1Uchiyama H. Suda T. Nakamura Y. Shirai M. Gemma H. Shirai T. et al.Alterations in smoking habits are associated with acute eosinophilic pneumonia.Chest. 2008; 133: 1174-1180Crossref PubMed Scopus (112) Google Scholar, 2Park H.N. Chung B.H. Pyun J.E. Lee K.C. Choung J.T. Lim C.H. et al.Idiopathic acute eosinophilic pneumonia in a 14-month-old girl.Korean J Pediatr. 2013; 56: 37-41Crossref PubMed Scopus (9) Google Scholar AEP is an eosinophilic alveolitis; thus, BAL is necessary because tracheal aspirates and/or bronchial washings are not sufficient to determine and characterize the cellular infiltrate present in the alveoli.4Janz D.R. O’Neal Jr., H.R. Ely E.W. Acute eosinophilic pneumonia: a case report and review of the literature.Crit Care Med. 2009; 37: 1470-1474Crossref PubMed Scopus (41) Google Scholar Patients with AEP have a predominance of eosinophils in BAL, with an average of 37% and 54% as described in 2 case series.5Pope-Harman A.L. Davis W.B. Allen E.D. Christoforidis A.H. Allen J.N. Acute eosinophilic pneumonia: a summary of fifteen cases and a review of the literature.Medicine. 1996; 75: 334-342Crossref PubMed Scopus (200) Google Scholar, 6Philit F. Etienne-Mastroianni B. Parrot A. Guerin C. Robert D. Cordier J.F. Idiopathic acute eosinophilic pneumonia: a study of 22 patients.Am J Respir Crit Care Med. 2002; 166: 1235-1239Crossref PubMed Scopus (251) Google Scholar In this case, the BAL eosinophil count was 23%, which is lower than the proposed percentage for diagnosis. One may speculate that 23% may not have been the peak percentage of lung eosinophils because it was performed quite early, but this case illustrates the importance of evaluating the overall picture for prompt diagnosis and treatment of AEP. In addition to helping with diagnosis, BAL can be and was helpful in excluding other causes of eosinophilic pneumonia such as infection.4Janz D.R. O’Neal Jr., H.R. Ely E.W. Acute eosinophilic pneumonia: a case report and review of the literature.Crit Care Med. 2009; 37: 1470-1474Crossref PubMed Scopus (41) Google Scholar Exclusion of other etiologies such as infection, medications, inhalants, recreational drugs, or malignancy is paramount because these agents or conditions have been reported as causes of lung eosinophilia.3Cottin V. Cordier J.F. Eosinophilic lung diseases.Immunol Allergy Clin N Am. 2012; 32: 557-586Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar, 7Bhatt N.Y. Allen J.N. Update on eosinophilic lung diseases.Semin Respir Crit Care Med. 2012; 33: 555-571Crossref PubMed Scopus (20) Google Scholar, 8Kelly K.J. Ruffing R. Acute eosinophilic pneumonia following the intentional inhalation of Scotchguard®.Ann Allergy. 1993; 71: 358-361PubMed Google Scholar, 9Weiler P.F. Eosinophilia and eosinophil-related disorders.in: Adkinson Jr., W.F. Bochner B.S. Busse W.W. Holgate S.T. Lemanske Jr., R.F. Simons F.E.R. Middleton’s allergy: principles and practice. 7th ed. Elsevier, Philadelphia2009: 859-877Crossref Google Scholar, 10Allen J.N. Davis W.B. Eosinophilic lung diseases.Am J Respir Crit Care Med. 1994; 150: 1423-1438Crossref PubMed Scopus (403) Google ScholarTable IDiagnostic criteria and epidemiologic associations of AEP of AllenData from Uchiyama et al,1Uchiyama H. Suda T. Nakamura Y. Shirai M. Gemma H. Shirai T. et al.Alterations in smoking habits are associated with acute eosinophilic pneumonia.Chest. 2008; 133: 1174-1180Crossref PubMed Scopus (112) Google Scholar Park et al,2Park H.N. Chung B.H. Pyun J.E. Lee K.C. Choung J.T. Lim C.H. et al.Idiopathic acute eosinophilic pneumonia in a 14-month-old girl.Korean J Pediatr. 2013; 56: 37-41Crossref PubMed Scopus (9) Google Scholar and Cottin and Cordier.3Cottin V. Cordier J.F. Eosinophilic lung diseases.Immunol Allergy Clin N Am. 2012; 32: 557-586Abstract Full Text Full Text PDF PubMed Scopus (46) Google ScholarDiagnostic criteria1. Acute respiratory symptoms (usually <7 d before seeking medical care) with fever2. Bilateral diffuse alveolar or mixed alveolar-interstitial infiltrates on imaging3. Evidence of hypoxia or hypoxemia4. Lung eosinophilia (≥25%) in BAL or eosinophilic pneumonia at lung biopsy5. The absence of determined cause including infection or exposure to drugs known to cause pulmonary eosinophilia (recent tobacco smoking onset or exposure to inhaled dusts may have occurred)Epidemiology and risk factors1. Recent initiation or alteration in smoking2. Adult predominance3. No history of asthma4. Male predominance Open table in a new tab This case also demonstrates how patients may present with a normal peripheral eosinophil count, but then may develop a peripheral eosinophilia days later. In Allen et al,11Allen J.N. Pacht E.R. Gadek J.E. Davis W.B. Acute eosinophilic pneumonia as a reversible cause of noninfectious respiratory failure.N Engl J Med. 1989; 321: 569-574Crossref PubMed Scopus (375) Google Scholar 3 of the 4 (75%) patients had normal peripheral eosinophil counts on presentation. In addition, 14 of 22 patients with AEP (64%) had no peripheral eosinophilia on presentation, but 7 went on to develop peripheral eosinophilia between 2 and 10 days after presentation.6Philit F. Etienne-Mastroianni B. Parrot A. Guerin C. Robert D. Cordier J.F. Idiopathic acute eosinophilic pneumonia: a study of 22 patients.Am J Respir Crit Care Med. 2002; 166: 1235-1239Crossref PubMed Scopus (251) Google Scholar These observations demonstrate that a normal peripheral eosinophil count does not rule out AEP. Moreover, if a BAL is not performed or is not diagnostic, a delayed peripheral eosinophilia may be the only manifestation of disease. In conclusion, this case of AEP demonstrates 3 clinical pearls. First, a normal peripheral eosinophil count on initial clinical presentation in patients with AEP does not rule out disease. Second, delayed peripheral eosinophilia may be the only delayed marker of AEP if a BAL is not performed or if it is not helpful in the diagnosis of AEP. Last, early evaluation with BAL did and will allow the discovery of pulmonary eosinophilia, which prompted allergists to initiate high-dose corticosteroids early in this disease course.