Case Presentation:

A 22–year–old man, on military deployment, presents to a remote clinic in Central Africa with 2 days of worsening dyspnea on exertion, fever, and fatigue; he denied a cough. His symptoms worsened despite treatment with azithromycin by the field medic. Though a nonsmoker, he had been smoking local cigarettes to stay awake during night patrols over the last 2 weeks. On physical exam, his temperature was 103.9oF, heart rate 120 beats per minute and respiratory rate 32 times per minute. Oxygen saturation was 80%. He had decreased air movement bilaterally and bilateral inspiratory crackles at the bases of the lungs. There was a tactile fremitus on the right side. Lab capabilities were limited, but rapid malaria and influenza was negative. Chest X–ray showed diffuse alveolar infiltrates and homogenous opacification of the right hemithorax. He was placed on continuous O2 and started on IV ceftriaxone and vancomycin. He was fluid resuscitated with normal saline, with modest effect on his heart rate. Attempts to wean his oxygen consumption were lead to an immediate desaturation to 80%. He was transported to a facility with more capabilities. Labs revealed a leukocytosis with no eosinophils. He underwent bronchoalveolar lavage (BAL) showing 30% eosinophils. A diagnosis of acute eosinophilic pneumonia was made and he was started on steroids. He experienced a rapid resolution of symptoms and was weaned off oxygen in 2 days. The next week he was released and returned to his unit.


Acute eosinophilic pneumonia (AEP) is part of a heterogenous group of disorders known as the eosinophilic lung syndromes. Though the pathophysiology has not been completely characterized, the syndrome typically consists of acute febrile illness, severe hypoxia, pulmonary infiltrates, increased eosinophils on BAL, and an absence of infection or other cause. The most commonly documented presenting signs and symptoms are dyspnea, fever, cough, and crackles on inspiration. Diagnosis is made based on pulmonary eosinophilia and ruling out chronic causes of eosinophilic pulmonary disease. Often pulmonary eosinophilia can exist without a peripheral eosinophilia due to a pulmonary eosinophil sequestration. Diagnosis often occurs after patients become worse despite broad spectrum antibiotic therapy.


Although there are idiopathic causes described in the literature, usually patients will have a history of airborne toxin exposure. One well–described key exposure is new onset smoking, seen with this patient. Typically, the patients described are in their mid–20s and develop symptoms consistent with AEP within one month of initiation of smoking. The treatment of AEP is steroids, typically IV methylprednisolone. Dosages vary, but the consensus is typically 60–125 mg of methylprednisolone every 6 h followed by an oral prednisone taper. Relapses of AEP have not been described in the literature, and the prognosis is typically excellent if identified rapidly and treated appropriately.