Case Reports

Another Reason Not to Smoke: Acute Eosinophilic Pneumonia

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Acute eosinophilic pneumonia is an uncommon but potentially life-threatening cause of respiratory failure if left untreated.



The following case was encountered and treated by Capt DellaVolpe during deployment with Operation Enduring Freedom-Trans Sahara on his tour as Special Operations Flight Surgeon with the Air Force Special Operations Command. The case highlights a rare but serious disease that can be particularly challenging to manage in military members serving overseas.

Case Presentation

After 2 days of worsening dyspnea on exertion, fever, and fatigue, a previously healthy 22-year-old man presented to a remote clinic established as part of a military deployment in central Africa. Despite having received azithromycin from a field medic, his condition continued to worsen. He had no cough, recent weight changes, or night sweats. The patient’s past medical history was unremarkable, including any prior history of pulmonary disorders.

The patient was a member of the U.S. Army Military Police Corps and had been deployed for 3 weeks. His job involved local patrols, and he had no history of airborne exposures, such as mold or chemical inhalants, or travel to sandy environments. Although he was previously a nonsmoker, he reported smoking local cigarettes to help him stay awake during night patrols over the past 2 weeks. The patient’s vaccination history included influenza, tetanus, measles/mumps/rubella, yellow fever, typhoid, hepatitis A/B, anthrax, meningococcus, and smallpox, all administered before deployment. At the time of evaluation, his temperature was 103.9°F, pulse 120 bpm, respiratory rate 32 breaths per minute, and blood pressure 110/70 mm Hg. His oxygen saturation was 80% on room air.

On examination, he was in significant distress and only able to speak in short sentences. There was no jugular venous distension or stridor. He was tachycardic, with a regular rhythm, without murmurs, rubs, or gallops. A pulmonary examination revealed decreased air movement bilaterally with bilateral inspiratory crackles at the bases. There was a tactile fremitus on the right side. He had no swelling or tenderness of the extremities, and no rashes were noted.

Laboratory capabilities were limited given the remote clinic location. Rapid malaria and rapid influenza were negative. A blood smear showed no organisms. A chest X-ray showed diffuse alveolar infiltrates and homogenous opacification of the right hemithorax.

The patient was placed on continuous oxygen by facemask and started on IV ceftriaxone and vancomycin. He was volume resuscitated with normal saline, with a modest effect on his heart rate. Attempts to wean his oxygen consumption were accompanied by an immediate oxygen desaturation to the low 80s. Because of the limited supply of oxygen available at the remote location as well as the patient’s poor response to broad-spectrum antibiotic coverage over the next 8 hours, he was evacuated by airborne casualty evacuation to the critical care team at Landstuhl Regional Medical Center in Germany.

Laboratory results revealed a peripheral leukocytosis with no eosinophilia. The patient underwent bronchoalveolar lavage (BAL), which showed 30% eosinophils. A diagnosis of acute eosinophilic pneumonia (AEP) was made, and the patient was started on IV methylprednisolone. He experienced a rapid resolution of symptoms and was completely weaned off oxygen 2 days later. The following week he was released from the hospital and able to return stateside to his unit.


This case illustrates an uncommon but potentially life-threatening cause of respiratory failure, AEP. First described as a reversible, noninfectious cause of respiratory distress, AEP is now characterized as an uncommon yet severe febrile illness, which typically presents with hypoxia, pulmonary infiltrates, and increased eosinophilia on bronchoalveolar lavage in the absence of other causes.1-3 Untreated, AEP can progress to respiratory failure and death.

Acute eosinophilic pneumonia belongs to a heterogeneous group of disorders known as the eosinophilic lung syndromes. Although the pathophysiology has not been completely characterized, it is theorized that AEP is caused by a hypersensitivity reaction to an airborne antigen.2 Interleukin-5 has been implicated in the preferential activation of eosinophils and granule release and may be responsible for the eosinophilic alveolar exudates. In addition, interleukin-5 has been established as an eosinophil chemotactant.4-6

Acute eosinophilic pneumonia is relatively uncommon. Most epidemiologic studies have been limited to retrospective analyses and case series.7 However, the presentation of the disease suggests that it may be underdiagnosed.6,8 The most common presenting signs and symptoms are dyspnea, fever, cough, and crackles on inspiration. Acute eosinophilic pneumonia has been documented in men and women of all ages with a 2:1 male predominance, typically occurring in previously healthy individuals aged 18 to 40 years.9,10 Reports of AEP in infants also exist.11

Although idiopathic cases have been described in the literature, patients, on average, will have a history of airborne toxin exposure, including smoke, sand, dust, mold, or chemicals. However, a causal relationship has not been proven.12

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