Diffuse Lung Disease |

An Uncommon Presentation of Lymphocytic-Variant Hypereosinophilic Syndrome as the Cause of Respiratory Failure in a Patient With Asthma FREE TO VIEW

Jonathan Wiesen, MD; Fred Hsieh, MD; Tarik Hanane, MD
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Cleveland Clinic Foundation, Cleveland, OH

Chest. 2013;144(4_MeetingAbstracts):436A. doi:10.1378/chest.1703011
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SESSION TITLE: Interstitial Lung Disease Cases II

SESSION TYPE: Affiliate Case Report Slide

PRESENTED ON: Monday, October 28, 2013 at 04:15 PM - 05:15 PM

INTRODUCTION: Although patients with asthma often get bacterial pneumonias, asthma is also associated with a number of other causes of pulmonary infiltrates, including Churg Strauss Syndrome, eosinophilic pneumonia and allergic bronchopulmonary aspergillosis. Respiratory failure with eosinophilia in patients with a history of asthma may be due to the underlying disease or any of the aforementioned syndromes. We present an uncommon cause of respiratory failure in a patient with a history of poorly controlled asthma.

CASE PRESENTATION: A 42 year old male with a past medical history of mild-moderate asthma presented to the intensive care unit for further management of multifocal pneumonia. He had recently seen his primary care physician four months prior to admission with a productive cough and bilateral lower lobe opacities on chest Xray. He was treated with antibiotics and subsequently developed a diffuse rash with leukocytosis ( WBC 23k/uL) and eosinophilia (87%). The eosinophilia did not completely resolve and a bone marrow aspirate did not show clonal eosinophilic disease or malignancy and workup was negative for autoimmune, parasitic, or other infectious disease. He presented to the emergency department with hypoxia. Laboratory examinations were significant for leukocytosis (39 k/uL, 73% eosinophils), thrombocytopenia (16 k/uL), acute kidney injury (creatinine 1.46 mg/dL), and elevated liver function tests. Computed tomography of the chest without contrast showed multifocal opacities consistent with pneumonia. Platelet factor four (PF4) testing was positive although the patient was not on heparinoids. Further imaging evaluation revealed diffuse systemic thrombosis, including blood clots in the bilateral upper and lower extremities, both left and right ventricles and the hepatic vein. An emergent inferior vena cava filter was placed and high dose corticosteroid therapy (125 mg of methylprednisolone every 6 hours) was initiated. Due to his extensive thrombosis he was anticoagulated with bivalrudin due to the concern for heparin induced thrombocytopenia (HIT). Broad spectrum antibiotics were administered as well. A diagnosis of lymphocytic-variant hypereosinophilic syndrome (HES) with possible concomitant HIT was proposed. With high dose glucocorticoid therapy his eosinophil count slowly normalized and his platelet counts recovered as well. He was discharged on a steroid taper and systemic anticoagulation with warfarin.

DISCUSSION: HES is common in patients with asthma, although it rarely presents with hypercoagulability and diffuse systemic thrombosis. It is uncommon to have biventricular mural thrombi with this condition. Like other forms of eosinophilic pneumonia, it is sensitive to treatment with corticosteroids.

CONCLUSIONS: This is the first reported case of HES with systemic hypercoagulability and a positive PF4.

Reference #1: Shannon JJ, Lynch JP. Eosinophilic pulmonary syndromes. Clinical Pulmonary Medicine. 1995; 2(1).

DISCLOSURE: The following authors have nothing to disclose: Jonathan Wiesen, Fred Hsieh, Tarik Hanane

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