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A Case of Acute Interstitial Pneumonitis With a Very Atypical Clinical Presentation, Radiologic Findings, and Response to Corticosteroid Therapy FREE TO VIEW

Joann Bolton, MD; Jeffrey Garland, MD
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Mayo Clinic Jacksonville, Atlantic Beach, FL

Chest. 2014;146(4_MeetingAbstracts):316A. doi:10.1378/chest.1987520
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SESSION TITLE: Critical Care Student/Resident Case Report Posters III

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: Acute Interstitial Pneumonitis (AIP) is a disorder with numerous etiologies which typically presents with rapidly progressive bilateral patchy airspace opacities and a clinical presentation consistent with the Acute Respiratory Distress Syndrome (ARDS). We present the case of a patient with AIP with a very atypical clinical presentation, radiographic findings, and response to treatment.

CASE PRESENTATION: A 46-year-old man with a history only significant for obstructive sleep apnea presented to the emergency department with 7 days of flu-like symptoms and dyspnea on exertion in the setting of recent sick contacts. On presentation he was found to be dyspneic with a respiratory rate of 20, and a room air oxygen saturation of 85%. He was febrile at 39.2 with WBC count of 4.7. Chest X ray and CT scan revealed bilateral lung opacities with a peripheral predominance and no evidence of pulmonary emboli. Over the next three days, despite treatment with both broad spectrum antibiotics and Tamiflu, he required endotracheal intubation, 100% FiO2, high levels of PEEP, and salvage therapy with nitric oxide (NO). Bronchoalveolar lavage was negative for infection and for eosinophils. Serologies were negative for connective tissue disease (CTD) and eosinophilia. Deemed too unstable for open lung biopsy (OLBX), empiric high dose steroids (methylprednisolone 60 mg IV q 6hrs) were started. Over the next 3 days, he improved, was off NO, and the FiO2 was down to 60%. OLBX was performed 11 days after starting steroid therapy and showed acute interstitial pneumonitis with microthrombi and lung infarction. He slowly improved and weened to nasal canula 27 days after starting corticosteroid therapy. He was discharged from the hospital at 29 days on 2 liters oxygen.

DISCUSSION: The etiology of this fulminant and aggressive steroid responsive disease is puzzling, with a broad differential diagnosis including, chronic eosinophilic pneumonia (CEP), cryptogenic organizing pneumonia (COP), a CTD-associated or other secondary cause of organizing pneumonia, a drug reaction, aspiration lung injury, or an extremely unusual case of sarcoidosis. The clinical presentation and laboratory findings did not clearly support any of these. With the patient too unstable for OLBX it was felt there was little to lose from a trial of high dose corticosteroids. It is impossible to say whether this was causal of or associated with the improvement. Findings on the OLBX may have been influenced by the corticosteroid treatment prior to the procedure. Finally, the findings of pulmonary emboli on OLBX were likely secondary events.

CONCLUSIONS: We present the case of a patient with AIP with a very atypical clinical and radiologic presentation with bilateral peripheral predominant infiltrates in whom it was deemed unsafe to obtain an OLBX. In such patients, an empiric course of salvage therapy with high dose corticosteroids should be considered.

Reference #1: Harrison’s Textbook of Medicine, 18th ed., 2013.

DISCLOSURE: The following authors have nothing to disclose: Joann Bolton, Jeffrey Garland

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