OCCUPATIONAL-HYPERSENSITIVITY PNEUMONITIS: A DIAGNOSIS NOT TO BE MISSED BY PROPER HISTORY TAKING

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: Hypersensitivity Pneumonitis (HP) is an inflammatory and/or fibrotic disease affecting the lung parenchyma. Radiographic or histopathological findings help to categorize HP as either fibrotic (mixed inflammatory plus fibrotic or purely fibrotic) or non-fibrotic (purely inflammatory), being the primary determinant of prognosis. Rarely acute respiratory decline can be the first manifestation of chronic HP that may develop within a wide timeframe from weeks to years of exposure. CASE PRESENTATION: A 38-year-old male with no comorbidities or smoking history, presented with one week of progressive shortness of breath. Further questions revealed that since childhood he was working in a car painting shop without using protective equipment. Vital signs: Temperature 36.9, pulse 98 beats/min, respiratory rate 22 breaths/min, blood pressure 116/96 mmHg, and oxygen saturation 37% on room air, improved to 98% via a non-rebreather mask. He was not in respiratory distress. Findings included diffuse bilateral crackles over the lung fields. CXR showed diffuse patchy bilateral alveolar opacities. WBC count and serum procalcitonin were within normal limits. SARS-CoV-2 PCR performed was negative. Chest CT showed extensive diffuse bilateral lung consolidations, ground-glass opacities, honeycombing, and prominent mediastinal lymph nodes. Given the patient symptoms, high-risk exposure to isocyanate which exists in paints, radiologic findings, and by ruling out infectious etiologies, the suspected diagnosis of HP was made and treatment with IV Methylprednisone 60mg twice daily initiated. After 2 days, clinical status improved and oxygen requirements decreased to 8 LPM via Nasal Cannula. Bronchoscopy showed erythema throughout the tracheobronchial tree. Bronchoalveolar lavage (BAL) was performed and cytology showed: Reactive bronchial cells (24% Lymphocytes, 31% macrophages, 44% neutrophils). Consequently, a diagnosis of chronic, non-fibrotic HP was confirmed. Finally, after completing 7 days of IV steroid treatment, he was discharged home with 2 LPM supplemental oxygen. Instructions regarding oral corticosteroid tapering over a 3 week-period were provided. DISCUSSION: Diagnosis of chronic HP is predominantly based on exposure identification, CT scan pattern, and bronchoscopic/histopathological findings. BAL in the majority of the patients with non-fibrotic chronic HP shows elevated cell count with greater than 20% lymphocytes and this group responds to steroid therapy significantly. CONCLUSIONS: We would like to emphasize the high value of taking detailed patient history to detect causative agent exposure. Unprotected exposure to isocyanate was the key leading to further investigation including performing BAL in our patient. We also recommend health care providers educate their patients regarding proper safety equipment use, in case of occupational exposure to HP inducers. Prevention is always better than cure! REFERENCE #1: Raghu G, Remy-Jardin M, Ryerson CJ, Myers JL, Kreuter M, Vasakova M, et. al. Diagnosis of hypersensitivity pneumonitis in adults. An official ATS/JRS/ALAT clinical practice guideline. Am J Respir Crit Care Med 2020;202(3):e36–e69. REFERENCE #2: Koster MA, Thomson CC, Collins BF, Jenkins AR, Ruminjo JK and Raghu G. Diagnosis of hypersensitivity pneumonitis in adults, 2020 clinical practice guideline: summary for clinicians. Ann Am Thorac Soc 2020. DISCLOSURES: no disclosure on file for Manish Gugnani;No relevant relationships by Irina Gutierrez Puentes, source=Web Response No relevant relationships by Julio Piedra Butina, source=Web Response No relevant relationships by Asieh TakallooBakhtiari, source=Web Response