A 40 years-old welder presented with sudden episode of massive hemoptysis without hemodynamic failure. Hemoptysis, in an amount of 4 cups, occurred suddenly after 8 h of welding in time of a few hours. The patient described the amount of bleeding as 1 L. He denied dyspnea, sputum production, fever, chest pain and any contact with tuberculous patients. Patient further reported a monthly headache with 6-7 days periods which increased especially after spending a long time with welding.
He had no history of drug use, systemic or pulmonary disease or coagulapathy, and reported no alcohol use. There was no family history of coagulopathy, or tuberculosis. He had a smoking history of 2 pack/years, and has been working as a welder for 8 years. On physical examination, he was anxious and mildly dyspneic with a pulse rate of 110/min, respiratory rate of 24/min and a blood pressure of 130/80 mmHg and oxygen saturation 95% on room air. There was no clubbing or lymphadenopathy. Oral or genital aphthous ulcers were not detected in physical examination or presented in past medical history. Bilateral hyperemic conjunctivas and basal crackles on auscultation were remarkable on physical examination. Rest of the physical examination was unremarkable. Although there was nothing then mild diffuse ground-glass opacity on his chest radiography, high resolution computed tomography scans revealed diffuse poorly defined centrilobular nodules with patchy ground-glass opacity predominantly on the lower lobes and right side (Figs. 1 and 2). Laboratory investigation showed a hemoglobin level of 12 gr/dL, a WBC count of 10.4 x 103 muL (92% neutrophils, 5% lymphocytes), haematocrit of 0.40, a platelet count of 162 x 103/muL. Prothrombin time and international normalized ratio were within normal limits. Sedimentation was 60 mm/h. His routine biochemical investigations including renal and liver functions, and urine analysis were all normal. Atypical cells in peripheral smear were not detected, platelets were aggregated. Antinuclear antibody, rheumatoid factor and anti-double-strand DNA, and anti-neutrophil cytoplasmic antibodies were all negative. Fiberoptic bronchoscopy revealed active bleeding bilaterally from the lower lobes and right middle lobe, with major bleeding on the right side. We made iced saline and Ankaferd Blood Stopper  (2 mL) lavage to the both of the lower lobes from the bronchoscope probe. Bleeding was decreased after this procedure. Hemoptysis diminished day by day, and disappeared on sixth day after acceptance. No other specific treatment for hemoptysis was used. Control bronchoscopy on fifteenth day of presentation was completely normal without any potential cause of bleeding such as intrabronchial mass or foreign body. Culture of bronchoalveolar washing was negative for fungal and acid-fast bacteria. The patient discharged on tenth hospital day without hemoptysis. There has been no recurrence for two years.