A 68-year-old man came to the ER (emergency room) with shortness of breath over the last 3 days, wheezing, a fever and a cough with purulent sputum. He had been experiencing cough and exercise-induced fatigue for one year. Earlier, he had two episodes of pulmonary tuberculosis. Five years earlier, he was treated by primary health care for six months with standard first-line tuberculosis drugs and declared cured but 2 years later he was diagnosed with pulmonary multi-drug resistant TB (MDR-TB). He took anti-tuberculosis therapy from December 30, 2014 until September 30th, 2016 with a regimen consisting of Km-Lfx-Eto-Cs-Z-E during the intensive phase and Lfx-Eto-Cs-Z-E for the continuation phase. Sputum culture converted to negative in the second month of this therapy. He has had Diabetes Mellitus for 5 years and has been on insulin therapy. He had a previous history of smoking 4.5 packs per year but stopped smoking 5 years ago. There was no history of asthma, food or drug allergies.
On physical examination, the patient was alert with respiration rate 28 cycles per minute, blood pressure 140/80 mmHg, a pulse of 100 beats per minute, axillary temperature 38.5  C. Thoracic examination showed symmetrical chest movement, sonorous percussion, bronchial sounds with rhonchi on the right side of the chest and bilateral wheezing.
Laboratory results were Hemoglobin 14.6 g/dL; Leukocytes 29.130 x 109/L; Thrombocyte 215.000 x 1012/L, BUN 19 mg/dL, Creatinine 1.12 mg/dL, AST 24 U/L, ALT 17 U/L, Total Bilirubin 2.30 mg/dL, Direct Bilirubin 1.42 mg/dL, CRP 307.6 mg/dL, Sodium 132,7 mmol/l, Potassium 3.51 mmol/l, Random blood glucose 379 mg/dL. Blood gas analysis with 3L oxygen were pH 7.50, PaCO2 26.6 mmHg, PaO2 94.5 mmHg, HCO3- 21.1 mmol/l, BE -2.2 mmol/L, SaO2 98.2%, A-aDO2 71.9 mmHg, P/F ratio 337.5. A chest X-ray on day 1 of hospital admission demonstrated fibrosis and consolidation was observed in the right lung field (Fig. 1B).
Sputum microscopy for acid fast bacilli staining was negative, Gram staining showed gram negative bacteria, Xpert MTB/RIF from sputum result was negative for tuberculosis. With aerobic culture of sputum, we found Acinetobacter baumanii (sensitive to Gentamycin, Amikacin, Ceftazidime, Cefoperazone-Sulbactam, Ciprofloxacin, Levofloxacin); MTB culture of sputum was negative. Total IgE serum was 242.9 IU/mL, no worm infection was found by faecal examination, differential count of sputum showed eosinophils 5%, basophils 1.1%, and neutrophils 6.6%. Spirometry was performed after pneumonia and COPD exacerbation resolved. Pre-bronchodilator spirometry results were FVC 3.66 L (107% of predicted), FEV1 2.46 L (94% of predicted), FEV1/FVC 67.2% and post-bronchodilator spirometry results were FVC 3.97 L (116% of predicted), FEV1 2.71 L (104% of predicted), FEV1/FVC 68.2%. Reversibility testing showed 10.1% (250 ml) increase on bronchodilator treatment.
Patient was diagnosed with pneumonia and eosinophilic COPD exacerbation based on findings of high total IgE serum and high eosinophil count of sputum. Eosinophilic COPD has several clinical characteristics, one of them is preserved FEV1. A corresponding finding was seen in this patient (predictable FEV1 is 94%). In this case, irreversible airflow obstruction (pre-bronchodilator FEV1/FVC 67.2% and post-bronchodilator FEV1/FVC 68.2%) is related to COPD and also previous episodes of pulmonary TB.
Oxygenation was given at 3 L/min, medications given were salbutamol + ipratropium bromide nebulizer solution every 6 hours, methylprednisolone 62.5 mg IV every 8 hours, continuous infusion of aminophylline 480 mg IV in 24 hours, infusion of Ceftazidime 1 g IV every 8 hours, subcutaneous short-acting insulin 10 IU 3 times before meals and long-acting insulin 14 IU at bedtime.
Patient's condition improved after a week of hospitalisation. Laboratory data showed a decrease of leukocyte count (8.020 x 109/L). A follow-up chest x-ray 2 weeks later showed resolution of consolidation in the right lung field (Fig. 2).