A 77-year-old woman presented to our hospital with complaints of persistent cough and low-grade fever for two months. Her medical history revealed glaucoma and osteoporosis seven years previously. Her vital signs were normal except for mild tachypnoea (respiratory rate, 24 breaths/min) and fever at 38.2°C. Physical examination showed decreased breath sounds at the right middle to lower lung fields. Chest X-ray taken at the first visit showed moderate right-sided pleural effusion and right hilar lymphadenopathies (Fig. ) confirmed by enhanced thoracic computed tomography (CT), which revealed a homogeneous enhanced mass as large as 3 cm in diameter (Fig. , arrow) with subcarinal lymphadenopathies (Fig. , arrow head). There was no calcification both in right hilar/mediastinal lymphadenopathies and in lung parenchyma.\nSerum laboratory data were normal except for mild elevation in white blood cell count at 17,000/μL (cell differential of neutrophil 63.3%, eosinophil 1.1%, basophil 0.8%, monocyte 13.3%, and lymphocyte 21.5%) and C-reactive protein at 1.19 mg/dL. Other data were normal; total protein (TP) of 7.1 g/dL, lactate dehydrogenase (LDH) of 217 IU/L, total cholesterol (T-cho) of 202 mg/dL, and triglyceride of 71 mg/dL. An interferon-gamma release assay was positive.\nAlthough thoracentesis of the right side was milky yellow in appearance (Fig. ), no pathogens were isolated including Mycobacterium, and polymerase chain reaction (PCR) for TB or Mycobacterium avium-complex (MAC) was also negative. No malignant cells were identified (class II). Chemical analysis revealed exudative pleural effusion (LDH 126 IU/L and TP 4.2 g/dL) as well as mild elevation of total cell count (1500/μL), predominantly lymphocytes (89%) followed by neutrophils (3%). Interestingly, the level of triglyceride (TG) in pleural fluid was markedly elevated (713 mg/dL), while the values of adenosine deaminase (ADA) (31.7 IU/L) and glucose (107 mg/dL) were normal. She thus met the criteria of chylothorax of TG greater than 110 mg/dL and a pleural to serum T-cho ratio less than 1 (0.48).\nOn the basis of the suspicion of a malignant disease-induced chylothorax, fluorodeoxyglucose–positron emission tomography–CT (FDG–PET–CT) was performed. The FDG–PET–CT demonstrated high FDG uptake in the right hilum, with a maximum standardized uptake value (SUV) of 7.04, and in the subcarinal lymphadenopathies, with a value of 9.65 (Fig. ).\nTwo weeks after the first visit, bronchoscopy was performed. Endobronchial ultrasound-guided transbronchial needle aspiration taken from the subcarinal lymph node showed necrotic tissue with abundant neutrophils or monocytes, which was of no diagnostic value. All retrieved respiratory samples were negative for bacterial or acid-fast culture or PCR methods on TB and MAC.\nOne month later, her symptoms and moderate right-sided pleural effusion persisted; thus, thoracoscopic surgery was performed. Curiously, a noticeable enlarged milky yellow lymphatic duct was found (Fig. , arrow) with its proximal portion seemingly compressed by the adjacent enlarged subcarinal lymphadenopathies (asterisk). Biopsied specimens obtained from the subcarinal lymph node showed epithelioid cell granulomas containing Langhans giant cells (Fig. , arrows) along with necrosis, fibrosis, fibrous venous occlusion, and lymphoid hyperplasia. Although no acid-fast organisms were detected by the Ziehl–Neelsen stain, these findings suggested mycobacterial lymphadenitis associated with TB, she was thus diagnosed with TB lymphadenitis-associated chylothorax. During the thoracoscopic surgery, cauterization of the lymphatic duct was performed, which resulted in a partial resolution of the pleural effusion. The patient rejected treatment for tuberculous lymphadenitis, and four months later (six months after the first visit), the amount of right pleural effusion had rapidly increased again. Thoracentesis found that the colour of the pleural fluid had changed from milky yellow to red (Fig. ) together with an elevation of ADA 77 IU/L and LDH 472 IU/L, suggestive of tuberculous pleuritis. Finally, she was treated with anti-tuberculous drugs, which led to the complete resolution of symptoms, right-sided pleural effusion, and mediastinal lymphadenopathies.
A 33-year-old man, diagnosed case of chronic kidney disease secondary to diabetes mellitus on maintenance dialysis presented to pulmonary medicine outpatient unit with complaints of intermittent fever and weight loss of 2 months duration. On examination, he was febrile (38.4 Celsius) with a respiratory rate of 20/min, pulse rate of 104/min, blood pressure of 140/90 mmHg, and oxygen saturation of 96% on room air. General examination revealed pallor and bilateral pitting pedal edema. His respiratory-, cardiac-, abdominal- and neurological examination was within normal limits. Laboratory examination showed hemoglobin of 7.2 g/dL (normal 11.5–16.5), platelet count of 22 × 109/L (normal 150–500), white cell count of 3.2 × 109/L (normal 4.3–10.8) with neutrophils 65%, lymphocyte 32%, and monocyte of 3%. His glycated hemoglobin was 5.6% (normal <6.5%) and liver function test revealed albumin of 2.2 g/dL (normal 3.5–5 g/dL). Rest of the biochemical investigations were within normal limits. HIV serology was negative. Even though, the patient had normal blood picture and reticulocyte count, bone marrow study was done for his leukopenia.\nChest X-ray posteroanterior (PA) view revealed increased bronchovascular markings [] and computed tomography (CT) thorax with abdomen [] showed bilateral mild pleural effusion with significant mediastinal and abdominal adenopathy. Ultrasound chest was done and it revealed minimal pleural effusion and the same was not tappable. CT-guided fine-needle aspiration was done from paraaortic lymph nodes. Histopathology from bone marrow and cytology of paraaortic lymph nodes showed caseous necrotic granulomatous inflammation suggestive of TB. Acid-fast culture of bone marrow tissue and lymph node aspirate revealed growth of pansensitive mycobacterium TB. He was initiated on modified antitubercular treatment for his kidney disease and the regimen included rifampicin 450 mg daily, isoniazid 300 mg daily, ethambutol 800 mg thrice weekly, and pyrazinamide 1250 mg thrice weekly.\nSix weeks postantitubercular treatment, he came to our casualty with complaints of fever and exertional breathlessness. Patient was febrile (38.6°C) with respiratory rate of 32/min, pulse rate of 120/mine, blood pressure of 150/92 mm of Hg, and oxygen saturation of 92% at room air. Respiratory examination was suggestive of right pleural effusion. Rest of the examination was within normal limits. Chest X-ray PA view showed features suggestive of right moderate to massive pleural effusion []. Diagnostic thoracocentesis revealed milky white fluid and analysis showed total protein 4.1 g/dL, glucose 117 mg/dL, total cholesterol 68 mg/dL, triglycerides 751 mg/dL, and chylomicrons 1050 mg/dL. Cytology of the pleural fluid was negative for malignant cells, cultures for bacteria and mycobacteria were negative. Hence, a diagnosis of chylothorax was made. Repeat CT thorax with abdomen showed an increase in the size of mediastinal and abdominal lymphadenopathy. Hence, the acute worsening in patient clinical condition was attributed to be part of PR/IRIS, developing secondary to antitubercular treatment. His antitubercular therapy was continued and was managed symptomatically with parenteral nutrition, therapeutic thoracocentesis, antipyretics, and oxygen; nonsteroidal anti-inflammatory drugs were deferred in view of renal disease. Despite these he was symptomatic, so initiated on tab prednisolone 1 mg/kg/day. In view of persisting breathing difficulty, increasing oxygen requirement and worsening pleural effusion radiologically after informed consent intercostal drain (ICD) was inserted. Post-ICD X-ray showed partial expansion of lung, so patient was connected to −20 cm water suction. Despite these lung failed to expand, thoracic surgery opinion was obtained and he underwent decortication and interruption of the thoracic duct. Histopathology of the operated specimen showed fibrous connective tissue, fibrinous, and acute inflammatory exudates. Postoperative chest X-ray showed good lung expansion and resolution of right pleural effusion []. Prednisolone 1 mg/kg daily was continued for 2 weeks, then, it was tapered to 0.5 mg/kg and the same was given for 2 more weeks. The patient was discharged on antitubercular treatment and was advised to continue the same for total of 6 months. On follow-up, patient showed good clinical recovery.