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 42-year-old male presented with pain in the epigastrium, radiating to the back and feeling of fullness of the abdomen for a duration of six months. He gave history of loss of appetite and weight loss of 5 kg over a period of six months. He complained of progressive breathlessness on exertion for a period of one month. He gave no history of cough, expectoration, fever, wheeze or hemoptysis. He did not give any history of trauma.\nHe was working as a casual laborer in the agriculture sector. He consumed alcohol on at least five days in a week and smoked at least two packets of beedis in a week.\nNine months back he was admitted to a hospital for treatment of acute abdominal pain. A diagnosis of acute on chronic calcified pancreatitis was made. The most probable cause for the chronic pancreatitis was due to excessive alcohol intake by the patient. A pancreatoduodenostomy was performed on him. He remained asymptomatic for a period of three months. A follow-up ultrasound done after three months showed multiple calcification of the head of the pancreas with bulky tail, and minimal ascites and one old calcified granuloma in the right lobe of the liver. He was put on a low-fat diet, small frequent feeds and received pancreatic enzyme supplements from the time he was operated upon.\nOn examination he was thin built and emaciated and was systemically well. There were no palpable lymphadenopathies. He had bilateral pitting pedal edema. On chest examination there was diminished movement of the right lower hemithorax when compared to the left. Percussion of the right hemithorax yielded a dull note in the right infraaxillary and infrascapular areas which persisted on deep inspiration. On auscultation diminished breath sounds in the right basal regions were apparent. On palpation his abdomen was distended, epigastric tenderness was present and bowel sounds were heard. Examinations of other systems were unremarkable.\nHis hemogram revealed low hemoglobin of 9.2 mg/dl and elevated erythrocyte sedimentation rate of 32 mm in half hour. Renal and liver function tests were within normal limits. Sputum smear examination for acid-fast bacilli was negative in the two samples obtained. The result of the Mantoux test done with 5 TU and read after 48 h was 0 mm. Peripheral smear examination for microfilaria was negative. Chest skiagram revealed apparent elevation of right hemidiaphragm with lateral peaking, a heterogeneous opacity in the right lower zone and loss of lung volume on the right hemithorax. A lateral decubitus view revealed tracking of fluid.\nUltrasonogram of chest was done and pleurocentesis was performed at the site marked for pleural fluid aspiration. The pleural fluid aspirated was milky white in color and odorless [ and ].\nWith pleural fluid triglyceride >110 mg/dl and pleural fluid to serum cholesterol ratio less than 1 a diagnosis of chylothorax was made.[] Pleural fluid cytology was negative for malignant cells. Ziehl-Neelsen staining of pleural fluid smear was 3 plus positive for AFBs []. Computed tomography (CT) scan of the chest showed right-sided hydrothorax with partial collapse of the right lower lobe and fluid in minor fissure []. CT scan of abdomen was suggestive of acute on chronic pancreatitis with ascitis. Ascitic fluid was so minimal that ascitic fluid aspiration could not be done. It did not reveal any evidence of mass lesion or enlarged lymph nodes.\nThe patient was started on antituberculous treatment with a four-drug regimen with isoniazid, pyrazinamide, rifampicin and ethambutol. He did not give consent for intercostal drainage or any surgical or interventional procedure, hence pleural aspiration was done in a staggered manner in three sittings with 500 ml being aspirated in each sitting. As octreotide was not available in our institution he was put on a low-fat diet, intravenous fluids and monitored. The patient's general condition improved and he was discharged from the hospital after three weeks.