An HIV-exposed uninfected 20-month-old boy presented to Chris\nHani Baragwanath Academic Hospital in Johannesburg, South Africa,\nwith a 2-day history of shortness of breath, cough and noisy breathing.\nHe had also experienced night sweats, fever and vomiting for a week.\nTwo weeks prior to this presentation, he had been diagnosed with\nbacteriologically unconfirmed PTB at a primary healthcare clinic and\nwas empirically started on a four-drug antituberculosis treatment\nregimen (rifampicin, isoniazid, pyrazinamide and ethambutol). The\ndiagnosis was based on a chest X-ray and a positive Mantoux\ntest. His father (a household contact) had been diagnosed with PTB,\nand had been on first-line antituberculosis treatment for 4 months. \nThe boy had had normal growth and development up to 1 year of age,\nbut had subsequently lost weight, and fallen from a weight-for-height\nz-score +2 to the median over the preceding 8 months.\nOn admission, he was apyrexial, tachycardic and in moderate\nrespiratory distress, with oxygen saturations of 97% in room air. He\nhad marked chest wall indrawing and bilateral posterior cervical\nand axillary lymph nodes (<0.5 cm in diameter). He was clinically\nhyperinflated, with bilateral wheezing. The rest of his clinical\nexamination was normal.\nHe was diagnosed with viral bronchiolitis, and therefore a chest\nX-ray was not performed. He was started on oxygen and hypertonic\nsaline nebulisation. He responded poorly to this initial treatment\nand was therefore started on oral corticosteroids and amoxicillin on\nday 2 of hospitalisation, and his first-line antituberculosis treatment\nwas continued. Gastric aspirate samples for microscopy for acid-fast\nbacilli, Xpert MTB/RIF (Cepheid, USA) and culture for mycobacteria\nwere negative.\nDuring his hospital admission period his wheezing persisted,\nand he remained in moderate respiratory distress. On the fifth day\nof admission, he developed percussion dullness and absent breath\nsounds over the right hemithorax.\nA chest X-ray at this point revealed a large right-sided pleural\neffusion . A computed tomography scan of the chest revealed\nhilar lymphadenopathy and a large right-sided pleural effusion. The\nthoracic duct could not be visualised. Diagnostic pleurocentesis\nconfirmed a chylothorax. It was suspected that tuberculous lymph\nnodes had eroded the thoracic duct causing the chylothorax, and\ntherefore a bronchoscopy was performed, which revealed caseating\nlymph nodes in the right main bronchus suggestive of TB, and 90%\nobstruction of the left main bronchus. The Xpert MTB/RIF (Cephaid,\nUSA) test on a bronchoalveolar lavage specimen identified rifampicinresistant Mycobacterium tuberculosis. Gastric aspirates, pleural fluid\nand bronchoalveolar lavage samples were all smear-negative for acidfast bacilli and mycobacterial culture-negative.\nThe chylothorax was managed with a low-fat diet (with additional\nmedium-chain triglycerides), therapeutic taps for worsening\nrespiratory distress and an octreotide infusion. The boy was\ncommenced on multidrug-resistant TB (MDR-TB) treatment\n(amikacin, levofloxicin, ethionamide, terizidone, pyrazinamide,\nethambutol and high-dose isoniazid) and oral steroids.\nFor further management, he was transferred to a hospital dedicated\nto the care of MDR-TB patients. One month later, he showed marked\nclinical improvement, with almost complete radiological resolution of\nthe chylothorax, and reduced hilar lymphadenopathy . The\nfull case overview is shown in .
A 17-year-old girl was admitted to the Korean University Ansan Hospital with a one-month history of fever, abdominal distention and dyspnea. The patient had been treated in another hospital for 10 days but the cause of ascites and pleural effusion had not been discovered. She was transferred to our hospital for further care. On admission, body temperature was 38.6℃, heart rate was 146/min and body weight was 56 kg. On chest auscultation, breathing sound was decreased on both lower lung fields. Abdominal examination revealed shifting dullness and the lower extremities were severely edematous. A chest radiograph taken on admission showed diffuse fine nodular opacities in both lungs and bilateral pleural effusion. Chest computed tomography (CT) showed pleural effusion of both sides, more serious on the left side, and pericardial effusion and multifocal nodular consolidation on both lung fields (). Abdominal CT showed a large amount of ascites with diffuse peritoneal thickening and multiple necrotic lymphadenopathy in the abdominal cavity, and enhanced wall thickening in the distal ileum and ascending colon (). Initial laboratory results were as follows: white blood cell count 6,670/mm3, hemoglobin 6.7 g/dL, serum total protein 4.6 g/dL and albumin 2.2 g/dL. Thoracentesis and paracentesis were performed to verify the nature of fluid apparent in the chest and abdominal CT images.\nPleural fluid () was turbid and whitish-colored, with pH 8.0, protein level 3.1 g/dL, lactate dehydrogenase of 5,855 IU/L, triglyceride 133 mg/dL and adenosine deaminase 121.6 IU/L. The lactate dehydrogenase ratio of pleural fluid versus serum was 15, consistent with exudate. Ascites () was milk-like and turbid in appearance, pH 8.0, albumin level 0.5 g/dL, triglyceride 864 mg/dL and adenosine deaminase 14.8 IU/L. We diagnosed chylothorax and chylous ascites because the triglyceride level of pleural fluid and ascites were higher than 110 mg/dL and 200 mg/dL, respectively. Direct smear of pleural fluid and ascites for acid fast bacilli (AFB) was positive only in pleural fluid. So, finally we diagnosed the patient as having TB associated with chylothrax and chylous ascites on the basis of positive AFB stain and abdomen CT. Initially, the patient received anti-TB treatment with quadritherapy including isoniazid 300 mg/day, rifampin 600 mg/day, pirazinamide 1,500 mg/day and etambutol 1,200 mg/day. The patient also was put on a high protein and low fat diet with medium chain triglyceride. Mycobacterium tuberculosis was cultured from sputum and pleural fluid on 28th day from admission and the isolate was susceptible to all anti-TB medications. The patient improved continuously after anti-tuberculosis medication, and pleural effusion and ascites were slightly decreased on follow-up chest and abdomen X-ray. The patient was discharged on day 60 of hospitalization with ongoing anti-tuberculosis treatment.