Case Report

570 www.thelancet.com Vol 382 August 10, 2013

Pleural eff usions in a patient with tuberculosis on dialysisHugh Ip, Lucy Ellen Eyre Schomberg, Liju Ahmed

A 63-year-old Ghanaian woman developed dyspnoea in the renal unit in June, 2012. She was on haemodialysis for hypertensive nephropathy (started Feb, 2011). Miliary tuber culosis had been diag nosed in May, 2012, by induced sputum, yielding a fully sensitive culture-positive organ-ism (initially smear nega tive). She had been living in the UK for 30 years, with no tuberculosis contacts. She was stable on (and adherent to) rifampicin 900 mg, isoniazid 900 mg, pyrazinamide 2 g, and moxifl oxacin 400 mg (three times per week) for 6·5 weeks. Clinical examination showed oxygen saturations of 80% on room air, respiratory rate of 28 breaths per min, blood pressure of 98/63 mm Hg, and heart rate of 113 beats per min. There was reduced expansion and a dull percussion note on the left side of the chest. Ultrasound scan showed a large left pleural eff usion. She had a normal white cell count of 7·4×10⁹/L (normal range 4–11×10⁹/L) and a raised C-reactive protein (CRP) concentration of 1086 nmol/L (0–38 nmol/L). A chest drain was inserted, draining yellow-green creamy fl uid. Intravenous tazocin was given for a pre sumed empyema. Dyspnoea improved after drainage, and oxygen saturations recovered to 97% on air. Pleural fl uid analysis showed no organisms on Gram stain and culture, and acid-fast bacilli smear was negative. Lactate dehydro genase was raised at 29 μkat/L (serum range 4–8 μkat/L), protein concentration suggested an exudate at 50 g/L (exudates >29 g/L), and triglyceride measurement was substantially raised at 12·71 mmol/L (<1·24 mmol/L).

A diagnosis of chylothorax was made. The patient’s chest drain produced over 400 mL of fl uid daily in the fi rst week. A respiratory opinion was sought. On review of a thoracic CT scan from May, 2012 (fi gure), a large soft tissue mass was found in the posterior mediastinum. Lymphadenopathy,

secondary to tuberculosis, probably obstructed or eroded the thoracic duct—leading to a chylothorax.1 A decision was made to treat conservatively with symptomatic aspiration and await the eff ects of anti-tuberculous therapy. The rate of fl uid production diminished after 4 months, during which she needed four aspirations. A repeat CT scan at the end of August, 2012, showed resolution of the mediastinal lymphadenopathy and miliary nodules. An important diff erential diagnosis was trauma to the thoracic duct. 6 weeks before this admission, a 14·5 French double lumen haemo dialysis catheter had been inserted into the right internal jugular vein. In view of the time lag, trauma was considered unlikely. Our patient was symptom free at last review in May, 2013. The lymph leakage stopped after successful anti-tuberculous therapy. After 3 months of quadruple therapy, she completed an additional 5 months of rifampicin and isoniazid.

Chylothoraces can be left sided (33·3%) when due to damage above the fi fth thoracic vertebra, right sided (50%) when due to thoracic duct damage below this level, or bilateral (16·7%).2 Other causes include malignancy, cardiac failure, sarcoidosis, goitre, as well as thoracic and upper gastrointestinal surgery. Importantly, the immuno-compromised state of patients on haemodialysis pre-disposes them to tuberculosis,3 usually an uncommon cause of chylothoraces. Less than 50% of chylothoraces have the classic milky appearance,4 so diagnosis depends on pleural fl uid analysis showing triglyceride concen-trations greater than 1·24 mmol/L (or the detection of chylomicrons). Lymphography can be considered for localisation of thoracic duct obstruction.5 Treatment of the underlying cause is crucial, often resulting in spontaneous cessation of chyle leakage. With a leak, thoracic duct ligation may be preferred, especially for a traumatic cause. Octreotide has been used with varying success. Ceasing fat intake will reduce chyle formation, requiring parenteral supplement of medium chain fatty acids. Thoracocentesis is benefi cial for symp tom relief but should be done cautiously to avoid immuno suppression from loss of chyle. Infections rarely occur in the pleural eff usion itself, since chyle is bacteriostatic.2

ContributorsAll authors looked after the patient. HI wrote the fi rst draft of the manuscript. LEES and LA contributed signifi cantly to the fi nal draft. Written consent to publish was obtained.

References1 Karapolat S, Sanli A, Onen A. Chylothorax due to tuberculosis

lymphadenopathy: report of a case. Surg Today 2008; 38: 938–41.2 McGrath EE, Blades Z, Anderson PB. Chylothorax: aetiology,

diagnosis and therapeutic options. Respir Med 2010; 104: 1–8.3 Ananthan VS, Siva KK. A rare case of acid-fast bacilli in chylothorax.

Lung India 2012; 29: 166–68.4 Huggins JT. Chylothorax and cholesterol pleural eff usion.

Semin Respir Crit Care Med 2010; 31: 743–50.5 Vennera MC, Moreno R, Cot J, et al. Chylothorax and tuberculosis.

Thorax 1983; 38: 694–95.Figure: Chest CT scan showing soft tissue mass in the posterior mediastinum (arrows)

Lancet 2013; 382: 570

Department of Respiratory Medicine, NHS

Foundation Trust, St Thomas’ Hospital, London, UK

(H Ip MRCP, L E E Schomberg MRCP,

L Ahmed MRCP)

Correspondence to:Dr Hugh Ip, Department of

Respiratory Medicine, St Thomas’ Hospital, London SE1 7EH, UK

hughip@gmail.com