A 32-year-old HIV seronegative female patient, currently working as a research assistant in a healthcare facility presented with a second episode of massive haemoptysis within a 5-month period. She had been diagnosed with microbiologically proven PTB 6 years prior to her admission and completed 6 months of therapy. However, this was complicated by fibro-cavitatory destruction of her left lung with post-TB bronchiectasis (Fig. 1). Over the course of her follow up at the pulmonology clinic, and 2 years prior to this current presentation, she developed apical mycetoma's, which were identified on computed topographical scan of the chest (Fig. 2) and due to evident haemoptysis, she was considered for a left pneumonectomy. Her lung function test showed a restrictive lung pattern with a FEV1 of 64%, a FVC of 67% (FEV1/FVC of 95) and a DLCO of 74. Furthermore, a nuclear medicine split perfusion scan indicated no discernible perfusion to the affected lung. An electrocardiogram and echocardiogram were performed, indicating the presence of pulmonary hypertension.
On examination during this admission, she was haemodynamically stable with a blood pressure of 127/82 mmHg and a sinus tachycardia of 110 beats/min. She was afebrile, her respiratory rate measured 20 breaths/min and she was a-cyanotic on room air with an oxygen saturation of 93%. Marked digital clubbing and subconjunctival pallor were noted. On respiratory examination, evidence of left sided volume loss was present with decreased expansion of the left chest wall and compensatory hyperinflation of the right. The breath sounds on the right were vesicular in nature but the left side had breath sounds of reduced intensity with amphoric breath sounds and coarse crackles predominantly in the upper zone. No evidence of decompensated cor-pulmonale was present on cardiovascular examination, but pulmonary hypertension and mediastinal shift to the left were evident. A para-sternal heave with a palpable P2 were elicited, as was a loud pulmonary component of the second heart sound. Her apex beat was displaced to the anterior axillary line in the fifth intercostal space with tracheal deviation to the left side. Initial laboratory results showed a microcytic hypochromic anaemia with a haemoglobin of 7.7 g/dL (MCV = 73.8fl; MCHC = 31.4g/dL) and a platelet count of 487 x 109/l. Further haematological work-up demonstrated an iron-deficiency anaemia with a ferritin of 37 mug/l, percentage saturation of 5% and associated morphological features. Her renal and liver function tests were normal. Her C-Reactive Protein was 32mg/L and her INR measured 1.28. An Xpert MTB/RIF assay was performed and was reported as negative for mycobacterium tuberculosis.
She was admitted to medical high care. Transfused 1 unit of packed red blood cells and initiated on oral codeine phosphate. An emergency computed topographical pulmonary angiogram (CTPA) was performed and suggested the presence of a Rasmussen's aneurysm but formal angiography was deemed necessary for confirmation. Direct angiography indicated a pulmonary arterial blush adjacent to the left upper lung cavity confirming the presence of a Rasmussen's aneurysm (Fig. 3). Despite difficult initial ventilation due to her diseased lung, selective right bronchial intubation was performed and successful arterial embolization was achieved. Following 48 hours of post-procedural monitoring in a high care setting, she was stepped down to the general medical ward where after 6 days of remaining haemoptysis free, she was discharged home and is currently awaiting left sided pneumonectomy.