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Before the widespread use of effective chemotherapy, artificial pneumothoraces were created by clinicians treating tuberculosis in an attempt to collapse and “rest” the affected lung and heal cavitating disease [4] . This strategy of collapsing part of the lung was thought to reduce aerobic conditions and hinder mycobacterial progress. In 1882, the Italian physician Carlo Forlanini performed detailed theoretical and animal studies and developed specialised instruments enabling the injection of air into the pleural cavity. Artificial pneumothoraces created by the instillation of larger volumes (<3 L of nitrogen) by surgical incision and with X-ray guidance followed [5] . By 1912, it received recognition and became the primary therapy for pulmonary tuberculosis until the 1950s, when streptomycin and rifampicin became the frontline of clinical practice. Cessation of recurrent haemoptysis in pulmonary tuberculosis by repeated unilateral and bilateral pleural insufflation of air/oxygen or nitrogen was also established in the late 19th century [6] . The use of endobronchial techniques or devices for the control of haemoptysis is established. Bronchoscopy is performed to identify the source of bleeding, isolate the remaining lung, and create tamponade until there is control of the bleeding. Haemorrhage management involves suction above the point of bleeding, administration of cold saline, diluted adrenaline (1 in 100,000 to 1 in 200,000 Massive haemoptysis is a medical emergency with variably successful outcomes depending on the source, cause, and institution of effective control measures. Haemoptysis as a complication of fibrocavitatory lung disease, tuberculosis being the exemplar, is well described and variously innocuous or catastrophic. In the early 19 th century, during his detailed correlations of clinical presentations with morbid anatomy, Laennec [1] suggested a pathological distinction between the common and often self-resolving “slight haemoptysis” and the universally catastrophic massive haemoptysis for which he developed the term pulmonary apoplexy. In these cases, he observed that the rupture of the aneurysmal pulmonary vessels (i.e., Rasmussen or intercostal artery) or rupture of often tortuous blood vessels with a weakened adventitia and media) traversing the tuberculous cavities were the main aetiological factor. It is suggested that budding capillaries in the granulation tissue increase the capillary bed supplied by the bronchial arteries, leading to increased load and hypertrophy [2] . Aspergillomas also lead to an extensive network of small vessels but usually from the pulmonary circulation. Several abnormal connections may exist in a single patient. In lung abscess, the pathogenesis of haemoptysis is not entirely clear but may be due to progression of local inflammatory processes causing necrosis of branches of the pulmonary artery [3] . Published online: April 20, 2017

Controlled Pressure: The Solution for a High-Pressure Situation - Aetiology and Techniques for Control of Airway Haemorrhage