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Viva — Haemoptysis
Q1. Define haemoptysis and tell me how you would distinguish it from haematemesis at the bedside.
Haemoptysis is the expectoration of blood originating from the respiratory tract below the vocal cords. True haemoptysis is bright red, frothy, alkaline (mixed with air and sputum) and coughed; it often persists over several days. Haematemesis is dark brown (coffee-ground) due to gastric-acid action on haemoglobin, acidic in pH and vomited, usually with a history of liver or upper-GI disease. A third category, pseudohaemoptysis, is blood from the upper airway (epistaxis, gingival, pharyngeal/laryngeal) or factitious — so I always inspect the nose, oropharynx and upper airway first. In practice, aspiration of haematemesis and swallowing of haemoptysis can blur the picture, so the act — cough versus vomit — is the decisive point in the history.
Q2. What is the commonest cause of haemoptysis worldwide, and how does that differ from the developed world?
Worldwide, and especially in TB-endemic regions such as India and South Asia, tuberculosis is the commonest cause — both active cavitary disease and the late sequelae (Rasmussen aneurysm, post-TB bronchiectasis and aspergilloma). In the developed world the leading causes are bronchogenic carcinoma, bronchiectasis, pneumonia and pulmonary embolism. After a full work-up, 7 to 25 percent of cases remain cryptogenic (idiopathic), and these need follow-up imaging because a small proportion harbour an occult malignancy.
Q3. Why does massive haemoptysis kill, and what does that mean for your priorities?
Over 90 percent of massive haemoptysis arises from the high-pressure BRONCHIAL arteries, so the bleed is brisk. But the cause of death is asphyxia, not exsanguination — only about 150 to 200 mL of blood in a segmental bronchus or one lung can collapse alveoli and spill into the contralateral lung, causing hypoxaemia and cardiac arrest long before hypovolaemic shock develops. So the priority is the airway: oxygen, place the BLEEDING LUNG DOWN to protect the good lung, suction, large-bore IV access and crossmatch, reverse anticoagulation, and intubate (large-bore at least 8 mm, or a double-lumen tube) if the airway is threatened.
Q4. Walk me through the definitive management of massive haemoptysis.
Once the airway is secure I localise and control the source: rigid bronchoscopy (preferred — ventilation, large-bore suction, tamponade) using iced saline lavage, topical adrenaline 1:20 000, balloon (Fogarty/bronchial blocker) tamponade, fibrin glue, APC or cryotherapy. If bronchoscopy cannot control the bleed, bronchial artery embolisation (BAE) is the first-line intervention — a pre-procedure CT angiogram maps the bronchial arteries, the culprit is embolised with PVA particles or microspheres; immediate success is 70 to 99 percent but 10 to 50 percent rebleed. Surgery (lobectomy) is the last resort for uncontrolled, localised, resectable bleeding in a fit patient — emergency mortality up to 40 percent. Throughout I treat the underlying cause (TB therapy, reversal of anticoagulants, immunosuppression for vasculitis).
Q5. What is the feared complication of BAE, and why?
Anterior spinal artery syndrome (paraplegia) from non-target embolisation of the artery of Adamkiewicz, the dominant feeding vessel of the anterior spinal artery, which may share a common origin with a bronchial artery. The interventional radiologist must identify and avoid it. Other complications include recurrence, contrast-induced nephropathy and ischaemia from other non-target embolisation.
Q6. How would you recognise diffuse alveolar haemorrhage, and why might you miss it?
Diffuse alveolar haemorrhage (DAH) presents with dyspnoea, anaemia and bilateral alveolar infiltrates — but, crucially, haemoptysis may be absent (blood is diffuse in the alveoli and not necessarily coughed up), so it can be missed. The clue is a pulmonary–renal syndrome — acute kidney injury with haematuria/red-cell casts. Causes are capillaritis from ANCA-associated vasculitis, anti-GBM (Goodpasture) disease, or immune-complex disease, or bland haemorrhage from coagulopathy, mitral stenosis or drug toxicity. I send ANCA, anti-GBM, ANA/dsDNA and complement, and treat with high-dose methylprednisolone (1 g IV daily for 3 days), cyclophosphamide, and plasma exchange for anti-GBM. Bronchoalveolar lavage shows progressively bloodier returns.
Q7. Give me three high-yield exam pearls.
(1) Commonest cause worldwide = TB; in the West = bronchial carcinoma. (2) Over 90 percent of massive bleeds arise from the high-pressure bronchial arteries; death is from asphyxia, not exsanguination — protect the airway first and put the bleeding lung down. (3) BAE is first-line intervention for massive haemoptysis; beware the artery of Adamkiewicz; surgery (lobectomy) is last resort. And — the Rasmussen aneurysm is a pulmonary artery pseudoaneurysm in a chronic TB cavity causing massive haemoptysis.