Chronic cough and haemoptysis

• In adults, cough lasting over 8 weeks is chronic, 3 to 8 weeks is subacute, and under 3 weeks is acute; in children chronic cough is usually taken as over 4 weeks.^[1][2][3][4] Duration is the first thing to establish because it narrows the list of causes.^[3]
• Most chronic cough in adults comes from four conditions: upper airway cough syndrome (UACS), asthma, nonasthmatic eosinophilic bronchitis (NAEB) and gastro-oesophageal reflux disease (GERD), often in combination.^[3][4] About 10% of adults worldwide have chronic cough.^[2]
• Red flags such as haemoptysis, fever, weight loss, hoarseness, recurrent pneumonia, smoking of 20 pack-years or more, or being a smoker over 45 years of age point to serious disease and need early investigation.^[4]
• Haemoptysis is bleeding from the lower respiratory tract. It is frightening but usually not exsanguinating; when massive, death comes mainly from flooding of the airways and asphyxiation.^[6][7]
• In over 90% of massive haemoptysis the bleeding comes from the bronchial (systemic) arteries, so the treatment is bronchial artery embolisation rather than surgery in most patients.^[5][6][7]

By the end of this page you should be able to:

1. Define chronic cough and haemoptysis, including the duration cut-offs, and separate mild, moderate and life-threatening haemoptysis.
2. List the common causes of chronic cough in adults and children by system and urgency, and recognise the four dominant causes in adults.
3. Take a focused history and examination that localises the cause, including the questions that separate bleeding from the lung from bleeding from the nose or stomach.
4. Use red flags to decide when to investigate promptly, and know when a chest radiograph, computed tomography (CT) or bronchoscopy is needed.
5. Follow a stepwise diagnostic and treatment algorithm for chronic cough, including trials of therapy and when to refer.
6. Manage life-threatening (massive) haemoptysis in order: stabilise, localise, escalate to bronchial artery embolisation or surgery.
7. Adapt the approach to low-resource settings, children and people with chronic respiratory disease.

Cough is a reflex that protects the airway. It is classified first by duration. For adult patients complaining of cough, acute cough is under 3 weeks, subacute cough is 3 to 8 weeks, and chronic cough is over 8 weeks.^[3] The German S2k guideline states the same cut-offs: acute up to 3 weeks, subacute 3 to 8 weeks, chronic more than 8 weeks.^[1] In children, cough is increasingly defined as chronic after more than 4 weeks.^[2][4] The reason duration matters is that the differential diagnosis changes with it: acute cough is most often infection or exacerbation of known disease, whereas chronic cough needs a structured search for underlying disease.^[3]

A cough can also be classified by sputum production, because this changes the cause list. A dry (non-productive) cough and a productive cough are not the same problem, and the amount of sputum is informative: in adults, more than about 30 mL of phlegm in 24 hours strongly suggests chronic infection or bronchiectasis, 5 to 30 mL deserves consideration of those diagnoses, and up to 5 mL makes them unlikely.^[1]

Haemoptysis is the expectoration of blood that originates from the lower respiratory tract, below the larynx. It must be distinguished from blood coming from the nose (epistaxis, blood that drips down the pharynx) and from the stomach (haematemesis). Clues that the blood is from the lung include a preceding cough or tickle in the throat, frothy bright red blood mixed with sputum, a salty taste, and symptoms of lower respiratory disease; clues that it is from the stomach include vomiting, dark "coffee ground" blood, abdominal pain and no cough. Bleeding from the upper airway, gums and tonsils should be excluded first in any acute presentation.^[6][7]

In adults the categories by volume are useful, although thresholds differ between sources. One working scheme defines mild haemoptysis as under 100 mL of blood per day, moderate as 100 to 300 mL per day, and severe (massive) as more than 300 mL within 24 hours or any amount causing haemodynamic instability or respiratory failure.^[6] Other authorities use "massive" for 100 mL or more in adults, because as little as 100 mL has been reported to be life-threatening, and 150 mL of blood occluding the tracheal dead space is enough to kill by asphyxiation.^[5][7] The 2025 Breathe review therefore advises replacing the word "massive" with "life-threatening" haemoptysis: any haemoptysis greater than 100 mL in 24 hours, or haemoptysis that causes abnormal gas exchange or airway obstruction or causes haemodynamic instability.^[5] Guidelines thus differ on the exact millilitre cut-off; what matters clinically is not the number but whether the airway patency, oxygenation or circulation are threatened. This topic uses "massive haemoptysis" and "life-threatening haemoptysis" interchangeably, with that caveat.^[5][6][7]

Massive haemoptysis is rarely encountered but life-threatening, with high morbidity and mortality.^[5] Mortality results from asphyxiation rather than from blood loss itself.^[6] A relatively small volume in the wrong place, an upper-lobe bleed pouring across the carina, can kill faster than a large bleed that drains out through the mouth. That is why a patient who can cough blood out and has good cardiopulmonary reserve may be observed, while a patient with weak airway reflexes needs early intubation.^[6][7]

Chronic cough is common: a meta-analysis estimated the global prevalence in the general adult population at about 10%, with higher prevalence in Europe, America and Oceania than in Asia and Africa.^[2] In a recent international survey of 10,032 adult patients attending specialist cough clinics, two-thirds were women and the most common age at presentation was in the sixth decade.^[2] Smoking is the major remediable cause of chronic cough and is inextricably linked to chronic obstructive pulmonary disease (COPD).^[2]

Chronic cough in children differs from adults in aetiology and management and is increasingly defined as cough lasting more than 4 weeks.^[2] In up to a third of adults no cause is ever found, giving the labels refractory or unexplained chronic cough.^[1]

Haemoptysis is far less common than cough; severe haemoptysis accounts for roughly 5% of presentations and needs immediate attention.^[6] Causes vary by region: pulmonary tuberculosis accounts for up to 40% of cases in low- and middle-income countries, and for roughly 40% to 79% of haemoptysis presentations in India, whereas malignancy, cardiovascular disease and bronchiectasis predominate in high-income regions.^[6] Common causes in Asia are tuberculosis, fungal infection or mycetoma, bronchiectasis and lung cancer.^[7]

The cause list is long, but it can be sorted by how often each cause occurs and whether it is dangerous. Smoking-related bronchitis and COPD, interstitial lung diseases, foreign body, obstructive sleep apnoea, post-COVID-19, tracheobronchomalacia, bronchiectasis, cystic fibrosis, medication side effects and swallowing problems all belong on the differential.^[1]

UACS is the most common cause of chronic cough.^[4] The prevalence of asthma in patients with chronic cough ranges from 24% to 29%; NAEB accounts for 10% to 30% of cases referred for subspecialist investigation, and in up to 13% of patients attending cough clinics eosinophilic bronchitis without asthma has been reported; the prevalence of GERD as a causative factor varies from 0% to 73%.^[4][2] These overlapping figures reflect that more than one cause often operates in the same patient.^[3]

Three subgroups of asthmatic cough are recognised: classic asthma, cough-variant asthma and NAEB. Eosinophilic bronchitis without bronchoconstriction or hyperresponsiveness behaves as part of an asthmatic spectrum and responds to anti-inflammatory treatment.^[2] Eosinophilic airway inflammation may be suspected when the blood eosinophil count exceeds 0.3 x 10^9/L.^[2] Other drugs can worsen cough: bisphosphonates and calcium channel antagonists can exacerbate pre-existing reflux, prostanoid eye drops such as latanoprost can irritate the pharynx, and sitagliptin deserves mention in the history.^[2][1]

Acute cough in adults is most often caused by respiratory infection, usually viral, followed by exacerbations of asthma or COPD and pneumonia; subacute cough is most often post-infectious cough plus exacerbations of underlying disease. Estimating duration narrows the list.^[3]

Rare pulmonary causes include recurrent small pulmonary emboli, cardiac causes of chronic cough, systemic diseases with lung involvement, rare isolated tracheobronchial diseases, and somatic cough syndrome or cough tic.^[1] Refractory unexplained chronic cough affects post-menopausal women in about two-thirds of cases.^[1]

The cause of haemoptysis follows the prevalence of disease in the region and the patient's age. Infectious causes dominate globally, with tuberculosis leading in low- and middle-income countries.^[6] The commonly cited causes are listed in the table.

In life-threatening haemoptysis the commonest causes are bronchiectasis, bronchogenic carcinoma, pulmonary tuberculosis and fungal infection such as aspergillosis.^[5] In cases reported by Mishra and colleagues the examples include bronchiectasis with copious sputum, aspergilloma, active tuberculosis, primary or metastatic lung cancer, aortopulmonary fistula, diffuse alveolar haemorrhage and coagulopathy.^[6]

Understanding where the blood comes from guides treatment. Pulmonary arteries provide about 99% of total blood flow to the lungs, but bronchial (systemic) arteries, although only about 1% of the lung blood supply, are the source of about 90% of clinically significant haemoptysis, and in over 90% of massive cases bleeding arises from high-pressure systemic circulation such as the bronchial vascular tree and collaterals from the intercostal, subclavian, internal mammary or aortic vessels. Pulmonary artery involvement accounts for only about 5% of cases.^{[6][7] [5]}

Red flags are symptoms or contexts suggesting a potentially life-threatening condition and demanding prompt investigation. Always screen for them.^[3] In acute and subacute cough they include haemoptysis, high fever, dyspnoea, suspected tumour, acute chest pain (pulmonary embolism, pleurisy, empyema, pneumothorax), stridor (airway obstruction from foreign body or laryngeal tumour or infection), and sudden onset of thin foamy sputum (pulmonary oedema).^[1]

In chronic cough, red flags needing immediate work-up include haemoptysis, night sweats, weight loss, hoarseness, fever, stridor, change in cough symptoms in older smokers (55 to 80 years), dysphagia with malnutrition and dehydration, severe immunosuppression and symptoms of systemic involvement such as oedema and weight gain from heart failure. ACE inhibitor and tumour must be considered. ^[1][4]

For any cough the following should trigger investigation without delay: fever; weight loss; haemoptysis; hoarseness; excessive dyspnoea or sputum; recurrent pneumonia; smoking history of 20 pack-years or more; or being a smoker over 45 years old. ^[4] A history of smoking of 20 pack-years or more or a smoker over 45 years is a red flag in itself.

Environmental and occupational exposure history is part of every cough assessment, and residents of or travellers to tuberculosis-endemic areas should be assessed accordingly. Tuberculosis should be considered even when the chest radiograph is normal. ^[3]

A good cough history often makes the diagnosis. Ask about timing, triggers and associated symptoms, because these reflect mechanism.

• Duration and course. Is it under 3 weeks, 3 to 8 weeks, or over 8 weeks? Did it start after an infection, a new drug, or a change in environment? ^[1][3]
• Character. Dry versus productive; morning cough; nocturnal cough; barking, honking or throat-clearing quality. The cough reflex can become hypersensitive, producing cough with trivial stimuli such as talking or temperature change; that pattern is typical of chronic refractory cough. ^[1]
• Sputum. Amount per day, colour, whether it is blood-streaked. Productive cough of more than 30 mL per day points to chronic infection or bronchiectasis. ^[1]
• Triggers. Exercise, cold air, smoke, fumes, perfumes, lying flat, eating, speaking, and laughing. These point to asthma, reflux, habit or upper airway causes.
• Associated symptoms. Breathlessness, wheeze, chest pain, fever, sweats, weight loss, reflux symptoms, dysphagia, pre-syncopal or syncopal episodes, and snoring or witnessed apnoeas (sleep apnoea).
• Medications. ACE inhibitors in about 15% of users (ERS 2020) to 35% (AAFP 2017 range 5% to 35%), plus bisphosphonates, calcium channel blockers, prostanoid eye drops and sitagliptin. ^[2][1]
• Risk factors. Smoking in pack-years; occupation (dusts, silica, asbestos); HIV and immunosuppression; endemic tuberculosis; travel.
• Haemoptysis history. Volume per episode and per 24 hours, colour, presence of clots, whether it is mixed with sputum, pain, shortness of breath, and any anticoagulant or antiplatelet drug. Distinguish epistaxis and haematemesis as above. ^[6][7]
• Past history. Asthma, COPD, tuberculosis, recurrent pneumonia, nasal polyposis, connective tissue disease, and cardiac disease.

Several systems are worth checking, and the findings often settle the diagnosis.

• General. Fever, cachexia, cyanosis, clubbing, lymphadenopathy, and signs of anaemia.
• Upper airway. Nasal mucosa and turbinates, septal deviation, polyps and post-nasal drip; the "cobblestone" pharynx of chronic UACS. Hoarseness and stridor suggest laryngeal disease and are red flags. ^[4]
• Chest. Inspection for pattern of breathing; palpation, percussion and auscultation for localised signs; wheeze, prolonged expiration, crackles, bronchial breathing. Fixed monophonic wheeze may be upper airway obstruction.
• Cardiovascular. A murmur of mitral stenosis is a cause of haemoptysis; right heart failure and raised jugular venous pressure suggest cor pulmonale; pulse and blood pressure for haemodynamic stability if bleeding.
• Abdomen. Hepatomegaly from right heart failure and signs of chronic liver disease.
• Skin and joints. Vasculitic rashes, telangiectasia, joint swelling, suggestive of autoimmune disease with diffuse alveolar haemorrhage.

In adults with haemoptysis, protect the airway first. A distressed or hypoxaemic patient takes precedence over further history. ^[7]

The basic work-up recommended as good practice is spirometry and a recent chest radiograph for all patients with chronic cough.^[2] Beyond that, investigation is cause-directed.

• Chest radiograph. First imaging to exclude most infectious, inflammatory and malignant thoracic conditions. ^[4]
• Spirometry with bronchodilator reversibility. Looks for asthma or COPD; essential if any suggestion of obstructive disease. ^[2]
• Full blood count and differential. Eosinophilia raises the possibility of asthma or NAEB; anaemia may be present with chronic disease. ^[2]
• Eosinophilic inflammation testing. In adults and children with chronic cough, assessment for eosinophilic inflammation is suggested. A blood eosinophil count greater than 0.3 x 10^9/L may indicate eosinophilic airway inflammation; the ERS 2020 paper prints 0.3 cells/uL for the same threshold and Kim 2025/BTS write 0.3 x 10^9/L. ^[2] Induced sputum eosinophil counts above 2 to 3% are used in some centres, though availability varies.
• Chest CT scan. Routine CT of the chest (and sinuses) is not necessary when examination is normal and no red flags are present; in adults with a normal chest radiograph and examination, routine chest CT is not suggested. ^[4][2]
• Bronchoscopy. Not part of initial evaluation without red flags or an abnormal radiograph; reserved for suspected foreign body, atypical infection, haemoptysis, or unexplained focal lesions. ^[4]
• Sinus imaging. Consider in suspected UACS when examination is normal; treat as a clinical diagnosis first.
• Reflux testing. Ambulatory pH monitoring is reserved for cases where reflux is suspected and standard measures fail; empiric acid suppression alone is no longer recommended for cough due to reflux in the absence of dyspeptic or reflux symptoms. ^[2][3]
• Bug-directed and malignancy work-up. Sputum for acid-fast bacilli and culture if tuberculosis is possible; low-dose CT of the chest in heavy smokers with red flags, guided by local lung cancer pathways. HIV testing when immunosuppression is suspected.

The intensity of investigation depends on whether the patient is stable.

• Chest radiograph. First radiological imaging of choice because it is accessible and rapid. Sensitivity is about 52% for localising bleeding and 25% for identifying the aetiology. ^[6][7] It is highly variable in massive haemoptysis. ^[7]
• Contrast-enhanced CT with bronchial angiography (CTBA/MDCT). Imaging of choice in stable patients. It has 90% to 98% sensitivity and nearly 100% specificity for localising the bleeding source, and is more efficient than bronchoscopy at identifying the underlying cause. It precisely identifies culprit vessels and the anatomy of bronchial, non-bronchial and pulmonary artery vasculature. ^[6][7]
• Flexible bronchoscopy. Sensitive for detecting the bleeding source in about 70% of cases, but diagnostic accuracy for cause is lower (30% to 50%) and depends on timing. Best performed within 48 hours of the episode, when early bronchoscopy improves localisation of site, lobe and lung. It is especially useful in unstable patients where CT must wait. ^[6][7]
• Laboratory tests. Arterial blood gas, full blood count, clotting screen, renal and liver function, group and cross-match, and blood cultures if infection is suspected. Correct coagulopathy actively.

A stepwise algorithm avoids over-investigation. Screen for red flags first, then by duration, then by the four dominant causes and by smoking, before referring. The standard sequence from the CHEST and ERS guidance is: estimate duration; screen for red flags; basic evaluation with history, examination, spirometry, chest radiograph; optimise therapy for known disease; then a cause-directed algorithm for the four dominant conditions, with a trial of treatment for each before adding the next. ^[3][2]

Notes on empiric therapy. The ERS guideline suggests a short-term trial of inhaled corticosteroids for 2 to 4 weeks in adults, with a high dose suggested empirically and no continuation if there is no response within 2 to 4 weeks; a short-term antileukotriene trial of 2 to 4 weeks is suggested in those with an asthmatic cough. ^[2] Anti-acid drugs are not routinely recommended unless the patient has peptic symptoms or evidence of acid reflux. ^[2] For refractory unexplained chronic cough, a trial of low-dose morphine 5 to 10 mg twice daily, gabapentin or pregabalin, and cough control therapy are suggested, together with referral to a recognised cough clinic. ^[2][4] The response to morphine in responders is rapid, usually within a week, and treatment is stopped if there is no response after 1 to 2 weeks. ^[2] Codeine is generally not recommended in the same review because of side effects and lack of efficacy. ^[2]

The principle is to treat the cause of the cough, not to suppress it indiscriminately, although cough suppressants have a limited role while treatment takes effect.

• UACS. Treat rhinosinus disease: intranasal corticosteroids, saline irrigation, and review of environmental allergens. Antihistamines and decongestants are not recommended in children under 6 years, and UACS is rare in that age group. ^[4]
• Asthma and cough-variant asthma. Inhaled corticosteroids as the mainstay, with bronchodilators according to control; response may take weeks. ^[2][4]
• NAEB. Inhaled corticosteroids; eosinophilia should resolve with treatment. ^[2]
• GERD or laryngopharyngeal reflux. Treat proven reflux; lifestyle advice; acid suppression if peptic symptoms or reflux are present. Empiric proton pump inhibitors are not recommended in children without a specific diagnosis. ^[2][4]
• Smoking. Cessation is the treatment. Smoking is the major remediable cause. ^[2]
• COPD. Bronchodilators, smoking cessation, rehabilitation; address exacerbations.
• ACE inhibitor cough. Stop the ACE inhibitor and substitute another antihypertensive. Resolution may take days to weeks. Cough is reported in about 15% (ERS 2020) to 35% (AAFP 2017 range 5% to 35%) of users and is more common in women. ^[2][4]
• Bronchiectasis. Chest physiotherapy, antibiotics for exacerbations, treat underlying disorder.
• Tuberculosis. Treat per local programme; isolate and trace contacts.
• Interstitial disease and malignancy. Refer to specialist services.

Children with isolated chronic wet, productive cough that settles after an antibiotic course have protracted bacterial bronchitis: ERS 2020 describes 2 to 4 weeks and AAFP 2017 describes 2 weeks of an appropriate oral antibiotic such as amoxicillin-clavulanate. The preferred antibiotic and duration are not firmly defined. ^[2][4]

If no cause is found after the work-up, reassess the history and check adherence, then consider a supervised therapeutic trial. Options include low-dose morphine 5 to 10 mg twice daily, gabapentin up to 1,800 mg per day or pregabalin 300 mg per day in conjunction with speech therapy, and cough control or speech and language therapy. ^[2][4] In a trial of gabapentin, symptoms improved within 4 weeks. ^[4] A response to speech therapy alone is also reported. ^[4] Morphine responders show benefit within a week. ^[2]

Review the patient 4 to 6 weeks after the initial visit to confirm response. ^[3] Persistent, refractory, or unexplained chronic cough warrants referral to a pulmonologist or otolaryngologist. ^[4] A recognised cough clinic is the appropriate destination in many systems. ^[3]

This section follows the Singapore 2026 frontline-management review, supported by the 2025 Breathe and 2026 Lung India reviews. ^[5][6][7]

Massive (life-threatening) haemoptysis is any haemoptysis that is greater than 100 mL in 24 hours, or any volume causing abnormal gas exchange or airway obstruction, or causing haemodynamic instability. ^[5][7] Other sources such as Mishra 2026 call severe haemoptysis more than 300 mL in 24 hours, or any amount causing respiratory failure or haemodynamic instability. ^[6] Life-threatening haemoptysis is therefore a clinical diagnosis as well as a numerical one. Death comes from asphyxiation, not from exsanguination: 150 mL of blood occluding the tracheal dead space is enough to cause rapid death, and the least amount reported to cause life-threatening haemoptysis is 100 mL. ^[6][7] Severe presentations account for about 5% of cases. ^[6]

A patient with a strong protective cough reflex and good cardiopulmonary reserve may be managed without intubation, if closely monitored. Patients with weak protective reflexes or poor reserve need early intubation. High-flow nasal oxygen and non-invasive ventilation are not indicated, because they do not protect the airway. ^[7]

Rapidly exclude an upper airway source (epistaxis) and haematemesis, and look for the underlying cause. ^[7]

For patients who expectorate at least 100 mL of blood at one time and are at risk of airway loss, or who have tachypnoea, orthopnoea, inability to lie supine, ongoing hypoxaemia (inability to maintain peripheral oxygen saturation of 90% despite supplemental oxygen), mean arterial pressure below 65 mmHg, or need massive transfusion, emergency stabilisation should be started. ^{[7] [1]}

Objectives of initial stabilisation:

1. Secure the airway with a cuffed endotracheal tube, size 8 or larger. A large bore tube (8.5 mm inner diameter or larger in some advice) allows therapeutic bronchoscopes and thrombus extraction. ^[7][5]
2. Suction and clear the airway.
3. Give fluid resuscitation and support circulation.
4. Correct coagulopathy.
5. Start empirical treatment of infection and reversible causes.
6. Localise the bleeding.
7. Bridge to definitive treatment with a multidisciplinary team. ^[7]

Once the bleeding side is known, position the patient with the bleeding side down to reduce spillage into the unaffected lung, while awaiting further management. ^[7]

Conventional coagulation targets in bleeding patients: haemoglobin above 7 g/dL, platelets above 50 x 10^9/L, international normalised ratio below 1.5, and fibrinogen above 1.0 g/L, achieved with blood products. ^[7] In stable non-bleeding patients a haemoglobin around 7 to 8 g/dL is generally acceptable. ^[6]

Evidence favours localised (nebulised) over intravenous (IV) tranexamic acid for non-massive haemoptysis. In one comparison, nebulised tranexamic acid achieved haemoptysis cessation at 30 minutes in 72.72% versus 50.91% with IV tranexamic acid; in another randomised trial, 96% of patients receiving nebulised tranexamic acid had complete resolution within 5 days compared with 50% with placebo. ^[5][6]

Because none of these trials were in patients with massive haemoptysis, IV tranexamic acid 1 g is advocated as frontline management in massive haemoptysis because of its availability, ease of use and minimal side effects. ^[7] Nebulised tranexamic acid is given as 500 mg in 5 mL normal saline three to four times daily. ^[6] Tranexamic acid given down the bronchoscope is 1 g diluted in 20 mL normal saline. ^[6][7] A rare minor side effect of nebulised tranexamic acid is bronchospasm. ^[6]

Adjuncts used through the bronchoscope: cold saline 10 to 20 mL aliquots at 4 degrees Celsius; adrenaline 10 mcg diluted in 10 mL normal saline aliquots; and tranexamic acid as above. Topical measures such as cold saline lavage and diluted adrenaline (1:10,000) provide immediate but temporary haemostasis by vasoconstriction. ^[6][7]

When bleeding is associated with anticoagulant therapy, reverse it promptly:

• Idarucizumab for dabigatran: IV 5 g. ^[7]
• Andexanet alfa for factor Xa inhibitors: IV 400 mg. ^[7]
• Vitamin K: up to 10 mg IV. ^[7]

Multidetector CT is the imaging modality of choice in massive haemoptysis when available and the patient is stable enough for transfer. ^[7][5] It is comparable to bronchoscopy for identifying bleeding sites and is better at identifying the underlying cause. ^[7] Chest radiograph has variable efficacy for identifying the side of bleeding and the aetiology. ^[7] Bronchoscopy in this setting is adjunctive: it identifies the bleeding source, clears blood and thrombus, and allows endobronchial interventions, but should not delay definitive treatment. ^[5][7]

Bronchial artery embolisation (BAE) is the first-line definitive therapy for localised severe haemoptysis. It is minimally invasive, rapidly effective, repeatable, and associated with shorter hospital stays and lower morbidity than surgery. It targets bronchial arteries and non-bronchial collaterals. Technical success rates exceed 90%, with immediate bleeding control in approximately 80% to 95% of cases; immediate success rates of 87% to 100% are reported. ^[6][7] Long-term success ranges from 70% to 85%, with a recurrence rate of 23.7%. ^[6] Recurrence rates across series vary from 9.8% to 57.5%. ^[7] Factors associated with recurrence include mycetoma, sarcoidosis, cystic fibrosis, and angiographic non-bronchial collaterals. BAE remains effective before surgery even when haemoptysis recurs. ^[7]

Complications of BAE include transient chest or back pain in 34% to 91% of patients and dysphagia in up to 30%; serious but rare risks include spinal cord ischaemia at 0.19%. ^[6] The safety profile is relatively benign overall. ^[5] Bronchial arteries supply about 90% of clinically significant bleeding, so pulmonary artery occlusion is rarely needed; BAE is far more commonly performed. ^[7]

Surgery is indicated for patients who fail BAE and bronchoscopy, are unlikely to respond to embolisation, have high risk of recurrence, or need concomitant surgical biopsy for diagnosis. Emergency surgery is associated with poorer outcomes than scheduled surgery performed after initial bleeding control; torrential bleeding with rapid instability is a surgical indication. Lobectomy is the typical operation. Elective limited resections and video-assisted thoracoscopic approaches have lower mortality and morbidity. ^[6][7]

Bronchoscopy-based temporisation in active bleeding can be attempted with scope or balloon tamponade and instillation of the agents above; rigid bronchoscopy is occasionally needed. ^[5][7]

About 90% of patients with life-threatening haemoptysis have a bronchial arterial source, which makes embolisation effective. ^[5] Initial control is achieved in most patients, but recurrence is not rare; continued treatment of the underlying cause (tuberculosis, bronchiectasis, aspergilloma) is what prevents further bleeding. ^[5][7]

• Chronic cough. Refer when red flags are present, when the initial work-up is unrevealing but cough persists, when refractory unexplained chronic cough is suspected, or when spirometry shows severe obstruction. ^[4][3]
• Haemoptysis. Any patient with haemoptysis needs assessment. Life-threatening haemoptysis is an emergency. Massive or uncontrolled bleeding, failure of bronchoscopy and BAE, or need for biopsy is an indication for surgical review. ^[7]
• Strongly suspected lung cancer or tuberculosis. Refer on local cancer or tuberculosis pathways without waiting for full work-up. ^[4][3]
• Children. Children with chronic cough over 4 weeks, especially with wet productive cough, recurrent pneumonia, or suspected foreign body, should be referred early. ^[2][4]

Children. Chronic cough in children is more often different from that in adults. Protracted bacterial bronchitis, asthma, upper airway cough syndrome, bronchiectasis and cystic fibrosis are common causes; GERD is less common and routine proton pump inhibitors are not recommended without a diagnosis. Antihistamines and decongestants are not recommended for UACS in children under 6 years. ^[2][4]

Older adults. A change in cough in a smoker aged 55 to 80 years is a specific red flag for lung cancer or pulmonary fibrosis, even if the chest radiograph has not been done recently. ^[1]

People with chronic respiratory disease. In COPD, asthma and bronchiectasis, a worsening or blood-streaked cough suggests acute infection, exacerbation or, later in life, malignancy. Haemoptysis in bronchiectasis is often the first presentation of the severity of the disease.

Pregnancy. Haemoptysis or a severe cough in pregnancy is managed by the usual principles, with imaging chosen to minimise fetal risk; the source texts reviewed here do not provide pregnancy-specific data, so local specialist advice is needed.

Immunocompromised patients. Tuberculosis, fungal infection and atypical mycobacteria are proportionally more likely; severe immunosuppression is a red flag in itself. ^[1]

• Treating chronic cough starts with the history, examination and a plain chest radiograph plus spirometry where available; avoid CT unless red flags exist. ^[4][2]
• Consider tuberculosis early in endemic areas, even with a normal chest radiograph, and use the local tuberculosis programme for sputum testing and treatment. ^[3]
• Empiric isoniazid or other antibiotics must not be given blind; algorithms should follow national tuberculosis guidance.
• Protracted bacterial bronchitis in children can be treated with an antibiotic course: AAFP 2017 describes 2 weeks and ERS 2020 describes 2 to 4 weeks of an appropriate oral antibiotic such as amoxicillin-clavulanate. ^[4]
• In massive haemoptysis, airway protection and positioning come before imaging: an upright or lateral bleeding-side-down position, suction, and the largest available cuffed tube. High-flow nasal oxygen and non-invasive ventilation are not indicated. ^[7]
• BAE requires interventional radiology; when it is unavailable, arrange the earliest possible transfer to a centre that can perform it. Emergency surgery is associated with worse outcomes than embolisation. ^[7]
• Where CT angiography is not available, chest radiograph and bedside bronchoscopy still help localise the bleed, though both have limited sensitivity. ^[6][7]

Chronic cough often coexists with asthma, chronic obstructive pulmonary disease, bronchiectasis, upper airway disease, tuberculosis and lung cancer; these are covered in their own topics and should be consulted when the history points that way. Haemoptysis may also relate to pulmonary embolism, diffuse alveolar haemorrhage, and interstitial lung disease.>>