Haemoptysis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Haemoptysis ranges from blood-streaked sputum to airway-threatening haemorrhage. A volume estimate is often unreliable because blood may be swallowed, retained in the lung or mixed with sputum. The immediate decision is therefore whether the patient can maintain an airway and gas exchange, followed by whether bleeding is ongoing. Common causes include infection, bronchiectasis, malignancy and iatrogenic or anticoagulant-associated bleeding; pulmonary embolism, tuberculosis, aspergilloma, diffuse alveolar haemorrhage, pulmonary arteriovenous malformation and vascular erosion are less common but important.

History should establish onset, recurrence, streaking versus frank blood, clots, associated sputum, fever, weight loss, pleuritic pain and breathlessness. Ask about smoking and asbestos, previous cancer, bronchiectasis, tuberculosis and travel, autoimmune symptoms, renal disease, menstruation-related episodes, procedures and trauma. Obtain an exact medicine and last-dose history for anticoagulants and antiplatelets. Examination prioritises airway and breathing, then looks for focal chest signs, clubbing, lymphadenopathy, venous thromboembolism, vasculitis, heart failure and upper-airway or gastrointestinal sources.

Stable minor haemoptysis still requires a documented diagnostic plan. NICE referral thresholds are cancer-safety rules, not a complete differential. A normal chest radiograph does not exclude an endobronchial tumour or bronchiectasis. Conversely, infection on radiography does not automatically explain recurrent haemoptysis in a higher-risk patient. Close the loop on CT, bronchoscopy and follow-up rather than treating blood-streaked sputum repeatedly with antibiotics.

Key points

First confirm the source: haemoptysis is coughed from below the larynx, while epistaxis, oral bleeding and haematemesis require different pathways.
Severity is physiological, not purely volumetric. Airway flooding, impaired gas exchange, haemodynamic instability or continuing brisk bleeding defines an emergency even when volume is uncertain.
Ask about lung-cancer risk, bronchiectasis, tuberculosis exposure, infection, pulmonary embolism, autoimmune disease, recent procedures and anticoagulant or antiplatelet treatment.
Unexplained haemoptysis in a person aged forty or over meets NICE criteria for a suspected lung-cancer pathway referral; an abnormal radiograph can trigger referral at any relevant age.
Chest radiography is a useful start in stable bleeding, but contrast-enhanced CT or CT angiography usually provides better localisation and cause assessment; CTPA is selected when embolism is the question.
Bronchoscopy is important for airway control, clot extraction, central lesions and persistent bleeding; it complements rather than automatically replaces CT.
Review anticoagulants, platelet inhibitors and coagulation abnormalities immediately, but do not assume treatment is the underlying cause until structural disease has been considered.
Bronchial arteries cause most severe haemoptysis; bronchial-artery embolisation is a key definitive treatment for ongoing or recurrent significant bleeding.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Airway infection and damage

Bronchitis, pneumonia, tuberculosis, bronchiectasis and cystic fibrosis inflame hypertrophied bronchial vessels and are common sources of respiratory bleeding.

Malignancy

Lung and endobronchial cancer erode friable tumour vessels or obstruct airways, making persistent or unexplained haemoptysis a cancer warning symptom.

Pulmonary vascular disease

Pulmonary embolic infarction, pulmonary hypertension and vascular malformations can bleed from low- or high-pressure circulations, and its contribution is interpreted alongside the other recognised causes.

Diffuse or treatment-related bleeding

Vasculitis, anti-basement-membrane disease, anticoagulation and coagulopathy may cause diffuse alveolar haemorrhage or amplify bleeding from another lesion.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Vessel disruption
Inflammation, tumour, ischaemia or abnormal vascular pressure breaches bronchial or pulmonary vessels into an airway or alveolus.
2
Airway contamination
Blood spreads through the tracheobronchial tree, provoking cough and potentially flooding previously functional lung, with effects that increase as the pathological process progresses.
3
Gas-exchange loss
Clot and liquid blood obstruct ventilation and create shunt, so airway compromise often threatens life before blood loss does.
4
Haemodynamic effect
Sustained high-volume bleeding can also cause anaemia and shock, compounding hypoxaemia and reducing oxygen delivery, and the downstream physiological effect determines clinical severity.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Life-threatening haemoptysisRed flag

Active bleeding with inability to clear blood, falling saturation, respiratory distress, reduced consciousness, hypotension or a rapidly filling airway requires simultaneous resuscitation and haemorrhage control. Reported millilitres should not delay escalation.

Malignancy patternRed flag

Unexplained recurrent bleeding, weight loss, persistent cough, hoarseness, clubbing, lymphadenopathy or focal/recurrent radiographic change is concerning, especially with age over forty, smoking or asbestos exposure. Minor streaking can still be the presenting feature.

Infective or suppurative pattern

Fever, purulent sputum and focal consolidation suggests infection; daily sputum, recurrent exacerbations and coarse crackles suggests bronchiectasis. Tuberculosis risk, prolonged systemic symptoms or cavitation needs isolation and specialist microbiology planning.

Pulmonary vascular patternRed flag

Pleuritic pain, sudden breathlessness, syncope, hypoxaemia or thrombosis risk raises pulmonary embolism. Recurrent unexplained hypoxaemia, telangiectasia or family history may suggest pulmonary arteriovenous malformation.

Diffuse alveolar haemorrhageRed flag

Haemoptysis with diffuse infiltrates, falling haemoglobin, hypoxaemia and renal, skin or systemic inflammatory features raises pulmonary capillaritis or another alveolar-haemorrhage syndrome. Haemoptysis may be absent despite substantial alveolar bleeding.

Pseudohaemoptysis

Blood seen after coughing may originate from nose, gums, pharynx or gastrointestinal tract. Inspect the upper airway and ask about nausea, melaena and coffee-ground material, but do not use an uncertain source to dismiss ongoing respiratory bleeding.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE assessment, continuous oximetry and quantified bleeding trendFirst step
Why
Determine whether haemoptysis is immediately threatening airway, ventilation or circulation.
Interpretation and limitations
Record frequency, visible volume and clots while prioritising physiology. A rising oxygen requirement, inability to clear blood or haemodynamic change mandates resuscitation and definitive-control planning rather than routine outpatient work-up.
02
Full blood count, coagulation profile, renal and liver function, and group-and-save
Why
Assess blood loss, treatment safety and reversible haemostatic contributors.
Interpretation and limitations
An initially normal haemoglobin does not exclude acute blood loss. Renal function affects anticoagulant exposure and contrast planning; normal conventional coagulation tests do not measure every direct oral anticoagulant effect.
03
Chest radiograph
Why
Identify mass, cavitation, consolidation, oedema, diffuse haemorrhage or an alternative process.
Interpretation and limitations
Obtain promptly in stable patients and compare prior images. Normal radiography does not exclude cancer, bronchiectasis, embolism or a small vascular lesion; focal opacity may represent retained blood rather than its cause.
04
Contrast-enhanced chest CT or CT angiography
Why
Localise bleeding, identify cause and map bronchial or pulmonary vessels before intervention.
Interpretation and limitations
Choose the protocol with radiology: CTPA answers suspected pulmonary embolism, while systemic arterial mapping may be needed before embolisation. Balance contrast and radiation risk against the urgency of active significant bleeding.
05
Flexible or rigid bronchoscopy
Why
Secure or inspect the airway, remove clot, localise active bleeding and sample a central lesion.
Interpretation and limitations
Urgent bronchoscopy is a therapeutic airway procedure in significant ongoing bleeding; in stable disease its timing follows CT and specialist review. A negative examination does not exclude peripheral disease.
06
Sputum microbiology and targeted immune testing
Why
Investigate infection, tuberculosis or diffuse inflammatory haemorrhage when clinically supported.
Interpretation and limitations
Send bacterial and mycobacterial samples according to sputum and epidemiology. Urinalysis, creatinine, ANCA and related tests are appropriate for a pulmonary-renal or vasculitic phenotype, not as a blanket haemoptysis panel.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Upper-airway bleeding

Epistaxis or oral bleeding may be coughed out; nasal and oropharyngeal examination identifies a source above the larynx.

Haematemesis

Nausea, coffee-ground material, altered blood and gastrointestinal symptoms suggest vomiting of blood rather than lower-respiratory bleeding.

Pulmonary embolism

Pleuritic pain, tachycardia and venous thromboembolism risk support infarction, requiring probability-led imaging rather than attribution to infection.

Bronchiectasis

Chronic purulent sputum, recurrent infections and CT bronchial dilatation point towards bleeding from hypertrophied bronchial arteries.

Lung cancer

Persistent bleeding, age and smoking risk, weight loss or focal imaging change require urgent malignancy assessment even when infection is also plausible.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01EmergencyLife-threatening active bleedingFirst stepAirway contamination, gas-exchange failure, haemodynamic compromise or continuing brisk haemoptysis.

1Activate major clinical support including anaesthesia, respiratory, interventional radiology and thoracic surgery; use high-flow suction, monitoring, large-bore access and blood preparation while protecting staff and patient.
2If the bleeding side is known, position that lung dependent where feasible to protect the other lung; provide oxygen and ventilation support, recognising that a large single-lumen airway may be required for suction and bronchoscopy.
3Withhold and reverse clinically significant anticoagulation according to the specific agent, timing, renal function and local major-bleeding protocol; correct major thrombocytopenia or coagulopathy with haematology input.
4Use urgent contrast CT/angiography if the patient can be transferred safely, or bronchoscopy when airway control cannot wait; proceed to bronchial-artery embolisation for a suitable ongoing systemic arterial source.
5Plan surgery only for selected uncontrolled bleeding or a surgically correctable lesion because emergency resection carries substantial risk.

02StableNon-massive haemoptysis assessmentBlood-streaking or small-volume haemoptysis with stable airway, oxygenation and haemodynamics.

1Confirm the source, examine nose, mouth and chest, establish cancer, infection, embolism and medicine risks, and obtain observations, blood count, coagulation/renal profile and chest radiograph.
2Refer through the suspected-cancer pathway when NICE criteria are met; use CT despite a normal radiograph when risk, recurrence or unexplained bleeding warrants it.
3Treat an established infection or bronchiectasis exacerbation using the relevant guideline and microbiology, while retaining a plan to exclude structural disease when bleeding is recurrent or disproportionate.
4Give explicit return advice for increasing volume, breathlessness, dizziness or recurrent bleeding and assign ownership of imaging and specialist results.

03RecurrentBleeding with no cause on first assessmentRecurrent haemoptysis or persistent clinical concern after initial radiography and treatment.

1Review the quality and protocol of previous imaging and arrange contrast CT with respiratory or thoracic radiology input; compare the anatomical site of bleeding with recurrent infiltrates.
2Use bronchoscopy for suspected central lesion, airway sampling or persistent unexplained bleeding, and pursue bronchiectasis, tuberculosis, aspergilloma, vascular malformation and immune causes according to phenotype.
3Reconcile antithrombotic need with recurrence risk through the relevant specialist; do not permanently stop stroke- or thrombosis-prevention treatment without a documented balance and restart decision.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Reduces ongoing anticoagulant effect during clinically significant or life-threatening pulmonary bleeding.

Agent-specific anticoagulant reversal

Use the locally adopted major-bleeding protocol for the exact anticoagulant, last dose, renal function and bleeding severity; obtain urgent haematology advice.

Reversal can increase thrombosis risk and is not a substitute for airway protection and source control. Conventional coagulation tests may not quantify direct oral anticoagulants reliably.

Treats infection when the clinical and microbiological phenotype supports it.

Antimicrobial therapy for a confirmed infective cause

Select agent, route and duration from the relevant pneumonia, bronchiectasis or tuberculosis guideline and current microbiology rather than treating haemoptysis empirically.

Antibiotics do not exclude cancer or vascular disease. Obtain cultures when feasible, check allergy and renal function, and reassess persistent or recurrent bleeding.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Airway obstruction

Blood and clot can block the trachea or major bronchi, causing asphyxia despite relatively preserved circulating volume.

Contralateral flooding

Bleeding from one lung can spill into the other, converting a local lesion into widespread shunt and respiratory failure.

Haemorrhagic shock

Ongoing major bleeding may reduce circulating volume and haemoglobin, causing hypotension and impaired tissue oxygen delivery.

Aspiration pneumonia

Retained blood and impaired airway protection encourage collapse and secondary infection after the acute event, and potentially prolonging treatment and functional recovery.

Recurrent haemorrhage

Temporary cessation does not remove an abnormal bronchial artery, tumour or vascular lesion, so further potentially larger bleeding can occur.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

In active bleeding continuously monitor airway clearance, respiratory rate, SpO2 and oxygen requirement, pulse, blood pressure, consciousness and observed bleeding burden.
Trend haemoglobin and transfusion requirement with clinical loss; an early haemoglobin can remain normal after acute haemorrhage.
After embolisation monitor puncture site, distal perfusion, chest pain, recurrent haemoptysis and new neurological symptoms that could signal a rare spinal complication.
Document withholding, reversal and planned review or restart of every anticoagulant and antiplatelet medicine.
Close the loop on CT, bronchoscopy, cytology and microbiology and arrange repeat assessment for any recurrent bleeding, even if the first episode was labelled infective.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Volume is an unreliable severity measure

Patients swallow blood, retain it in distal airways or estimate mixtures with sputum. The rate, airway impact and cardiopulmonary reserve determine danger more reliably than a remembered cupful.

Bleeding side down protects

When unilateral bleeding is known, dependent positioning can reduce contamination of the unaffected lung. This is a bridge to airway and definitive management, not a substitute for it.

Most severe bleeding is systemic arterial

Hypertrophied bronchial arteries operate at systemic pressure and cause most life-threatening haemoptysis, explaining why bronchial-artery embolisation is central even though blood exits through the pulmonary airway.

Opacity may be consequence, not cause

Fresh alveolar blood can produce focal or diffuse radiographic opacity. Correlate with CT angiographic and clinical findings rather than diagnosing pneumonia solely from a new shadow.

Anticoagulation can reveal disease

An anticoagulant may increase bleeding from tumour, bronchiectasis or infection but should not be accepted as the sole diagnosis. Structural investigation and a deliberate restart decision are both required.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for a precise millilitre threshold while the airway is filling with blood.
02
Sending an unstable actively bleeding patient to CT without airway and transfer planning.
03
Assuming a normal chest radiograph excludes endobronchial malignancy.
04
Attributing recurrent bleeding entirely to anticoagulation and missing structural lung disease.
05
Treating every blood-streaked sputum episode with antibiotics without cancer or bronchiectasis assessment.
06
Stopping antithrombotic treatment indefinitely without documenting thrombosis risk and a review date.