Haemoptysis

OVERVIEW

Haemoptysis is the expectoration of blood from the respiratory tract (below the cords).

• The spectrum varies from minor blood-streaked sputum to life-threatening haemorrhage
• There is no universal definition of massive or life-threatening hemorrhage 

“Life-threatening” haemoptysis (the main focus of this CCC entry) in practical terms is:

• Any bleeding causing respiratory failure, airway obstruction, or haemodynamic compromise
• Often >500 mL/24 h or >100 mL/h, but clinical impact is more important than volume
• The key life threat is asphyxiation from “airway flooding”, not exsanguination.

Haemoptysis must be distinguished from “pseudo-haemoptysis”, the expectoration of blood originating from sources other than the respiratory tract (i.e. nasopharynx, oropharynx, larynx, or gastrointestinal tract).

DEFINITIONS

Volume‑based definitions (traditional)

• Historically defined by the amount of blood expectorated over time:
  • >200–1000 mL over 24 hours in older literature
• Common contemporary thresholds:
  • >500 mL in 24 hours
  • >100 mL/hour 
• Limitations
  • Blood volume is difficult to estimate accurately
  • Does not account for patient reserve or physiological impact

Physiological definition — preferred for clinical relevance

• Massive haemoptysis is any bleeding that causes life‑threatening consequences, including:
  • Airway obstruction
  • Hypoxaemia or respiratory failure
  • Haemodynamic instability 
• The adult airway holds only ~150 mL so relatively small volumes can be fatal due to airway flooding and asphyxiation 

CAUSE

Common causes

• Infectious
  • Tuberculosis (global leading cause)
  • Necrotising pneumonia, lung abscess
  • Aspergilloma/mycetoma
• Structural lung disease
  • Bronchiectasis
  • Cystic fibrosis
• Malignancy
  • Bronchogenic carcinoma (esp. squamous)
  • Endobronchial tumours
• Vascular
  • Pulmonary embolism/ infarction
  • AVMs, aneurysms (e.g. Rasmussen aneurysm)
• Autoimmune
  • Vasculitis (GPA, SLE, anti-GBM)
  • Diffuse alveolar haemorrhage
• Cardiac
  • Mitral stenosis
  • Pulmonary oedema
• Iatrogenic
  • Bronchoscopy, biopsy, pulmonary artery catheter
• Drugs/toxins
  • Anticoagulants, antiplatelets
  • Cocaine, bevacizumab
• Bleeding disorders
  • Thrombocytopaemia
  • DIC
  • Factor deficiencies
• Cryptogenic
  • 7–25% of cases

PATHOGENESIS

Dual pulmonary circulation:

• Pulmonary arteries: low-pressure (12–16 mmHg)
• Bronchial arteries: systemic pressure ~100 mmHg

Bleeding source in life-threathening haemoptysis

• Bronchial arteries ~90% 
• Non-bronchial systemic collaterals ~5%
• Pulmonary arteries ~5%

Mechanisms

• Chronic inflammation results in bronchial artery hypertrophy and tortuosity
• Angiogenesis (VEGF) produces fragile neovessels prone to rupture
• Bronchopulmonary anastomoses enlarge causing high-pressure bleeding

Consequences

• Airway flooding
  • hypoxaemia and asphyxiation (leading cause of death)
  • Ventilation/perfusion mismatch
• Aspiration to contralateral lung
• Haemodynamic collapse (less common)

Complications

• Respiratory failure (common, major cause of death)
• Mortality
  • 9–38% (for life-threatening haemoptysis)
• Rebleeding after embolisation
  • 10–60%

CLINICAL ASSESSMENT

History

• Symptoms
  • Cough with blood (universal)
  • Dyspnoea (variable; more common if large volume)
  • Fever (infection)
  • Weight loss (malignancy, chronic infection)
• Key features
  • Volume and rate of bleeding (mL/h)
  • Ability to clear airway (critical)
  • Sentinel bleeding episodes (common in malignancy ~80%)
• Ask specifically:
  • TB exposure, prior lung disease
  • Immunosuppression
  • Anticoagulants/ antiplatelets or other bleeding diathesis
  • Other bleeding sites/ problems
  • Autoimmune symptoms (rash, renal disease)
  • Rule out pseudohaemoptysis (epistaxis, haematemesis)
  • Recent lung procedures

EXAMINATION

• Vital signs
  • Hypoxaemia (frequent in severe cases)
  • Tachycardia, hypotension (advanced)
• Respiratory
  • Reduced breath sounds (localised disease)
  • Crackles or consolidation (infection)
• Signs of cause
  • Clubbing (chronic lung disease)
  • Cachexia (malignancy)
  • Rash/purpura (vasculitis)

INVESTIGATIONS

Bedside tests

• ECG
  • Hypoxia-related changes, arrhythmia
• Blood gas
  • Hypoxaemia ± hypercapnia (severe cases)
• Blood glucose
  • Baseline
• Spirometry
  • Not indicated acutely
• POCUS
  • Consolidation, effusions

Laboratory tests

• FBC
  • Anaemia (severity), thrombocytopenia
• Coagulation profile
• Crossmatch
• U&E, LFTs
• Autoimmune screen (if DAH suspected)
• Microbiology (sputum, TB testing)
• TEG/ ROTEM if available

Imaging

• CXR
  • Localises bleeding in ~46%
  • Identifies cause ~35%
• CT chest (contrast / CT angiography)
  • Localisation: 70–88%
  • Aetiology: 86% – better than bronchoscopy (Chalumeau-Lemoine et al, 2013)
  • Defines vascular anatomy for embolisation
  • Best to perform earlier as ongoing bleeding may obscure pathological site and aetiological features
• MRI
  • Limited role

Other

• Bronchoscopy
  • Localization similar to CT (~70%)
  • Aetiology: 70% – worse than CT chest (Chalumeau-Lemoine et al, 2013)
  • May be essential for airway clearance and bleeding control
  • Often not required in patients maintaining a patent and protected airway and a causative lesion identified on CT chest
• Angiography
  • Diagnostic + therapeutic (BAE)

MANAGEMENT

Resuscitation

• Coordinated team-based approach to resuscitation in a suitably equipped setting to address the following life threats:
  • Airway obstruction from blood
    • intubate with ETT ≥8.0 mm (to facilitate bronchoscopy) if:
      • Ineffective cough, severe respiratory distress, worsening respiratory failure, or to facilitate diagnostics/ interventions (e.g. Ct scan / procedures)
      • Avoid intubation if possible (e.g. effective cough, able to protect airway, and patient able to oxygenate and ventilate safely)
      • Anticipate difficulty due to blood obscuring laryngoscopic view
    • Use suction and bronchoscopy (perform awake and unintubated if possible)
    • Hypoxaemia / respiratory failure
      • If SpO₂ <90% → administer high-flow oxygen
      • If severe/ refractory consider intubation and mechanical ventilation
    • V-V ECMO if other oxygenation strategies fail
  • Aspiration to contralateral lung
    • position bleeding side down If bleeding side known
  • Inadequate ventilation due to airway flooding
    • Consider selective mainstem intubation or bronchial blocker
      • Bronchial blocker preferred over double-lumen endotracheal tube for ease of placement, more selective lung isolation, and lower risk of malposition/ displacement.
    • V-V ECMO if other ventilation strategies fail
  • Ongoing haemorrhage
    • If active bleeding then perform urgent bronchoscopy ± embolisation
  • Coagulopathy
    • target INR >1.5, platelets >50, fibrinogen >1.5, treat hypocalcaemia
    • consider DDAVP for uraemia and other anticoagulant reversal agents.

SPECIFIC THERAPY

• Bronchoscopy (first-line temporising)
  • Topical adrenaline (epinephrine) (various regimens described)
    • Use adrenaline 1:10,000 (100 mcg/mL)
    • Instill 1–2 mL aliquots directly onto the bleeding segment
    • Maximum total dose 6 mL (600 mcg) initially
    • Monitor ECG and blood pressure continuously
  • Balloon tamponade / bronchial blockers
  • Cold saline lavage (50 mL aliquots)
    • Uncertain effectiveness
• Tranexamic acid
  • IV: 1 g every 8 h
  • Nebulised: 500 mg 8–12 hourly
    • Effective in an RCT of patients with “non-massive” haemoptysis (wand et al, 2018)
  • Endobronchial administration has also been described (500 mg in 15 mL saline) (Marquez-Martin et al, 2010)
• Bronchial artery embolisation (BAE)
  • First-line definitive therapy
  • Success: 70–99%
    • Less effective for large central masses fed by multiple vascular territories
  • Recurrence: 9–57%
    • Repeat BAE can still be successful
    • Risk factors for recurrence after BAE (Davidson & Shojaee, 2020):
      • aspergillomas, tuberculosis, bronchiectasis, and non-bronchial systemic collateral circulation, and bronchopulmonary shunting.
• Endobronchial therapies
  • Argon plasma coagulation
  • Laser (avoid if FiO₂ >0.4)
  • Stents, glue, spigots
• Surgery (selected cases)
  • Indications:
    • Failed BAE
    • Recurrent bleeding
    • Localised disease (e.g. aspergilloma)
  • Mortality:
    • Emergent ~35–40%
    • Elective markedly lower

SUPPORTIVE CARE AND MONITORING

• FASTHUGSINBED Please
  • Withhold chemical thromboprophylaxis if bleeding
  • Nurse bleeding side down

SEEK & TREAT COMPLICATIONS

• Rebleeding
  • Repeat BAE (effective)
• Aspiration pneumonia
  • Antibiotics
• Respiratory failure
  • Escalate ventilatory support
• BAE complications
  • Chest pain (common 1.4–34%)
  • Spinal cord ischaemia (<5%)
• Anaemia
  • Transfusion as required

DISPOSITION

• ICU admission
  • All life-threatening haemoptysis
  • High risk patients
    • Worsening respiratory failure
    • Poor physiological reserve due to underlying disease
    • Large volumes of blood
    • Concerning CT (e.g. consistent with large volumes of blood in lung and/or high risk pathology such as an eroding malignancy or infection)
    • Rapid progression
• HDU / ward
  • Minor haemoptysis only
• Consult:
  • Respiratory
  • Interventional radiology (urgent)
  • Thoracic surgery
• Consider transfer to tertiary centre if embolisation unavailable

MNEMONIC APPROACH / CHECKLIST

A–B–C–D–E

• Airway, Block it, Clot it, Deal with it, Everything else

A — ASSESS THE AIRWAY

• Airway aspiration
• Artificial airway (intubation):
  • Endotracheal intubation
  • Mainstem bronchus intubation
  • Double lumen intubation
• Anaesthesia consult

B — BLOCK THE BLOOD

• Bad side down (lateral decubitus)
• Bronchoscopy
• Bronchial blocker

C — CAUSE A CLOT

• Compression (tamponade, wedge)
• Cold (ice cold saline)
• vasoConstriction (e.g. adrenaline)
• Coagulants (thrombin, fibrin, tranexamic acid)
• Cautery (electrocautery / APC / laser)

D — DEFINITIVE THERAPY

• Interventional radiology consult (bronchial artery embolisation)
• Surgery consult
• Rigid bronchoscopy

E — EVERYTHING ELSE

• Eye on the patient (vital sign review, volume resuscitation)
• Evaluate labs (ABG, Urea / BUN, CBC, Coagulation profile, Group & crossmatch)
• Ensure coagulation:
  • Medication review
  • Correct coagulopathies

PROGNOSIS

• Overall mortality ~9–38% for life-threatening haemoptysis
• Favourable factors:
  • Rapid bleeding control
  • Localised disease amenable to therapy
• Poor prognostic factors:
  • Need for mechanical ventilation
  • Multilobar disease
  • Pulmonary artery involvement
  • Malignancy, aspergillosis
• Recurrence is common – up to 60% after BAE

CONCLUSION

Life-threatening haemoptysis is primarily lethal due to airway obstruction and hypoxaemia

• Bronchial arterial bleeding accounts for ~90% of cases

Management priorities:

• Secure airway and isolate bleeding lung (e.g. bronchial blocker)
• Localise source (CT and/or bronchoscopy)
• Control bleeding (BAE first-line)
• Anticipate rebleeding, which is common and requires definitive management (e.g. BAE, endobronchial therapies, and/or surgery)

REFERENCES

LITFL

• CCC – Diffuse alveolar haemorrhage

Journal articles

1. Chalumeau-Lemoine L, Khalil A, Prigent H, Carette MF, Fartoukh M, Parrot A. Impact of multidetector CT-angiography on the emergency management of severe hemoptysis. Eur J Radiol. 2013 Nov;82(11):e742-7. doi: 10.1016/j.ejrad.2013.07.009. Epub 2013 Aug 6. PMID: 23932395.
2. Charya AV, et al. Management of life-threatening hemoptysis in the ICU. J Thorac Dis. 2021;13(8):5139-5158. PMID: 34527355
3. Davidson K, Shojaee S. Managing massive hemoptysis. Chest. 2020;157(1):77-88. PMID: 31374211
4. Kathuria H, Hollingsworth HM, Vilvendhan R, Reardon C. Management of life-threatening hemoptysis. J Intensive Care. 2020 Apr 5;8:23. doi: 10.1186/s40560-020-00441-8. PMID: 32280479; PMCID: PMC7132983.
5. Márquez-Martín E, Vergara DG, Martín-Juan J, Flacón AR, Lopez-Campos JL, Rodríguez-Panadero F. Endobronchial administration of tranexamic Acid for controlling pulmonary bleeding: a pilot study. J Bronchology Interv Pulmonol. 2010 Apr;17(2):122-5. doi: 10.1097/LBR.0b013e3181dc8c17. PMID: 23168726.
6. Wand O, Guber E, Guber A, Epstein Shochet G, Israeli-Shani L, Shitrit D. Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial. Chest. 2018 Dec;154(6):1379-1384. doi: 10.1016/j.chest.2018.09.026. Epub 2018 Oct 12. PMID: 30321510.

FOAM and web resources

• Deranged Physiology – Causes and management of massive haemoptysis
• EMCrit IBCC – Severe hemoptysis (2021)
• EMCrit 199 – Management of Massive Hemoptysis with Oren Friedman (2017)
• Emergency Medicine Cases – Ep 188 Hemoptysis – ED Approach and Management