Hemoptysis

 Hemoptysis 

🔹 Introduction

Hemoptysis refers to expectoration of blood originating from the lower respiratory tract (below the glottis). It is a potentially life-threatening emergency when massive, as it can cause airway obstruction, asphyxiation, or hypoxemic respiratory failure, even before exsanguination occurs.


🔹 Classification

Type

Definition

Volume / Clinical Relevance

Non-massive hemoptysis

Blood-streaked sputum or <100–200 mL/day

Usually benign, common in bronchitis or mild infections

Massive hemoptysis

Traditionally >200–600 mL in 24 hr, or any volume causing airway compromise or hemodynamic instability

True emergency — high mortality if not controlled rapidly

Clinical definition preferred:
➡️ Any hemoptysis that causes respiratory distress, airway obstruction, or hemodynamic instability should be treated as massive, irrespective of volume.


🔹 Pathophysiology

1. Vascular sources

  • Bronchial circulation (90%) — systemic high-pressure system from thoracic aorta.
  • Pulmonary circulation (10%) — low-pressure system, but involvement in vasculitis, AV malformations, or trauma.

2. Mechanisms

  • Erosion or rupture of bronchial artery due to chronic inflammation or neoplasm.
  • Neovascularization with fragile vessels (e.g., bronchiectasis, TB).
  • Alveolar capillary leakage (e.g., diffuse alveolar hemorrhage).


🔹 Common Causes of Hemoptysis

1. Infectious

  • Tuberculosis (active or sequelae) – cavitary lesions erode bronchial vessels.
  • Bronchiectasis – chronic suppurative infection with fragile neovascularity.
  • Lung abscess, necrotizing pneumonia, or fungal infections (Aspergilloma).

2. Inflammatory / Autoimmune

  • Goodpasture’s syndrome (anti-GBM disease)
  • Granulomatosis with polyangiitis (Wegener’s)
  • Microscopic polyangiitis
  • SLE, Behçet’s disease

3. Neoplastic

  • Bronchogenic carcinoma – central tumors may erode vessels.
  • Metastatic lesions – especially choriocarcinoma, renal cell carcinoma.

4. Cardiovascular

  • Mitral stenosis – pulmonary venous hypertension rupture of bronchial veins.
  • Pulmonary embolism / infarction
  • AV malformations, aneurysm of pulmonary artery (Rasmussen’s aneurysm)

5. Iatrogenic / Traumatic

  • Bronchoscopy, biopsy, tracheostomy, catheter-induced injury, or mechanical ventilation.

6. Coagulopathy / Drugs

  • Anticoagulants, antiplatelet therapy, DIC, thrombocytopenia.

7. Idiopathic

  • Up to 30% of cases — particularly in smokers and chronic bronchitics.


🔹 Differential Diagnosis — “Pseudohemoptysis”

Source

Key Features

Upper airway (epistaxis, gingival bleeding)

Blood seen on posterior pharyngeal wall; not associated with cough

GI tract (hematemesis)

Coffee-ground appearance, acidic pH, mixed with food particles, melena

True hemoptysis

Alkaline pH, bright red, frothy, preceded by cough

  • Most common cause worldwide: Tuberculosis
  • Most common cause in developed countries: Bronchiectasis
  • Most common cause of death: Asphyxiation
  • Definitive treatment for massive hemoptysis: Bronchial artery embolization
  • DAH hallmark on BAL: Hemosiderin-laden macrophages
  • Rasmussen’s aneurysm: Pulmonary artery aneurysm adjacent to TB cavity



🔹 Clinical Evaluation

1. History

  • Onset: sudden (PE, bronchiectasis) vs gradual (malignancy).
  • Associated symptoms: fever, weight loss, hematuria (vasculitis), chest pain.
  • Risk factors: smoking, TB exposure, anticoagulants, recent procedures.

2. Physical Examination

  • Vital signs, oxygenation, hemodynamic stability.
  • Inspection for clubbing, cyanosis, signs of vasculitis, murmurs (mitral stenosis).
  • Auscultation: crackles, bronchial breath sounds, wheeze, cavity signs.


🔹 Investigations

1. Initial

  • CBC, renal and liver function, coagulation profile, ABG.
  • Chest X-ray – localize lesion (cavity, mass, infiltrate, consolidation).
  • Sputum for AFB, cytology, Gram/fungal stain.

2. Advanced

  • CT chest (HRCT or CECT)first line if patient is stable, best for localization, detecting bronchiectasis, malignancy, aspergilloma, PE.
  • Bronchoscopy (Flexible or Rigid)
    • Diagnostic & therapeutic.
    • Allows localization, suctioning, tamponade, instillation of vasoconstrictors or iced saline.
    • first line if patient is unstable

3. Specific

  • Autoimmune panel: ANA, ANCA, anti-GBM.
  • Urinalysis: red cells, casts (DAH).
  • Echocardiography: evaluate mitral stenosis, cardiac causes.


🔹 Diffuse Alveolar Hemorrhage (DAH)

Definition: Bleeding into alveolar spaces due to capillaritis or non-inflammatory causes.

Causes:

  • ANCA-associated vasculitis
  • Anti-GBM disease
  • SLE
  • Drugs (amiodarone, cocaine, anticoagulants)

Clinical triad:

  • Hemoptysis (may be absent in 30%)
  • Anemia
  • Diffuse pulmonary infiltrates

Bronchoalveolar lavage (BAL): sequentially more bloody aliquots, hemosiderin-laden macrophages.


🔹 Management Approach

1. Immediate Priorities (ABCDE)

  • Airway protection – main cause of death is asphyxiation, not exsanguination.
    • Intubate with large-bore single-lumen ETT (>8.5 mm) for bronchoscopy access.
    • Selective mainstem intubation of non-bleeding lung if bleeding side known.
    • Can use bronchial blocker
  • Breathing: supplemental oxygen, mechanical ventilation if required.
  • Circulation: IV access, fluids, transfusion for anemia/shock.

2. Localization of Bleeding

  • CT chest followed by bronchoscopy — often both needed.
  • If site identified, position patient bleeding side down (dependent position).

3. Specific Therapy

 a. Medical Measures

  • Stop anticoagulants, correct coagulopathy (FFP, PCC, platelets).
  • Tranexamic acid500–1000 mg IV or via nebulization; may reduce bleeding duration.
  • Cold saline lavage, topical epinephrine (1:20,000) via bronchoscope.
  • Treat underlying cause — antibiotics, antituberculars, immunosuppressants.

 b. Bronchoscopic Interventions

  • Balloon tamponade, fibrin glue, topical hemostatics.
  • Rigid bronchoscopy preferred in massive cases (better suction, airway control).

 c. Definitive Therapies

  • Bronchial Artery Embolization (BAE):
    • First-line definitive therapy for massive hemoptysis.
    • Success: 70–90%, recurrence 10–30%.
    • Embolic agents: PVA particles, coils, glue.
    • Avoid spinal artery embolization (paraplegia risk).
  • Surgical Resection:
    • Indicated when embolization fails or if resectable localized lesion (aspergilloma, tumor, destroyed lobe).
    • High mortality if done emergently; prefer elective once stabilized.


🔹 ICU and Critical Care Aspects

  • Massive hemoptysis = Airway emergency immediate airway control.
  • Maintain PEEP cautiously to avoid dislodging clot.
  • Prone positioning may aid dependent drainage.
  • Blood conservation: monitor hemoglobin and coagulation closely.
  • Multidisciplinary team: pulmonologist + interventional radiologist + thoracic surgeon.


🔹 Prognosis

  • Depends on etiology and bleeding severity.
  • Mortality in massive hemoptysis: >50% without intervention, <10% with early embolization.
  • Recurrence common in bronchiectasis and TB sequelae.


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