1. Haemoptysis

2. Haemoptysis
Spitting of blood derived from the lungs or bronchial tubes as a result of pulmonary or bronchial hemorrhage
Non-massive vs Massive: based on volume of blood loss  but no uniform definitions
Massive haemoptysis = potentially life-threatening haemoptysis
Massive hemoptysis = potentially life-threatening. Therefore the amount varies among individuals.

3. Pulmonary circulation
Mostly (95%): low-pressure pulmonary arteries  pulmonary capillary bed
Others (5%): high-pressure bronchial arteries
Originate at the aorta
Supply major airways and supporting structures

4. Haemoptysis Blood usually from bronchial circulation
Rarely from pulmonary circulation
Usually produce small-volume haemoptysis
Others mimickers:
Pseudohaemoptysis (blood that does not come from the lungs or bronchial tree)
Haematemesis

5. Differential diangoses
Broad range of DDx

7. Differential Diagnoses
Source other than the lower respiratory tract
Upper airway (nasopharyngeal) bleeding
Gastrointestinal bleeding
Tracheobronchial source
Neoplasm (bronchogenic carcinoma, endobronchial metastatic tumor, Kaposi’s sarcoma, bronchial carcinoid)
Bronchitis (acute or chronic)
Bronchiectasis
Broncholithiasis
Airway trauma
Foreign body
Pulmonary parenchymal source
Lung abscess
Pneumonia
Tuberculosis
Mycetoma (“fungus ball”)
Goodpasture’s syndrome
Idiopathic pulmonary
hemosiderosis
Wegener’s granulomatosis
Lupus pneumonitis
Lung contusion

8. Differential Diagnoses
Primary vascular source
Arteriovenous malformation
Pulmonary embolism
Elevated pulmonary venous pressure (especially mitral stenosis)
Pulmonary artery rupture secondary to balloon-tip pulmonary artery catheter manipulation
Miscellaneous and rare causes
Pulmonary endometriosis /Catamenial hemoptysis
Systemic coagulopathy or use of anticoagulants or thrombolytic agents

9. Infection Most common cause of haemoptysis
Superficial mucosal inflammation and edema  rupture of the superficial blood vessels
Bronchitis, pneumonia ,tuberculosis
Bacteria (e.g. Staph. aureus, Pseudmonas aeruginosa) TB
Rarer cause: fungi (e.g. Aspergillus)
I don’t think aspergillus is the commonest infective agent. It is less common than bacterial and TB in our locality.

10. Tumour
Superficial mucosal invasion, erosion into blood vessels, or highly vascularised tumour
Obstruction  secondary infection
Metastatic tumour less likely to bleed

11. Pulmonary venous hypertension
Left ventricular systolic heart failure
Mitral stenosis

12. Idiopathic
7-34% patient with haemoptysis has no identifiable cause after careful evaluation
Prognosis is good
Most had resolution of haemoptysis in 6 months

13. Assessment Airway, Breathing, Circulation
Haemoptysis vs Haematemesis vs Pseudohaemoptysis (e.g . from naso/oro-pharynx)

14. Assessment
History usually provides clues for differentiating haemoptysis vs haematemesis vs pseudohaemoptysis

15. Haemoptysis? Haematemesis?
History
Absence of nausea and vomiting
Lung disease
Asphyxia possible
Sputum examination
Frothy
Liquid or clotted appearance
Bright red or pink
Laboratory
Alkaline pH
Mixed with macrophages
and neutrophils
Haematemesis
Presence of nausea and vomiting
Gastric or hepatic disease
Asphyxia unusual
Rarely frothy
Coffee ground appearance
Brown to black
Acidic pH
Mixed with food particles

16. Pseudohaemoptysis History of epistaxis Expectorating without cough
Usually suggest blood from upper resp tract

17. Assessment If Hx and PE findings suggest haemoptysis
Amount of blood has to be estimated
Difficult to quantify clinically and frequently overestimated
Nature of haemoptysis
Blood stained sputum
Clots
Fresh blood
Use of graduated container
?On-going haemoptysis
Amount or frequency of bleeding DOES NOT correlate with the diagnosis or incidence of cancer

18. Further history Clinical clues Anticoagulant use
Association with menses
Dyspnea on exertion, fatigue, orthopnea, paroxysmal nocturnal dyspnea, frothy pink sputum
Fever, productive cough
History of breast, colon, or renal cancers
History of chronic lung disease, recurrent lower respiratory track infection, cough with copious purulent sputum
HIV, immunosuppression
Nausea, vomiting, melena, alcoholism, chronic use of nonsteroidal anti-inflammatory drugs
Pleuritic chest pain, calf tenderness
Tobacco use
Travel history
Weight loss
Suggested diagnosis*
Medication effect, coagulation disorder
Catamenial hemoptysis
Congestive heart failure, left ventricular dysfunction, mitral valve stenosis
Upper respiratory infection, acute sinusitis, acute bronchitis, pneumonia, lung abscess
Endobronchial metastatic disease of lungs
Bronchiectasis, lung absces
Neoplasia, tuberculosis, Kaposi’s sarcoma
Gastritis, gastric or peptic ulcer, esophageal varices
Pulmonary embolism or infarction
Acute bronchitis, chronic bronchitis, lung cancer, pneumonia
Tuberculosis, parasites (e.g., paragonimiasis, schistosomiasis, amebiasis, leptospirosis), biologic agents (e.g., plague, tularemia, T2 mycotoxin)
Emphysema, lung cancer, tuberculosis, bronchiectasis, lung abscess, HIV
Please match the two columns

19. CXR Essential Underlying cause
Site of bleeding, to guide further treatment

20. Clues on CXR CXR findings
Cardiomegaly, increased pul vascular distribution
Cavitary lesions
Diffuse alveolar infiltrates
Hilar adenopathy or mass
Hyperinfilation
Lobar or segmental infiltrates
Mass lesion, nodules, granulomas
Normal or no change from baseline
Patchy alveolar infiltrates (multiple bleeding sites)
Suspected diagnosis
CHF, MS
Lung abscess, TB, necrotizing CA
CHF, pul edema, aspiration, toxic injury
CA, met, infections, sarcoid
COPD
Pneumonia, thromboembolism, obstructing CA
CA, met, Wegener’s granulomatosis, septic embolism, vasculitides
Bronchitis, URI, sinusitis, pul embolism
Bleeding disorders, idiopathyic pulmonary haemosiderosis, Goodpasture’s syndrome

21. Laboratory findings White cell count/differential
Elevated WCC & left shifts  infections
Hb, Hct
Anaemia
Plt
Thrombocytopenia
PR/INR/APTT
Anticoagulant use/coagulopathy
ABG
Hypoxia/hypercarpnia
D-dimer PE
Sputum C/ST, AFB smear, C/st
Pneumonia, abscess, TB
Sputum cytology
Neoplasia
HIV serology
TB, Kaposi’s sarcoma
ESR
Infections, autoimmune disorders, +/-neoplasia

22. Management
Acute treatment depends on the amount/cause of haemoptysis

23. Massive haemoptysis
No standardised magic figures for amount of blood loss
Usually quoted as >200ml/24hr

24. Massive Haemoptysis
Mortality rate from massive haemotpysis depends on the bleeding rate and aetiology
Airway protection
Primary mechanism of death is asphyxiation, not exasnguination
Positioning maneurvers: decubitus position if one is sure of the site of bleeding
Intentional single lung intubation/use of double lumen ET tube
Obstruction of the bronchus leading to the bleeding lung, e.g bronchial blocker
Ventilatory support
Circulatory support

25. Double lumen ET tube

26. Double lumen ET tube

27. Double lumen ET tube

28. Endobronchial Blocker

29. Endobronchial blocker

30. Treatment Emergency treatment for control of haemoptysis
Treatment targeting underlying aetiology
E.g. treatment of infection in haemoptysis associated with infective exacerbation of bronchiectasis

31. Fibreoptic Bronchoscopy
Limited in massive haemoptysis
Localisation of bleeding site
diagnosis
Guide intubation
Cold saline
Adrenaline
Tamponade
Argon plasma coagulation, electrocautery, laser
Argon plasma coagulation, electrocautery, laser: can be done using the flexible bronchoscope

32. Rigid Bronchoscopy
Merits of rigid bronchoscopy over flexible bronchoscopy:
Better airway control
Larger field of view
Better suctioning
Better for therapeutic interventions
Direct pressure
Laser therapy
Cauterization
Adrenaline/vasopressin injection
Isolation of the bleeding pulmonary segment
Not readily available!!!
What do you mean by embolization using a rigid bronchoscope?

33. Surgery Lobectomy Pneumonectomy
Others surgical treatments directed to underlying causes, e.g.
Emergent mitral valvulotomy for haemoptysis due to severe MS

34. Bronchial Arterial Embolisation
Main stay for emergency management of massive haemoptysis
Effective, long and short term bleeding control
Safe: complication rates generally low and minor; major complications infrequent