Approach 2 PDF

Assessment of
haemoptysis
The right clinical information, right where it's needed
Last updated: Jan 24, 2019

Table of Contents
Summary 3
Overview 5
Aetiology 5
Emergencies 8
Urgent considerations 8
Diagnosis 10
Step-by-step diagnostic approach 10
Differential diagnosis overview 14
Differential diagnosis 16
Diagnostic guidelines 42
References 43
Images 48
Disclaimer 54
Summary
◊ Haemoptysis is the coughing of blood from a source below the glottis.[1] It can range from a small
amount of blood-streaked sputum to massive bleeding with life-threatening consequences due to
airway obstruction, hypoxaemia, and haemodynamic instability.
In one study of patients in a UK primary care database, the incidence of haemoptysis was found
to be 1 case in 1000 patients per year.[2] Massive haemoptysis occurs in around 5% to 15% of
patients presenting with haemoptysis as a chief presenting symptom.[3] The rate of bleeding has
been described as the most important factor determining mortality.[4]
◊ Pseudohaemoptysis versus haemoptysis :

The initial diagnostic assessment should aim to differentiate between haematemesis (i.e., the
vomiting of blood), pseudohaemoptysis (i.e., the coughing of blood from a source other than the
lower respiratory tract), and haemoptysis. Pseudohaemoptysis can occur when:[5]
• Haematemesis is aspirated into the lungs
• Bleeding from the upper airway or the mouth stimulates a cough reflex
• Material is expectorated that looks like blood but is not (e.g., Serratia marcescens infection).
Characteristically, haemoptysis tends to be indicated by bright red, frothy sputum that is alkaline.
Blood from extrapulmonary sources tends to be darker, may have admixed food particles, and is
acidic.[5] [6] The exception is when brisk bleeding in the gastrointestinal tract overcomes the acidic
environment of the stomach. Bleeding from the posterior nasal passage or nasopharynx may mimic
haemoptysis without obvious epistaxis. Examining the oral and nasal cavities can provide important
clues to the source of the bleeding (e.g., telangiectasia in the mouth or nose, etc).
◊ Massive haemoptysis :
Various definitions of massive haemoptysis exist. A common definition is the expectoration of blood
from a source below the glottis exceeding 600 mL of blood over a 24-hour period or 150 mL of blood
(which may flood the lung dead space) over a 1-hour period. Massive haemoptysis is a medical
emergency and should be addressed immediately. Initial priorities are stabilisation of the patient and
protection of the non-bleeding lung.
◊ Common causes :
Haemoptysis has numerous possible causes, including tracheobronchial, pulmonary parenchymal,
and pulmonary vascular diseases. In the primary care setting, major causes are acute and chronic
bronchitis, tuberculosis, lung cancer, pneumonia, and bronchiectasis.
◊ Vascular origin :
Clinical, radiological, and pathological evidence has demonstrated that the bronchial or systemic
circulation is responsible for most cases of haemoptysis.[7] However, the pulmonary circulation
has also been implicated, as is the case in catheter-induced pulmonary artery rupture, vasculitis,
pulmonary artery aneurysms due to collagen vascular disease, or hereditary haemorrhagic
telangiectasia.[8] [9]
Assessment of haemoptysis Overview
Aetiology
Acute and chronic bronchitis, and less commonly tuberculosis and bronchiectasis, have been reported
as major causes of haemoptysis.[10] [11] Malignancy is a common cause of massive or life-threatening
OVERVIEW
haemoptysis.[3]
Pulmonary vascular anatomy

The tracheobronchial tree and the lungs have a dual circulation:
• Bronchial arteries (systemic circulation)

• Pulmonary arteries.
The bronchial arteries are branches of the aorta or its tributaries, the intercostal arteries, and carry systemic
arterial pressures that perfuse the adjacent airways to the level of the terminal bronchioles. Bronchial arteries
supply the mediastinum, hilar lymph nodes, and visceral pleura.
The pulmonary artery is a low-pressure system, with normal systolic pressures ranging from 15 to 20
mmHg and diastolic pressures of 5 to 10 mmHg. These vessels supply the pulmonary parenchyma and the
respiratory bronchioles. The anastomotic connections between the bronchial circulation and the pulmonary
circulation contribute to physiological right-to-left shunt.[1]
Clinical, radiological, and pathological evidence has demonstrated that the systemic circulation (bronchial
arteries) is responsible for most cases of haemoptysis.[7] However, the pulmonary circulation has also
been implicated, as is the case in catheter-induced pulmonary artery rupture, vasculitis, pulmonary artery
aneurysms due to collagen vascular disease, necrotic pulmonary infection, or pulmonary arteriovenous
malformation as in hereditary haemorrhagic telangiectasia.[8] [9]
Infectious
Infection is one of the most common causes of haemoptysis.
• Pneumonia can cause haemoptysis by causing necrosis of adjacent bronchial vessels or local
mucosal ulceration.
• In chronic fibrotic tuberculosis, haemoptysis is caused by rupture of Rasmussen's aneurysms or
ectatic pulmonary arteries (with a weakened adventitia and media vessels) traversing the tuberculous
cavities.
• In bronchiectasis, chronic airway inflammation results in increased bronchial artery tortuosity, as
well as proliferation of the capillary beds and peribronchial vascular plexus. Recurrent inflammatory
destruction and healing lead to bronchopulmonary vascular anastomoses.[12] [13] [14]
• In lung abscess, the pathogenesis of haemoptysis is not entirely clear but may be due to progression
of local inflammatory processes causing necrosis of branches of the pulmonary artery.[15]
Neoplastic
In malignancy, there is an increase in the bronchial artery supply to the region of the tumour. Haemoptysis
results from necrosis, mucosal invasion, or direct local invasion of a blood vessel. Massive haemoptysis may
happen when tumour invasion into a blood vessel and its adjacent airway results in vascular airway fistula.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jan 24, 2019.
BMJ Best Practice topics are regularly updated and the most recent version
5
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2019. All rights reserved.
Iatrogenic
Haemoptysis may occur with traumatic intubation, bronchoscopy, and endobronchial therapeutic
manoeuvres. Massive fatal haemoptysis may rarely happen from erosion of a tracheostomy or laryngectomy
into an innominate (brachiocephalic) artery. Other causes include catheter-induced pulmonary artery rupture
OVERVIEW
or infarct. Drug-induced haemoptysis may occur with exposure to anticoagulants, aspirin, and thrombolytic
agents.
Vasculitic
Haemoptysis may be found in patients with pulmonary haemorrhage from a small-vessel vasculitis (such as
granulomatosis with polyangiitis [formerly Wegener's granulomatosis]), and may be the presenting symptom
in some patients.
The mechanisms responsible for haemoptysis in vasculitis are multiple. However, the most important is
pulmonary haemorrhagic alveolar capillaritis. This involves neutrophilic infiltration of the alveolar septa,
where disruption of the alveolar-capillary basement membranes results in extensive haemorrhage into
the alveolar spaces.[16] [17] Though performing diffusing capacity measurements is often difficult in the
acutely bleeding patient and is only infrequently clinically feasible, an elevated value of diffusing capacity can
indicate alveolar bleeding because intra-alveolar blood adsorbs carbon monoxide avidly.
Cardiac
In left ventricular failure and mitral stenosis, blood-streaked sputum is caused by rupture of pulmonary
veins or capillaries, or by anastomoses between bronchial and pulmonary arteries distended by elevated
intravascular pressure or pulmonary venous hypertension.[12] [18] [19]
Vascular
Vascular anomalies such as Dieulafoy's disease, characterised by the presence of a tortuous dysplastic
artery in the submucosa, can be a cause of haemoptysis. Pulmonary arteriovenous malformation may also
cause haemoptysis. Pulmonary thromboembolic disease that progresses to pulmonary infarct may result in
haemoptysis and bloody pleural effusion.
Haematological
Haemoptysis can be caused by bleeding- and coagulation-related disorders or abnormalities, such as
thrombocytopenia, coagulopathies, or disseminated intravascular coagulation.
Congenital
Congenital lung malformations such as bronchogenic cyst can cause haemoptysis.
Idiopathic
Idiopathic haemoptysis is a diagnosis of exclusion. In approximately one third of patients presenting with
haemoptysis, the underlying cause is not identified even after careful assessment.
Factitious
Factitious haemoptysis is a diagnosis of exclusion with more than 20 reported cases. However, factitious
haemoptysis is likely to be both under-reported and under-diagnosed. Because factitious haemoptysis is
6 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Jan 24, 2019.
an exclusionary diagnosis, patients with factitious disorders frequently undergo multiple invasive and non-
invasive studies before the diagnosis is made.[20] [21]
OVERVIEW
7
Assessment of haemoptysis Emergencies
Urgent considerations
(See Differential diagnosis for more details)
Massive haemoptysis
A patient with massive haemoptysis, defined as the expectoration of blood from a source below the glottis
exceeding 600 mL of blood over a 24-hour period or 150 mL of blood (which may flood the lung dead space)
over a 1-hour period, is a medical emergency and should be addressed immediately. The rapidity of blood
loss and the identification of poor underlying cardiopulmonary reserve are critical in determining the urgency
and level of intervention.
Awareness of prognosis in haemoptysis may also inform management. An analysis of 1087 patients with
haemoptysis gave rise to a model-based score (using clinical characteristics such as chronic alcoholism,
pulmonary artery involvement, and radiographic patterns) for early prediction of in-hospital mortality with
haemoptysis.[22]
EMERGENCIES
Experts recommend a stepwise approach to treat massive haemoptysis:
1. Initial stabilisation
Initial priorities are assessment of the need for intubation or mechanical ventilation, and the patient's
haemodynamic stability. Attending to ABC (Airway, Breathing, and Circulation) is paramount. Coagulopathy,
thrombocytopenia, and platelet dysfunction should be identified and reversed immediately, and blood
products should be readily available.
2. Protection of the non-bleeding lung
If haemoptysis is active and unilateral, there is risk of blood spillage into the non-bleeding lung, and rapid
action should be taken to protect the non-bleeding lung. The patient may be placed in a lateral decubitus
position with the bleeding lung downward in a dependent position. Alternatively, the non-bleeding lung may
be selectively intubated with the largest endotracheal tube available. A double-lumen endotracheal tube
has a very limited role in managing massive haemoptysis due to the complexity of its proper placement, the
need for significant operator experience, and the small lumen sizes, which do not allow room for therapeutic
bronchoscopy.
3. Airway intervention and control of bleeding
Once the patient has been stabilised and the non-bleeding lung has been protected, early bronchoscopy
should be performed. Airway control can be attained by flexible bronchoscopy through a large-bore
endotracheal tube or through the barrel of a rigid bronchoscope. Rigid bronchoscopy is a safe, effective
way of securing the airway with therapeutic control of bleeding.[6] [23] [24] [25] An endobronchial blocker or
Fogarty balloon may be placed into the bleeding bronchus for tamponade of the bleeding site.
Bronchial arteriography with embolisation of the source of bleeding can be used as a diagnostic and
therapeutic intervention when available.[26] In cystic fibrosis, bronchial artery embolisation is effective in
controlling haemoptysis, but the recurrence rate is high.[27] [28]
4. Surgical consideration
Assessment of haemoptysis Emergencies
For patients who do not respond to embolisation or other minimally invasive techniques, surgery is the
treatment of choice. Some causes of haemoptysis, such as mitral stenosis, leaking aortic aneurysm,
iatrogenic pulmonary artery rupture, traumatic injury to the chest, tracheo-innominate fistula, focal
bronchiectasis, or aspergilloma resistant to other therapies, should be treated surgically. The thoracic
surgeon should be involved early in the care of patients with massive haemoptysis, and a multi-disciplinary
approach is needed to optimise the outcome.[29]
5. Other
Bridging therapies with potential to reduce bleeding time and severity include nebulised or bronchoscopic
tranexamic acid, bronchoscopic fibrinogen-thrombin injection, and tissue glue.[30] [31] [32] [33] [34] [35]
EMERGENCIES
9
Assessment of haemoptysis Diagnosis
Step-by-step diagnostic approach

Haemoptysis has variously been defined as anything from a small amount of blood-streaked sputum through
to massive bleeding with life-threatening consequences due to airway obstruction and haemodynamic
instability.[4] [6] [18] [36] [37] [38] [39] Although arbitrary and variable in the literature, the following definitions
allow haemoptysis to be clinically characterised by the volume of expectorated blood:
• Mild haemoptysis: <30 mL over 24 hours

• Frank or moderate haemoptysis: ≥30 mL and <600 mL over 24 hours
• Massive haemoptysis: 600 mL or more over 24 hours.
Pathophysiologically, it is intuitive to consider >150 mL haemoptysis as life-threatening, as this volume of

blood could flood the conducting airways completely (i.e., fill the anatomic dead space to the level of gas-
exchanging lung units). It is important to distinguish between haemoptysis and massive haemoptysis, as the
differential diagnosis is narrower for the latter, and therapeutic urgency is greater.
The initial diagnostic assessment should aim to:
• Differentiate between haematemesis (the vomiting of blood), pseudohaemoptysis (the coughing of

blood from a source other than the lower respiratory tract), and haemoptysis
• Identify the site of bleeding
• Narrow the differential diagnosis.
History and physical examination

A detailed history and physical examination can help to rule out haematemesis or pseudo-haemoptysis,
and may provide clues to the site and cause of the haemoptysis. Pseudohaemoptysis can occur when
haematemesis is aspirated into the lungs, or when bleeding from the nasopharynx, sinuses, or oral cavity
stimulates a cough reflex.[5] Other rare causes of pseudohaemoptysis include pneumonia due to Serratia
marcescens producing a red-pigmented sputum, or sputum pigmentation due to rifampicin use.[40]
DIAGNOSIS
Characteristically, haemoptysis tends to be indicated by bright red, frothy sputum that is alkaline and with
an oxygen saturation (SaO₂) similar to peripheral arterial saturation. Blood from gastrointestinal sources
tends to be darker, may have admixed food particles, is acidic, and has an SaO₂ similar to that found in
venous blood.[5] [6] The exception is when brisk bleeding in the gastrointestinal tract overcomes the acidic
environment of the stomach.
Key features of the history include the following points.
• A history of untreated tuberculosis, lung cancer, or extrapulmonary metastatic cancer, and significant
weight loss increase the risk for haemoptysis.
• A history of smoking or of exposure to asbestos or silica confers an increased risk of lung cancer.
• A history of chronic mucopurulent sputum production with chronic lung disease is suggestive of
bronchiectasis.
• A history of exertion, orthopnoea, or paroxysmal nocturnal dyspnoea suggests the presence of
congestive heart failure or mitral stenosis.
• Detailed medication history: the use of anticoagulation therapy may indicate coagulopathy. A
history of deep venous thrombosis, pulmonary embolism, or hypercoagulable state with inadequate
anticoagulation suggests the possibility of pulmonary embolism as the source of haemoptysis.
• Travel history to endemic areas: this may point to potential endemic sources of lung infection, such
as: histoplasmosis in the Midwest river valleys of the US; coccidioidomycosis in the southwestern US;
paragonimiasis in East Asia; or schistosomiasis in the tropics of South America, Africa, and the Far
East.
Physical findings are uncommon but may help to establish the cause of haemoptysis.
• The presence of ecchymoses and/or petechiae suggests haematological diseases.

• The presence of clubbing may be associated with non-small-cell bronchogenic carcinoma,
bronchiectasis, and chronic lung abscess.
• A unilateral wheeze may be heard in cases of bronchial adenoma or endobronchial carcinomas that
block the laminar flow of air.
• The presence of a diastolic rumble, with an opening snap, loud S1, and loud P2 in the precordial
examination, suggest the presence of mitral stenosis.
• Other systemic findings such as arthralgias, synovitis, and/or nose deformity are clues
to rheumatological causes such as granulomatosis with polyangiitis (formerly Wegener's
granulomatosis).
Chest x-ray and chest computed tomography scan

After a careful history and examination, a chest x-ray (CXR) should be obtained. This has been shown to
localise the site of bleeding in 47% of patients.[41] It may also provide clues to any specific entity that may
be responsible for haemoptysis, including tuberculosis, malignancy, bronchiectasis, aspergilloma, and lung
abscess.
Aspiration of blood into the contralateral lung can cause the CXR to be misleading in determining the side of
bleeding.[42] In addition, some causes of haemoptysis may not produce changes on a CXR; these include
bronchitis, mild bronchiectasis, small areas of infection, angioma, infarction, aortopulmonary fistula, or an
endobronchial lesion that is not large enough to cause bronchial occlusion.[6] [43]
If diagnosis remains unclear, further imaging with a chest computed tomography (CT) scan is indicated.[44]
DIAGNOSIS
The American College of Radiology recommends the use of CT chest with contrast for optimal enhancement
of the systemic arterial circulation most commonly implicated in haemoptysis.[44]
If pulmonary embolism is suspected due to acute shortness of breath with or without pleuritic chest pain, a
chest CT angiogram or a ventilation/perfusion (V/Q) scan is indicated.
Bronchoscopy
If the history, exam, and chest imaging do not identify a clear cause for the haemoptysis, bronchoscopy is
indicated. Bronchogenic carcinoma is found in 9.6% of patients with haemoptysis with normal CXR.[45]
The flexible bronchoscope is the instrument of choice for evaluating non-massive haemoptysis, as flexible
bronchoscopy (FB) can be performed in the outpatient setting, or at the bedside under moderate sedation.
FB allows for sub-segmental visualisation of the airways, including the upper lobe orifices.[12] To identify
the bleeding site, FB is the most accurate method during active bleeding, with a success rate of 86%, and
is widely recognised as the study of choice.[46] [47] [48] It can also be used as a therapeutic tool to block
the bleeding site, and to introduce mechanical or thermal tools to treat it.[24] Although identification of the
bleeding bronchopulmonary segment cannot be achieved in every patient, the yield can be increased by
examining and performing diagnostic washing in every bronchial orifice. Sometimes, a bleeding tumour can
11
be identified in the sub-segmental bronchus. All abnormalities must be appropriately biopsied, brushed,
or lavaged for adequate specimens when possible. The bronchoscopist should pay special attention and
document vascular capillaries, bronchial inflammation, and subtle mucosal abnormalities.
[Fig-1]
Available studies show a higher success rate when bronchoscopy is carried out early.[46] [49] [50]
Identification of the bleeding site allows the clinician to focus on appropriate treatment. The flexible
bronchoscope can be used to evacuate clots from the airway, obtain diagnostic sampling, and deliver local
heat- or cold-based therapy.
The use of a rigid rather than a flexible bronchoscope in massive haemoptysis is debated. The choice
is mostly driven by the experience of the operator and the clinical scenario. The advantages of the rigid
bronchoscope (airway control, larger lumen, the opportunity to use larger instruments, and suction capability)
may be offset by the disadvantages (need for an available operating theatre, general anaesthesia, and
reduced reach into distal airways).[23]
Flexible bronchoscopy and rigid bronchoscopy are considered to be complementary techniques by many
experts.[12] [24] [51]
Other imaging techniques

Bronchial arteriography can be used as a diagnostic and therapeutic intervention if available. This technique
involves injecting radiocontrast dye into the thoracic aorta to visualise and localise the major systemic
arteries to the lung, often guided by localisation of the bleeding source on bronchoscopy. Once the feeding
vessels are localised, selective bronchial arteriography can be performed and abnormal vessels identified.
Abnormalities may include dilation, tortuosity, hypervascularity, and contrast extravasation. Once the
bleeding source is identified, an embolising agent (e.g., polyvinyl alcohol particles, gelfoam, dextran
microspheres, or metal coils) can be injected. A post-embolisation arteriogram is performed to ensure
complete blockage of the bleeding vessel. The success rates reported with bronchial arteriography range
from 60% to 95%, with a recurrence rate of 13% to 43%.[26] [28] [52] [53] [54] [55] [56] [57] [58] [59] [60]
Angiography has been compared with flexible bronchoscopy (FB) for the diagnosis of the bleeding
DIAGNOSIS
site in haemoptysis.[50] FB appeared to have a higher diagnostic yield (particularly when performed
early), but angiography was able to identify the bleeding site in 2 out of 8 patients with non-diagnostic
bronchoscopies.[50]
CT angiography is useful for identifying airway and parenchymal disease and vascular anatomy and
anomalies. In patients presenting with haemoptysis, it has been shown to provide new diagnostic information
in 47%, to clarify abnormalities in 15%, and to localise the site of bleeding in 88%.[42] With the use of
iterative model reconstruction and ECG-synchronised prospective-triggered technology in multi-detector-
row CT angiography, the bronchial anatomy can be depicted in patients with haemoptysis.[61] In patients
with haemoptysis of unknown source and a normal CXR, such CT technology may help identify the possible
source of bleeding. The 3-dimensional volume rendering reconstruction allows a virtual trip down the
airways and may facilitate the bronchoscopic procedure.[62] This technology, while interesting, is not
universally available and its role in the work-up of patients with haemoptysis remains unclear. From a
practical standpoint, CT angiography should be the CT of choice in the initial work-up of patients presenting
with haemoptysis, a non-diagnostic CXR, and clinically suspected pulmonary thromboembolic disease. If
pulmonary thromboembolism is ruled out, information gleaned from the CT angiogram is usually adequate
to map the way for bronchoscopy and for subsequent bronchial artery embolisation, should the latter
become necessary. In most cases, identifying a bronchial artery source of haemoptysis is most useful in
guiding therapy, which usually means embolisation of the vessel. Virtual bronchoscopy and CT angiogram,
despite the high quality of image renderings, still require conventional bronchial angiography for therapeutic
purposes.
Urgent bronchoscopy in an unstable patient facilitates the introduction of a balloon-tip catheter into the
bleeding bronchus to tamponade the haemorrhagic site, thereby protecting the non-bleeding lung from
aspiration.[63]
Laboratory assessment
The laboratory assessment should be focused towards the suspected diagnosis.
• Full blood count may help to identify infection, chronic blood loss, or a haematological disorder (e.g.,
leukaemia).
• Coagulation studies may suggest treatable coagulopathies that facilitate the occurrence of
haemoptysis.
• Arterial blood gases are indicated, particularly when haemoptysis is severe or there is concern about
respiratory failure.
• Uraemia should be considered as a factor contributing to haemoptysis due to the adverse effect of
uraemia on platelet aggregation.
• Urinalysis may help identify a pulmonary-renal syndrome or vasculitis. If there is clinical suspicion for
a pulmonary-renal syndrome, an anti-glomerular basement membrane antibody test, anti-neutrophil
cytoplasmic antibody test, and/or renal biopsy should be considered.
• Sputum and serum studies should be obtained if an infectious cause is suspected. If there is
suspicion for granulomatous or cavitary lung infection, sputum collection for acid-fast bacilli and
fungal cultures should be obtained. If endemic fungal infection (e.g., histoplasmosis, blastomycosis,
coccidioidomycosis) is suspected, fungal serologies should be obtained.
ECG and echocardiogram
DIAGNOSIS
If a cardiac cause of haemoptysis is suspected, an ECG and echocardiogram can help to identify the
presence of pulmonary hypertension, left ventricular failure, endocarditis, mitral stenosis, or ischaemic heart
disease.
[VIDEO: How to perform an ECG animated demonstration ]
Predictors of mortality
Retrospective data indicate that mechanical ventilation at the time of referral, cancer, aspergillosis, chronic
alcoholism, pulmonary artery involvement, and infiltrates involving two quadrants or more on admission are
independent predictors of increased mortality among in-hospital patients with haemoptysis.[22]
13
Differential diagnosis overview
Common
Acute/chronic bronchitis
Pulmonary tuberculosis
Lung abscess
Pneumonia
Primary lung cancer
Lung metastasis
Anticoagulants, thrombolytic agents
Toxic inhalation
Bronchiectasis
Pulmonary thromboembolism
Mitral valve stenosis
Left ventricular failure

DIAGNOSIS
Coagulopathy
Thrombocytopenia
Disseminated intravascular coagulation
Uncommon
Aspergilloma
Endobronchial carcinoid
Aspiration of foreign body
Aspiration of gastric contents
Broncholithiasis
Uncommon
Tracheo-oesophageal fistula
Bronchial telangiectasia
Airway trauma
Dieulafoy's disease
Thoracic endometriosis
Pulmonary artery aneurysm
Fat embolism
Tumour thromboembolism
Arteriovenous malformation
Pulmonary haemorrhagic syndromes
Granulomatosis with polyangiitis (formerly Wegener's granulomatosis)
Systemic vasculitis
Congenital heart disease
Tricuspid endocarditis
DIAGNOSIS
Bronchogenic cyst
Factitious haemoptysis
15
Differential diagnosis
Common
◊ Acute/chronic bronchitis
History Exam 1st Test Other tests
frequent cough with may be normal, cough »chest x-ray: normal »bronchoscopy:
excessive mucus with variable degrees or faint diffuse infiltrates non-diagnostic, or
production; chest of haemoptysis, normal small amount of blood
»sputum culture:
pressure or pain; to mildly elevated in airways, signs of
bacteria most
triggers include tobacco temperature, rhonchi, often recovered: chronic inflammation
smoke, cannabis, air expiratory wheezing In minor haemoptysis,
Haemophilus
pollutants, and various bronchoscopy may not
influenzae ,
infectious agents Streptococcus be needed if the chest
pneumoniae ,
x-ray is normal, and
Moraxella catarrhalis
, less commonly a history of acute or
Bordetella pertussis ; chronic bronchitis can
viral agents: respiratory be elicited.
syncytial virus,
rhinovirus, echovirus, Diagnosis of bronchitis
parainfluenza, herpes
is clinical.
virus, Coxsackie virus,
influenza, coronavirus,
adenovirus
Viral agents are
the most common
infectious causes of
acute bronchitis.
DIAGNOSIS
This is not an initial test

in patients with chronic
bronchitis.
history of travel to cachexia, fever, »chest x-ray: primary »bronchoscopy:

endemic areas, lymphadenopathy, TB: paratracheal and localised gelatinous
exposure to people with rales, consolidation, hilar lymphadenopathy, granulation tissue; red
tuberculosis (TB), risk decreased breath segmental or lobar mucosa, nodular or
factors for HIV, history sounds if pleural consolidation, pleural ulcerated mucosa
of incarceration or effusion is present effusions (mostly External compression
homelessness; cough, unilateral); postprimary from lymph nodes or
dyspnoea, weight loss, TB: upper lobe
fever, joint aches, night infiltrates, cavitation, mucosal erosion can be
sweats bronchogenic nodules, seen.
pleural effusions,
Common

fibrotic changes, or Tuberculous stenosis is
miliary pattern a common complication
Active cavitary and
of endobronchial TB,
non-cavitary TB can
occurring in 10%
cause haemoptysis.
to 37% of patients
»contrast-enhanced with TB who undergo
chest computed bronchoscopy.[64] [65]
tomography [66]
scan: primary TB:
mediastinal tuberculous Absence of
lymphadenitis
with central endobronchial findings
node attenuation does not affect the
and peripheral probability of TB
enhancement, infection.
delineated cavities;
postprimary TB: »interferon-gamma
centrilobular nodules release assay:
and tree-in-bud pattern positive
Bronchiectasis can Interferon-gamma
be seen in chronic release assay (IGRA)
cases. Haemoptysis is based on the
usually originates from amount of interferon-
bronchial arteries, gamma released by
but Rasmussen's the patient’s WBC
aneurysms from a in response to TB
DIAGNOSIS
pulmonary artery antigens. This test
adjacent to a cavity is used increasingly
can be the source of in the US in patients
bleeding. with prior vaccination
with Bacillus Calmette-
Residual bronchiectasis
Guérin (BCG) vaccine
from old TB can cause
or those unlikely to
haemoptysis.
return for purified
»sputum acid-fast protein derivative (PPD)
bacilli stain and interpretation.
cultures: positive for
acid-fast bacilli PPD and IGR assays
are useful for identifying
M tuberculosis
infection but cannot be
used alone to diagnose
active disease.
17
Common

»purified protein
derivative: positive
skin test
In the US, a result of
≥5 mm of induration
is considered a
positive test in high-
risk populations; ≥10
mm in individuals at risk
of exposure; ≥15 m in
presumed healthy, non-
exposed individuals.
A positive test only

determines exposure
to tuberculosis. This
should be interpreted
in the context of
the overall clinical
picture, including local
epidemiology, potential
exposures, immune
system status, and
prior exposure to BCG
DIAGNOSIS
vaccine.
This is not an initial test

in BCG-using countries.
PPD and interferon-

gamma release assays
are useful for identifying
M tuberculosis
infection but cannot be
used alone to diagnose
active disease.
◊ Lung abscess
high fever (>38.5°C fever, cardiac murmur, »FBC: leukocytosis, »contrast-enhanced

[>101°F]), productive signs of gingival anaemia chest CT scan: thick-
Common
◊ Lung abscess

cough, purulent disease, cachexia, »chest x-ray: walled, usually round
sputum, weight loss, halitosis, amphoric consolidation with cavity with irregular
malaise, fever, night or cavernous breath central cavitation and margins forming an
sweats, alcoholism, risk sounds, inspiratory air-fluid level, cavity wall acute angle with
factors for aspiration; crackles and/or thick and irregular chest wall, no signs
massive haemoptysis bronchial breathing, of compression of
»sputum Gram
may occur with chronic decreased breath surrounding lung
stain: one predominant
abscesses sounds; nail clubbing Useful for evaluating
gram-positive or -
may occur with chronic endobronchial
negative organism and
abscesses neutrophils in aerobic obstruction as a cause
infections; mixed flora
of abscess.
with many neutrophils
in anaerobic infections
»sputum culture:
often only see growth
of normal respiratory
flora in polymicrobial
anaerobic infections;
growth of infecting
organism in aerobic
infections
»blood culture:
positive for infecting
organism in aerobic
infections, bacteraemia,
and septic embolism;
seldom positive in
anaerobic infections
DIAGNOSIS
◊ Pneumonia
fever, cough, dyspnoea, dullness to percussion, »chest x-ray: lobar or

chest pain, malaise fever, unilateral rales, segmental infiltrates
hypoxaemia Radiographic
presentations of
common aetiological
agents are focal
(pleural effusion,
usually bacterial), cavity
(bacterial abscess,
fungal, acid-fast
bacilli, Nocardia ),
rapid progression/
multifocal ( Legionella
19
Common
◊ Pneumonia

, pneumococcal,
staphylococcal), and
interstitial (viral,
Pneumocystis ,
Mycoplasma ,
Chlamydia psittaci ).
»sputum Gram
stain: visualisation of
suspected infecting
organisms such as
gram-negative rods,
gram-positive cocci
»sputum culture:
growth of infecting
organism
»blood culture: may
be positive for infecting
organism
Primary lung cancer
new cough, dyspnoea clubbing, focal »chest x-ray: »PET-

(worse at night or in wheezing, diminished may be normal or fluorodeox yglucose
DIAGNOSIS
recumbent position), breath sounds in show segmental scan: positive

chest pain, weight loss, pleural effusion or atelectasis, lobar uptake of 18-
occurrence of para- central obstruction collapse, obstructive fluorodeoxyglucose
neoplastic syndrome pneumonitis, pleural (FDG) in metabolically
effusion active nodules
Tracheal tumours are Uptake of FDG
seen on standard indicates metabolically
radiographs in 23% to active disease.
45% of cases. This can occur
[Fig-3] with malignancy
or in the setting of
»chest CT scan: from
active infection or
solitary lung nodule
to endobronchial inflammatory lung
obstruction with diseases.
atelectatic lobe or
lung, mediastinal/hilar False-positive
lymphadenopathy, and/ tests may occur
or pleural effusion
with infectious
or inflammatory
Common
Primary lung cancer

»bronchoscopy: granulomas. False
vascular lesions: negatives may occur
may obstruct airways
distal to tumour, subtle with sub-solid nodules
granular appearance, and carcinoids.
or erythematous
mucosa; polypoid or
papillary infiltrative with
superficial erosions
Airway tumours tend
to necrose when they
outgrow their vascular
supply. Deeper biopsies
should be done in these
cases.
Lung metastasis
symptoms related to clubbing, focal »chest CT scan: one »PET-

the primary neoplastic wheezing or multiple nodules of fluorodeox yglucose
site, pain, weight variable sizes, from scan: increased uptake
loss, malaise, cough, diffuse micronodular in pulmonary nodules
dyspnoea shadows (miliary) to and at primary site
well-defined masses, In metastatic disease,
DIAGNOSIS
often irregular, often a PET scan aids in
in the periphery of
the lower lung zones, the identification of the
sometimes with primary site, and allows
cavitation; may see for appropriate staging
lymphadenopathy whenever malignancy
A search for the
is confirmed.
primary site should
be performed. It may »bronchoscopy with
include abdominal biopsy: positive for
malignant cells
and pelvic CT scans
The accurate sampling
accompanied by
of a nodule depends
imaging of the brain
on the location and
with CT scanning or
size of the nodule,
MRI. Extrapulmonary
presence of bronchus
cancers that
sign (e.g., a bronchus
metastasise to the lung
leading directly to a
include melanoma,
peripheral pulmonary
sarcomas, and
21
Common
Lung metastasis

adenocarcinoma of the lesion visible on CT),
colon, breast, kidney, or and local expertise
testicle. and availability of
fluoroscopy.
Endobronchial
lesions may occur
as metastases of
a wide variety of
cancers, including
renal cell carcinoma,
thyroid carcinoma,
oesophageal cancer,
ovarian cancer,
melanoma, breast
cancer, colorectal
cancer, and sarcomas.
Bronchoscopy has
a very high yield for
endobronchial lesions.
[Fig-4]
[Fig-5]
DIAGNOSIS
»sputum cytology:
positive for malignant
cells
Yield is higher in large
endobronchial lesions
or large masses.
exposure to ecchymosis, petechiae, »INR: may be »bronchoscopy:

anticoagulants, may be normal prolonged bleeding
antiplatelet therapy, The metabolism of Endobronchial signs of
thrombolytic agents the specific drug coagulopathy.
will determine the [Fig-6]
appropriate test and its
effect in the coagulation
cascade.
Common

»PTT: may be
prolonged
The metabolism of
the specific drug
will determine the
appropriate test and its
effect in the coagulation
cascade.
Toxic inhalation
exposure to smoke may be normal, cough »chest x-ray: »bronchoscopy:

inhalation, solvents, with variable degrees of atelectasis; airspace bleeding
trimellitic anhydride haemoptysis opacity Sloughing of mucosal
»ABG with surfaces, soot in
carbox yhaemoglobin airways.
(CO-Hg) level: severe
metabolic acidosis; CO-
Hg level >15%
»pulse oximetry:
hypoxaemia
»ECG: arrhythmias,
ischaemia
DIAGNOSIS
◊ Bronchiectasis
frequent cough with cough almost »chest x-ray: »bronchoscopy:

excessive mucus always present, with increased number small amount of blood
production and little variable degrees of of bronchovascular in airways, signs of
seasonal variation, haemoptysis, crackles, markings, crowding of chronic inflammation
dyspnoea, pleurisy, wheezing, clubbing bronchi, cystic spaces, Bronchoscopy is useful
fatigue, weight loss; linear shadows ('tram in identifying the site of
history of cystic fibrosis, tracking')
alpha-1 antitrypsin bleeding, and micro-
Abnormal in 87% of
deficiency, underlying organisms infecting or
cases but usually non-
immunodeficiency colonising the airway.
specific.
»chest CT scan: Bronchoalveolar lavage

dilated bronchi with or washings may isolate
thickened walls micro-organisms.
extending to the lung
23
Common
◊ Bronchiectasis

periphery; bronchial »spirometry:
diameter larger obstructive physiology
than accompanying with decrease in FEV1/
pulmonary artery, FVC ratio below normal
creating 'signet limit
ring' appearance,
endobronchial mucus
impaction
CT scan has sensitivity
of 97% and specificity
of 93% to 100%
for the diagnosis of
bronchiectasis.
»sputum culture:
pathogens most
often recovered:
Pseudomonas
, Haemophilus
influenzae ,
Streptococcus
pneumoniae ,
Moraxella catarrhalis ,
Mycobacterium avium
, Aspergillus , viral
pathogens
DIAGNOSIS
dyspnoea, pleuritic tachycardia, unilateral »chest x-ray: non- »ventilation-

chest pain, syncope lower-extremity specific parenchymal perfusion (V/Q)
oedema, split S2 with infiltrates, atelectasis, radionuclide scan:
loud P2, diaphoresis, hemidiaphragm pulmonary embolism
tachypnoea elevation, pleural likely when an area
effusion of ventilation is not
CXR may be normal. perfused; a negative
V/Q scan effectively
Decreased vascularity excludes pulmonary
embolism
in one lung
V/Q scan is a radiation-
(Westermark's sign)
and medium-sparing
causing unilateral
procedure and may be
lucency has been
appropriate for patients
described.
with contraindications
or relative
Common

Prominence of a central contraindications to CT
pulmonary artery (e.g., contrast allergy,
or a wedge-shaped moderate to severe
peripheral infiltrate renal failure, pregnancy,
(Hampton's hump) may young patients).[67]
be seen.
A large central
pulmonary artery
with abrupt tapering
(Fleischner sign) may
also be observed.
Atelectasis and pleural

effusions are common
but non-specific.
»chest CT
angiogram: low-
attenuation filling
defects within a well-
opacified pulmonary
artery, clot, vessel cut-
off, rim sign
Use of intravenous
contrast with a
DIAGNOSIS
pulmonary embolism
protocol is necessary
to reliably identify
pulmonary embolism.
Indirect findings include

pulmonary infarct,
large pulmonary
artery, pleural effusion,
atelectasis, and mosaic
attenuation.
»D-dimer: positive
A negative test in a low-
probability case has
a very high negative
predictive value,
thus ruling out deep
25
Common

venous thrombosis and
pulmonary embolism as
the cause.
A high pre-test
probability or a positive
result requires further
work-up with imaging
techniques.
Due to the non-specific

nature of the assay, the
D-dimer should be used
only in low-probability
settings, as many
other conditions (e.g.,
surgery, malignancy,
active infection,
vascular disease,
trauma) increase the D-
dimer level.

DIAGNOSIS
chronic dyspnoea, reduced pulse »chest x-ray: dilated

dyspnoea on pressure, elevated left atrium, variable
exertion, orthopnoea, jugular venous cardiomegaly, calcified
paroxysmal nocturnal distension, plethoric mitral valve, increased
dyspnoea, palpitations; cheeks, right ventricular interstitial markings with
may become clinically lift, atrial fibrillation, Kerley-B lines
apparent with diastolic rumble, »ECG: atrial fibrillation
pregnancy-induced opening snap, loud S1, with right ventricular
haemodynamic loud P2, hoarseness hypertrophy, left atrial
changes; history of (recurrent laryngeal enlargement with
recurrent respiratory nerve impingement by long P wave (>120
infections (group the left atrium) milliseconds), broad
A haemolytic notched P waves in
streptococci) during lead II
childhood, rheumatic
fever, rheumatic »transthoracic
heart disease, living echocardiogram:
in endemic areas leaflet thickening,
for mitral stenosis, commissural fusion,
Common

atherosclerotic heart chordal shortening,
disease, and/or mitral chordal fusion
annular calcification
history of hypertension, neck vein distension, »transthoracic

diabetes mellitus, hepatojugular reflux, echocardiogram:
dyslipidaemia, rales, S3 gallop, systolic heart failure:
or tobacco use; cardiomegaly, depressed and
coronary, valvular, or tachycardia dilated left and/or
peripheral vascular right ventricle with
disease; dyspnoea, low ejection fraction;
palpitations, chest diastolic heart failure:
discomfort, orthopnoea, left ventricular ejection
paroxysmal nocturnal fraction normal but left
dyspnoea, fatigue ventricular hypertrophy
and abnormal diastolic
filling patterns
»ECG: evidence of
previous infarct, left
ventricular hypertrophy,
or atrial enlargement;
may be conduction
abnormalities and
DIAGNOSIS
abnormal QRS duration
»chest x-ray:
cardiomegaly,
pulmonary vascular
congestion, Kerley B
lines, pleural effusions
»serum electrolytes
(including calcium
and magnesium):
decreased sodium
(usually <135 mmol/L
[<135 mg/dL]), altered
potassium
»Urea and
creatinine: normal to
elevated
»blood glucose:
elevated in diabetes
»LFTs: normal to
elevated
27
Common

»thyroid function
tests: hypothyroidism:
elevated thyroid-
stimulating hormone
(TSH), decreased
free triiodothyronine
(FT3), decreased
free thyroxine (FT4);
hyperthyroidism:
decreased TSH,
elevated FT4
»blood lipids:
elevated in
dyslipidaemia,
decreased in end-stage
heart failure, especially
in the presence of
cardiac cachexia
»B-type natriuretic
peptide (BNP)/N-
terminal pro BNP
levels: elevated
Coagulopathy

DIAGNOSIS
association with petechiae, »INR and PTT: »specific

advanced liver and small capillary elevated coagulation factor
kidney disease, haemorrhages, deficiency: decreased
»urea and
haematological ecchymoses, or absent
creatinine: elevated
malignancy, haematomas, »thrombin time:
recent cytotoxic haemarthrosis elevated
chemotherapy,
specific disorders of
coagulation cascade
(factor deficiency);
menorrhagia
Thrombocytopenia
may present with purpura, mucosal »peripheral blood »LFTs: may be

purpura or be bleeding, epistaxis, smear: thrombotic normal; may be
associated with signs of liver disease microangiopathy elevated aspartate
gestation, HIV, (schistocytes) aminotransferase/
liver disease, alanine
Common
Thrombocytopenia

myelodysplastic »FBC with aminotransferase/
syndrome; may be differential: low bilirubin and/or
drug-induced platelet count decreased synthetic
Repeat platelet count function (albumin)
in order to rule out »lactate
pseudothrombocytopenia. dehydrogenase:
elevated in haemolysis
»haptoglobin: low
level with haemolysis
»INR/PTT: elevated
in disseminated
intravascular
coagulation
»fibrinogen: low
in disseminated
intravascular
coagulation
»D-dimer: elevated
in disseminated
intravascular
coagulation
Disseminated intravascular coagulation
DIAGNOSIS
fever, cough, dyspnoea, petechiae, »FBC with
confusion, epistaxis, gastrointestinal or differential:
bleeding gums; genitourinary tract pancytopenia
possible history of bleeding, hypotension, »peripheral blood
sepsis, obstetric tachycardia, pleural smear: thrombotic
complications friction rub microangiopathy
such as placental (schistocytes)
abruption, snake bite,
malignancy (e.g., »serum INR and
acute promyelocytic activated PTT:
leukaemia), or tissue elevated
trauma (e.g., surgery) »serum fibrinogen:
low
»D-dimer: elevated
29
Uncommon
Aspergilloma
mostly asymptomatic, cough, variable »chest x-ray:

commonly secondary to haemoptysis upper lobe mobile
underlying chronic lung intracavitary mass with
disease; weight loss, an air crescent in the
chronic cough, malaise periphery
»high-resolution
chest CT scan: upper
lobe cavitary mass with
intracavitary contents
and adjacent pleural
thickening
A CT scan provides a
better yield than a CXR.
[Fig-2]
◊ Endobronchial carcinoid
asymptomatic; often normal »chest x-ray: may

may cause cough, examination, unilateral be normal or show
dyspnoea, wheezing if wheezing may be segmental atelectasis,
nodule is endobronchial present lobar collapse,
obstructive pneumonitis
»chest CT scan:
solitary lung nodule,
DIAGNOSIS
endobronchial nodule,
parenchymal nodule
Approximately 20%
present as solitary
lung nodules. May
cause post-obstructive
pneumonia.
About 80% of lung

cancers appear as an
endobronchial nodule,
20% as a parenchymal
nodule, with smooth
borders, rounded, and
highly vascularised.
Less than 10% are
calcified.
Uncommon
◊ Endobronchial carcinoid

»bronchoscopy
with biopsy: raised,
pinkish, vascular,
lobulated lesions;
biopsy positive for
malignant cells
Endobronchial biopsy
is usually required to
differentiate from small-
cell carcinoma.
Despite risk of
bleeding, endobronchial
biopsies are indicated.
may be asymptomatic, focal wheezing, choking »chest x-ray: »chest CT scan:

cough paroxysms, crisis, focal decrease in atelectasis, pulmonary associated air trapping,
localised wheezing, breath sounds infiltrates atelectasis
choking crisis; most Only a small In cases where
common in children percentage of foreign aspiration occurred
<15 years of age;
associated with alcohol bodies are radiopaque. months or years
DIAGNOSIS
abuse, sedative previously,
use, poor dentition, Aspiration may have bronchial stenosis,
neurological disease, occurred many years bronchiectasis, or an
loss of consciousness, previously. Comparison
seizure in older adults endobronchial mass or
with old films is key. granulation tissue can
Suspect foreign be seen.
body aspiration in
cases of recurrent
focal pneumonias.
Occasionally expiratory
films show air trapping
that can be missed on
inspiratory films.
»bronchoscopy:
chronic foreign body
usually covered with
mucus and granulation
tissue
31
Uncommon

Findings depend on the
characteristics of the
object and chronicity of
the aspiration.
Flexible and rigid

bronchoscopes are
complementary tools.
The choice depends
on the operator's
expertise, size of the
object, age of the
patient, and clinical
presentation.
[Fig-7]
◊ Aspiration of gastric contents
history of GORD, age fever, crackles, »chest x-ray: patchy »chest CT scan:
>70 years, male sex, wheezing, dyspnoea airspace consolidations opacities in dependent
general anaesthesia, segments
cerebrovascular Chest CT scan
DIAGNOSIS
disease; fever, delineates the location

intractable cough,
dyspnoea, alcohol of the lobar and
misuse segmental opacities.
In advanced cases,
the findings may be
indistinguishable
from those of acute
respiratory distress
syndrome.
Necrosis, cavity
formation, and
empyema are potential
complications of
aspiration that are
visualised better with
Uncommon
◊ Aspiration of gastric contents

CT than with plain
chest x-ray.
◊ Broncholithiasis
chronic cough, rarely wheezing due to »chest CT scan: »bronchoscopy:

occasional chest pain, airway obstruction calcified mediastinal splayed or irregular
may be asymptomatic, adenopathy or carinas
history of recurrent bronchial obstruction When broncholith
pneumonias in same erodes into the airway,
location
it can be seen as an
irregular hard white-
grey stone, which
may partially or totally
obstruct the airway.
◊ Tracheo-oesophageal fistula
feeding difficulties, laboured breathing, »chest x-ray: »bronchoscopy:

recurrent aspiration coughing, choking, mediastinal air, gas- presence of a fistula
DIAGNOSIS
pneumonia, cough and cyanosis are non- filled gastrointestinal
specific findings tract, dependent
infiltrates; insertion
of a nasogastric tube
may show coiling in the
upper pouch
»upper
gastrointestinal
series: spilling of
contrast into the
trachea
Thickened water-
soluble contrast should
be used.
33
Uncommon
◊ Bronchial telangiectasia
sometimes associated mucocutaneous »CT angiography: »bronchoscopy: non-

with hereditary telangiectasia, presence of specific network of
haemorrhagic pulmonary bruit, arteriovenous submucosal dilated
telangiectasia, stigmata of right-to- malformations vessels
recurrent epistaxis left shunting such as
cyanosis and clubbing
◊ Airway trauma
recent history of high- tachypnoea, wheezing, »chest x-ray: »bronchoscopy:

velocity accident, blunt chest or neck pain; presence of widened distal haemorrhage,
trauma to neck or external signs may mediastinum pulmonary contusion,
chest, or exposure or may not indicate This is a non-specific aspirated material
to explosive blast; magnitude of trauma finding but suggests Bronchoscopy serves
iatrogenic haemoptysis as a diagnostic tool,
may occur with vascular injury, rib
traumatic intubation, fractures, or patchy but it may also help to
bronchoscopy, infiltrates. secure the airway by
and endobronchial guiding endotracheal
therapeutic »chest CT scan: intubation. The trans-
manoeuvres fractures, haematomas,
oral route is preferred.
patchy or diffuse
infiltrates in the lung
parenchyma that do not
conform to segmental
DIAGNOSIS
or lobar anatomy
◊ Dieulafoy's disease
congenital origin; Dieulafoy's disease is »bronchoscopy:

history of comorbidities: a vascular anomaly arterial bleeding in
cardiovascular disease, characterised by the area of ulcer or nodule;
hypertension, chronic presence of a tortuous raised nipple or visible
renal failure, diabetes, dysplastic artery vessel without an ulcer,
or alcohol abuse in the submucosa; in absence of bleeding
cases involving a sub- »endoscopy: arterial
epithelial bronchial bleeding in area of
artery have caused ulcer or nodule; raised
haemoptysis; most nipple or visible vessel
cases involve the without an ulcer, in
gastrointestinal tract absence of bleeding
Uncommon
◊ Thoracic endometriosis
catamenial symptoms no physical findings; »no test required: »chest CT scan: may
(within 24-48 pelvic tenderness, cul- diagnosis is clinical be negative; pulmonary
hours of onset of de-sac nodularity may or pleural nodules seen
menstruation); may be present during menses
have dysmenorrhoea,
dyspareunia; chest
pain, shortness of
breath
◊ Pulmonary artery aneurysm
congenital or related non-specific; chest pain »CT angiography:

to pulmonary artery may be present presence of pulmonary
catheter complication artery aneurysm
◊ Fat embolism
dyspnoea, fever, hypoxaemia, »no test required:

changes in mental tachypnoea, changes diagnosis is clinical
status; usually 24-72 in mental status;
hours after long-bone petechiae in the head,
fracture or liposuction neck, anterior chest,
DIAGNOSIS
and axillae
◊ Tumour thromboembolism
history of tachypnoea, »CT angiography: »ECG: right-heart

mucin-secreting hypoxaemia, diagnosis is made strain
adenocarcinomas tachycardia in conjunction with »surgery:
(breast, lung, stomach, high clinical suspicion; histopathological
colon), hepatoma, isolated vascular filling demonstration of
prostate cancer, defect may be difficult tumour cells in the
choriocarcinoma, or to distinguish from pulmonary vasculature
renal cell carcinoma blood clot
35
Uncommon
◊ Arteriovenous malformation
dyspnoea; history pulmonary bruit; »chest CT with »pulmonary

of stroke, brain arteriovenous contrast: round or oval angiography:
abscess, cirrhosis communications or nodule(s) with feeding confirms presence
(hepatopulmonary telangiectasia in skin, artery and draining and location of
syndrome); personal mucous membranes, vein; pulmonary malformations,
or family history and other organs; arteriole enlargement in identifies feeding
of hereditary cyanosis, clubbing; dependent portions of arterial and venous
haemorrhagic neurological signs from the lungs structures
telangiectasia cerebral aneurysms, Most common in lower In cases of significant
cerebral emboli, or lobes. Multiple lesions haemoptysis, a
metastatic abscess;
stigmata of advanced are seen in 30% of pulmonary angiogram
liver disease (jaundice, cases. Usually round or is combined with
small liver, ascites, skin oval. Also known as an bronchial artery
spider angiomata) arteriovenous fistula. embolisation.
Patients with multiple »transthoracic

arteriovenous contrast
echocardiography:
malformations in delayed shunting
the lung usually suggests
have arteriovenous transpulmonary
communications in the shunting
skin, mucosa, and other »radionuclide
perfusion scanning:
organs.
does not typically
define a pulmonary
Osler-Weber-Rendu
arteriovenous
DIAGNOSIS
syndrome (hereditary malformation

haemorrhagic anatomically, but can
telangiectasia) may be confirm or identify the
presence of a right-to-
considered.
left shunt
The test involves
In patients with
intravenous injection
cirrhosis with
of macroaggregated
hepatopulmonary
albumin labelled with
syndrome, pulmonary
technetium-99m. In
artery enlargement
the presence of right-
in dependent lungs
to-left shunts, the
creates intrapulmonary
radiolabelled particles
shunt.
traverse through the
lungs and become
trapped in the brain
and kidneys. The shunt
fraction is calculated
by quantifying the
Uncommon
◊ Arteriovenous malformation

renal uptake as a
percentage of the total
administered dose.
»ABG analysis:
decreased partial
pressure of oxygen,
decreased oxygen
saturation when
arteriovenous flow is
severe
In cases of severe
systemic arteriovenous
malformation, chronic
hypoxaemia may
cause polycythaemia.
However, more
commonly, epistaxis
may result in anaemia.
◊ Pulmonary haemorrhagic syndromes
cough, fever, dyspnoea; usually negative; »chest x-ray: alveolar »erythrocyte
DIAGNOSIS
history of bone marrow presence of infiltrates, usually sedimentation rate:
transplant; history leukocytoclastic patchy or diffuse usually elevated
of connective tissue vasculitis, arthritis, or »FBC: decreased »urinary sediment:
disease or vasculitis synovitis, indicative haemoglobin level may be present
of connective tissue
»bronchoscopy with If present may indicate
disease
bronchoalveolar pulmonary-renal
lavage: sequential syndrome.
lavage yields
progressively more »ANA, C-ANCA, anti-
haemorrhagic fluid; GBM, and anti-DNA
cytology shows antibodies: may be
haemosiderin-laden positive
macrophages ANA: antinuclear
antibodies.
C-ANCA: anti-
neutrophil cytoplasmic
antibodies.
37
Uncommon
◊ Pulmonary haemorrhagic syndromes

Anti-GBM: anti-
glomerular basement
membrane antibodies.
Anti-DNA: antibodies to
double-stranded DNA.
If positive may point

to the underlying
connective tissue
disease.
»pulmonary
function test with
diffusing capacity of
the lung for carbon
monoxide: usually
restrictive pattern with
elevated diffusing
capacity of the lung for
carbon monoxide
◊ Granulomatosis with polyangiitis (formerly Wegener's

granulomatosis)

DIAGNOSIS
cough, chest pain, palpable purpura, »chest CT scan: »bronchoscopy:

dyspnoea, rhinorrhoea, painful ulcers, uveitis, solitary or multiple lung presence of necrotising
epistaxis, ear/sinus wheezing, sinus nodules; airways are granulomatous
pain, hoarseness, tenderness frequently affected inflammation and pauci-
fever, fatigue, anorexia, immune vasculitis in
»anti-neutrophil
weight loss small and medium
cytoplasmic
blood vessels on biopsy
antibody: usually
positive Granulomas on
Anti-neutrophil tissue obtained by
cytoplasmic antibody bronchoscopy should
(ANCA) testing results also be stained and
depend on the extent cultured for infectious
and severity of the agents.
disease.
A positive biopsy is
Generalised strongly supportive
granulomatosis with of a diagnosis of
polyangiitis is >90% vasculitis, and biopsies
are recommended to
Uncommon
◊ Granulomatosis with polyangiitis (formerly Wegener's

granulomatosis)

cytoplasmic ANCA assist in establishing
positive. a new diagnosis and
for further evaluation
Limited granulomatosis of patients suspected
with polyangiitis is 60% of having relapsing
ANCA positive. vasculitis.[68]
»CT-guided
transthoracic
needle aspiration:
presence of necrotising
granulomatous
inflammation
Granulomas on tissue
obtained by CT-guided
transthoracic needle
aspiration should
be identified by a
pathologist and stained
for infectious agents
before a non-infectious
cause is assumed.
◊ Systemic vasculitis
DIAGNOSIS
complaints of specific organ »erythrocyte »biopsy of affected

arthralgias, myalgias, involvement, which sedimentation rate: tissue: vessel wall
malaise, fatigue for may demonstrate a >100 mm/hour necrosis, fibrinoid
several months before pattern of disease necrosis, karyorrhexis
»C-reactive protein:
more specific signs or (e.g., Churg-Strauss (destructive
elevated
symptoms develop syndrome is associated fragmentation of the
with refractory asthma) »antineutrophil nucleus of a dying
cytoplasmic cell), red blood cell
antibody: positive extravasation
»urea and Histological
creatinine: normal or examination of biopsy
elevated material is useful in
»urinalysis: confirming a diagnosis
haematuria, proteinuria,
in the context of
red blood cell casts
clinical findings and
laboratory data. A
39
Uncommon
◊ Systemic vasculitis

negative biopsy does
not necessarily exclude
disease, and a positive
biopsy does not always
indicate the presence of
disease.[69]
◊ Congenital heart disease
from asymptomatic to frothy pink sputum, »echocardiogram:

disabling symptoms: stigmata of right-to- reflects the congenital
progressive heart left shunting (cyanosis, cardiac defect
disease, dyspnoea, clubbing), heart In congenital heart
fatigue, orthopnoea, murmur disease, haemoptysis
paroxysmal nocturnal
dyspnoea can be caused by post-
capillary pulmonary
hypertension or mitral
stenosis.
◊ Tricuspid endocarditis

DIAGNOSIS
history of intravenous fever, Janeway lesions, »FBC: elevated white »urinalysis: red blood
drug use, mitral valve Osler's nodes, splinter blood cells cell casts, white blood
prolapse, or congenital haemorrhages, cardiac cell casts, proteinuria,
»blood cultures:
heart disease; fever, murmur pyuria
bacteraemia,
malaise, fatigue, chest fungaemia
pains, weakness, night
sweats, palpitations »ECG: prolonged
PR interval; non-
specific ST/T wave
abnormalities;
atrioventricular block
»echocardiogram:
mobile valvular
vegetations
Uncommon
◊ Bronchogenic cyst
usually asymptomatic asymptomatic; cough, »chest x-ray: sharply

unless infected or dyspnoea circumscribed, round or
results in airway oval opacity in medial
obstruction; incidental third of lower lobe
finding When infection occurs,
an air-fluid level may be
seen.
Slow growth can occur

over a period of years.
»chest CT scan:
non-enhancing
homogeneous
attenuation near water
density; a smooth, thin
wall; typically presents
as a cystic mediastinal
mass
If higher-than-water
density is seen,
this is related to
proteinaceous material
or calcium deposits.
◊ Factitious haemoptysis
DIAGNOSIS
frequently young absence of an »clinical history

patients, healthcare alternative aetiology on and examination:
workers; evidence of work-up diagnosis is clinical
self-inflicted wounds or with a high index of
interventions capable suspicion; tests may
of causing haemoptysis not be indicated
supports the diagnosis
41
Diagnostic guidelines
Europe
Diagnosis and treatment of hemoptysis
Published by: Spanish Society of Pneumology and Thoracic Surgery (SEPAR)

Last published: 2016
North America
Hemoptysis: evaluation and management
Published by: American Family Physician

ACR appropriateness criteria: hemoptysis
Published by: American College of Radiology

DIAGNOSIS
Assessment of haemoptysis References
Key articles
• Sakr L, Dutau H. Massive hemoptysis: an update on the role of bronchoscopy in diagnosis and
REFERENCES
management. Respiration. 2010 Jan 8;80(1):38-58. Full text Abstract
• Comforti J. Management of massive hemoptysis. In: Simoff MJ, Sterman DH, Ernst A, eds.
Thoracic endoscopy: advances in interventional pulmonology. Malden, MA: Blackwell Publishing;
2006:23:330-43.
• Shigemura N, Wan IY, Yu SC, et al. Multidisciplinary management of life-threatening massive

hemoptysis: a 10-year experience. Ann Thorac Surg. 2009 Mar;87(3):849-53. Abstract
• Miller A, Chan M, Wiik A, et al. An approach to the diagnosis and management of systemic vasculitis.
Clin Exp Immunol. 2010 Jan 12;160(2):143-60. Full text Abstract
References
1. Stoller JK. Diagnosis and management of massive hemoptysis: a review. Respir Care. 1992
Jun;37(6):564-81. Full text
2. Jones R, Charlton J, Latinovic R, et al. Alarm symptoms and identification of non-cancer diagnoses in
primary care: cohort study. BMJ. 2009 Aug 13;339:b3094. Full text Abstract
3. Sakr L, Dutau H. Massive hemoptysis: an update on the role of bronchoscopy in diagnosis and
management. Respiration. 2010 Jan 8;80(1):38-58. Full text Abstract
4. Holsclaw DS, Grand RJ, Schwachman H. Massive hemoptysis in cystic fibrosis. J Pediatr. 1970
Jun;76(6):829-38. Abstract
5. Lyons HA. Differential diagnosis of hemoptysis and its treatment. Basics Respir Dis. 1976;5:26-30.
6. Comforti J. Management of massive hemoptysis. In: Simoff MJ, Sterman DH, Ernst A, eds.
Thoracic endoscopy: advances in interventional pulmonology. Malden, MA: Blackwell Publishing;
2006:23:330-43.
7. Rabkin JE, Astafjev VI, Gothman LN, et al. Transcatheter embolization in the management of
pulmonary hemorrhage. Radiology. 1987 May;163(2):361-5. Abstract
8. Khalil A, Parrot A, Nedelcu C, et al. Severe hemoptysis of pulmonary arterial origin: signs and role of
multidetector row CT angiography. Chest. 2008 Jan;133(1):212-9. Abstract
9. Hannan AT, Brown M, Bigman O. Pulmonary artery catheter-induced hemorrhage. Chest. 1984
Jan;85(1):128-31. Abstract
43
10. Johnston H, Reisz G. Changing spectrum of hemoptysis. Underlying causes in 148 patients
undergoing diagnostic flexible fiberoptic bronchoscopy. Arch Intern Med. 1989 Jul;149(7):1666-8.
Abstract
REFERENCES
11. Santiago S, Tobias J, Williams AJ. A reappraisal of the causes of hemoptysis. Arch Intern Med. 1991
Dec;151(12):2449-51. Abstract
12. Patel SR, Stoller JK. The role of bronchoscopy in hemoptysis. In: Wang K, Mehta AC, Turner JF, eds.
Flexible bronchoscopy. 2nd ed. Malden, MA: Blackwell Publishing; 2004:210-24.
13. Liebow AA, Hales MR, Lindskog GE. Enlargement of the bronchial arteries, and their anastomoses
with the pulmonary arteries in bronchiectasis. Am J Pathol. 1949 Mar;25(2):211-31. Full text Abstract
14. Boaventura R, Shoemark A, Chalmers JD. Pathophysiology. In: Chalmers JD, Polverino E, Aliverti S,
eds. Bronchiectasis: European Respiratory Society monograph. 2018:8-28. Full text
15. Thoms NW, Wilson RF, Puro HE, et al. Life-threatening hemoptysis in primary lung abscess. Ann
Thorac Surg. 1972 Oct;14(4):347-58. Abstract
16. Jennette JC, Falk RJ. Small-vessel vasculitis. N Engl J Med. 1997 Nov 20;337(21):1512-23. Abstract
17. Lara AR, Schwarz MI. Diffuse alveolar hemorrhage. Chest. 2010 May;137(5):1164-71. Abstract
18. Amirana M, Prater R, Tirschwell P, et al. An aggressive surgical approach to significant hemoptysis in
patients with pulmonary tuberculosis. Am Rev Respir Dis. 1968 Feb;97(2):187-92. Abstract
19. Wolfe JD, Simmons DH. Hemoptysis: diagnosis and management. West J Med. 1977
Nov;127(5):383-90. Full text Abstract
20. Kokturk N, Ekim N, Aslan S, et al. A rare cause of hemoptysis: factitious disorder. South Med J. 2006
Feb;99(2):186-7. Abstract
21. Baktari JB, Tashkin DP, Small GW. Factitious hemoptysis. Adding to the differential diagnosis. Chest.
1994 Mar;105(3):943-5. Abstract
22. Fartoukh M, Khoshnood B, Parrot A, et al. Early prediction of in-hospital mortality of patients with
hemoptysis: an approach to defining severe hemoptysis. Respiration. 2012 Jan;83(2):106-14. Full text
Abstract
23. Wahidi MM, Herth FJ, Ernst A. State of the art: interventional pulmonology. Chest. 2007
Jan;131(1):261-74. Abstract
24. Folch E, Mehta AC. Airway interventions in the tracheobronchial tree. Semin Respir Crit Care Med.
2008 Aug;29(4):441-52. Abstract
25. Jeon K, Kim H, Yu CM, et al. Rigid bronchoscopic intervention in patients with respiratory failure
caused by malignant central airway obstruction. J Thorac Oncol. 2006 May;1(4):319-23. Abstract
26. Panda A, Bhalla AS, Goyal A. Bronchial artery embolization in hemoptysis: a systematic review. Diagn
Interv Radiol. 2017 Jul-Aug;23(4):307-17. Full text Abstract
REFERENCES
27. Flume PA, Mogayzel Jr PJ, Robinson KA, et al; Clinical Practice Guidelines For Pulmonary Therapies
Committee. Cystic fibrosis pulmonary guidelines: pulmonary complications: hemoptysis and
pneumothorax. Am J Respir Crit Care Med. 2010 Aug 1;182(3):298-306. Full text Abstract
28. Flight WG, Barry PJ, Bright-Thomas RJ, et al. Outcomes following bronchial artery embolisation for
haemoptysis in cystic fibrosis. Cardiovasc Intervent Radiol. 2017 Mar 13;40(8):1164-8. Abstract
29. Shigemura N, Wan IY, Yu SC, et al. Multidisciplinary management of life-threatening massive
hemoptysis: a 10-year experience. Ann Thorac Surg. 2009 Mar;87(3):849-53. Abstract
30. Solomonov A, Fruchter O, Zuckerman T, et al. Pulmonary hemorrhage: a novel mode of therapy.
Respir Med. 2009 Feb 28;103(8):1196-200. Full text Abstract
31. Tsukamoto T, Sasaki H, Nakamura H. Treatment of hemoptysis patients by thrombin and fibrinogen-
thrombin infusion therapy using a fiberoptic bronchoscope. Chest. 1989 Sep;96(3):473-6. Abstract
32. Bhattacharyya P, Dutta A, Samanta AN, et al. New procedure: bronchoscopic endobronchial sealing; a
new mode of managing hemoptysis. Chest. 2002 Jun;121(6):2066-9. Abstract
33. Chawla RK, Madan A, Aditya C. Glue in hemoptysis. J Bronchology Interv Pulmonol. 2016
Oct;23(4):e40-2. Full text Abstract
34. Bellam BL, Dhibar DP, Suri V, et al. Efficacy of tranexamic acid in haemoptysis: a randomized,
controlled pilot study. Pulm Pharmacol Ther. 2016 Jul 25;40:80-3. Abstract
35. Prutsky G, Domecq JP, Salazar CA, et al. Antifibrinolytic therapy to reduce haemoptysis from any
cause. Cochrane Database Syst Rev. 2016 Nov 2;(11):CD008711. Full text Abstract
36. Bobrowitz ID, Ramakrishna S, Shim YS. Comparison of medical v surgical treatment of major
hemoptysis. Arch Intern Med. 1983 Jul;143(7):1343-6. Abstract
37. Corey R, Hla KM. Major and massive hemoptysis: reassessment of conservative management. Am J
Med Sci. 1987 Nov;294(5):301-9. Abstract
38. Crocco JA, Rooney JJ, Fankushen DS, et al. Massive hemoptysis. Arch Intern Med. 1968
Jun;121(6):495-8. Abstract
39. Garzon AA, Cerruti MM, Golding ME. Exsanguinating hemoptysis. J Thorac Cardiovasc Surg. 1982
Dec;84(6):829-33. Abstract
40. Gale D, Lord JD. Overgrowth of Serratia marcescens in respiratory tract, simulating hemoptysis. J Am
Med Assoc. 1957 Jul 20;164(12):1328-30. Abstract
41. Revel MP, Fournier LS, Hennebicque AS, et al. Can CT replace bronchoscopy in the detection of the
site and cause of bleeding in patients with large or massive hemoptysis? AJR Am J Roentgenol. 2002
Nov;179(5):1217-24. Full text Abstract
45
42. Haponik EF, Britt EJ, Smith PL, et al. Computed chest tomography in the evaluation of hemoptysis.
Impact on diagnosis and treatment. Chest. 1987 Jan;91(1):80-5. Abstract
REFERENCES
43. Strickland B. Investigating haemoptysis. Br J Hosp Med. 1986 Apr;35(4):242, 246-51. Abstract
44. American College of Radiology. ACR appropriateness criteria: hemoptysis. 2014 [internet publication].
Full text
45. Thirumaran M, Sundar R, Sutcliffe IM, et al. Is investigation of patients with haemoptysis and normal
chest radiograph justified? Thorax. 2009 May 19;64(10):854-6. Full text Abstract
46. Pursel SE, Lindskog GE. Hemoptysis. A clinical evaluation of 105 patients examined consecutively on
a thoracic surgical service. Am Rev Respir Dis. 1961 Sep;84:329-36. Abstract
47. Irwin RS, Curley FJ. Hemoptysis. In: Rippe JM, Irwin RS, Alpert JS, et al, eds. Intensive care
medicine. 2nd ed. Boston, MA: Little, Brown; 1991:513-24.
48. Ingbar DH. A systematic workup for hemoptysis. Contemp Intern Med. 1989 Jul-Aug;1:60-70.
49. Gong H Jr, Salvatierra C. Clinical efficacy of early and delayed fiberoptic bronchoscopy in patients with
hemoptysis. Am Rev Respir Dis. 1981 Sep;124(3):221-5. Abstract
50. Saumench J, Escarrabill J, Padró L, et al. Value of fiberoptic bronchoscopy and angiography for
diagnosis of the bleeding site in hemoptysis. Ann Thorac Surg. 1989 Aug;48(2):272-4. Abstract
51. Haponik EF, Fein A, Chin R. Managing life-threatening hemoptysis: has anything really changed?
Chest. 2000 Nov;118(5):1431-5. Abstract
52. Fernando HC, Stein M, Benfield JR, et al. Role of bronchial artery embolization in the management of
hemoptysis. Arch Surg. 1998 Aug;133(8):862-5. Full text Abstract
53. Barben J, Robertson D, Olinsky A, et al. Bronchial artery embolization for hemoptysis in young
patients with cystic fibrosis. Radiology. 2002 Jul;224(1):124-30. Abstract
54. Bustamante M, García-Valtuille R, Agüero R, et al. Bronchial embolization in the treatment of

hemoptysis [in Spanish]. Arch Bronchoneumol. 1998 Nov;34(10):479-83. Abstract
55. Cohen AM, Doershuk CF, Stern RC. Bronchial artery embolization to control hemoptysis in cystic
fibrosis. Radiology. 1990 May;175(2):401-5. Abstract
56. Corr PD. Bronchial artery embolization for life-threatening hemoptysis using tris-acryl microspheres;
short-term result. Cardiovasc Intervent Radiol. 2005 Jul-Aug;28(4):439-41. Abstract
57. Cremaschi P, Nascimbene C, Vitulo P, et al. Therapeutic embolization of bronchial artery: a successful
treatment in 209 cases of relapse hemoptysis. Angiology. 1993 Apr;44(4):295-9. Abstract
58. Kato A, Kudo S, Matsumoto K, et al. Bronchial artery embolization for hemoptysis due to benign
diseases: immediate and long-term results. Cardiovasc Intervent Radiol. 2000 Sep-Oct;23(5):351-7.
Abstract
59. Mal H, Rullon I, Mellot F, et al. Immediate and long-term results of bronchial artery embolization for life-
threatening hemoptysis. Chest. 1999 Apr;115(4):996-1001. Abstract
REFERENCES
60. Park HS, Kim YI, Kim HY, et al. Bronchial artery and systemic artery embolization in the
management of primary lung cancer patients with hemoptysis. Cardiovasc Intervent Radiol. 2007 Jul-
Aug;30(4):638-43. Abstract
61. Gang Q, Xu J, Wang J, et al. Electrocardiography-gated computed tomography of the bronchial

arteries with iterative image reconstruction: clinical evaluation and image quality. J Comput Assist
Tomogr. 2017 Nov/Dec;41(6):970-5. Abstract
62. Chung JH, Kanne JP. Multidetector-row computed tomography of diffuse tracheal disease: pictorial
review. J Bronchol Intervent Pulmonol. 2009 Jan;16(1):28-36. Abstract
63. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med. 2000
May;28(5):1642-7. Abstract
64. Kim YH, Kim HT, Lee KS, et al. Serial fiberoptic bronchoscopic observations of endobronchial
tuberculosis before and early after antituberculosis chemotherapy. Chest. 1993 Mar;103(3):673-7.
Abstract
65. So SY, Lam WK, Yu DY. Rapid diagnosis of suspected pulmonary tuberculosis by fiberoptic
bronchoscopy. Tubercle. 1982 Sep;63(3):195-200. Abstract
66. McIndoe RB, Steele JD, Samson PC, et al. Routine bronchoscopy in patients with active pulmonary
tuberculosis. Am Rev Tuberc. 1939;39:617-28.
67. Konstantinides SV, Torbicki A, Agnelli G, et al. 2014 ESC guidelines on the diagnosis and
management of acute pulmonary embolism. Eur Heart J. 2014 Aug 29;35(43):3033-69, 3069a-k. Full
text Abstract
68. Yates M, Watts RA, Bajema IM, et al. EULAR/ERA-EDTA recommendations for the management of
ANCA-associated vasculitis. Ann Rheum Dis. 2016 Jun 23;75(9):1583-94. Full text Abstract
69. Miller A, Chan M, Wiik A, et al. An approach to the diagnosis and management of systemic vasculitis.
Clin Exp Immunol. 2010 Jan 12;160(2):143-60. Full text Abstract
47
Assessment of haemoptysis Images
Images
IMAGES
Figure 1: Hypervascular endobronchial mucosa

From the personal collection of Dr Erik Folch
IMAGES
Figure 2: Aspergillus infection
From the personal collection of Dr Jeffrey Kanne, with permission
Figure 3: Tracheal tumour

49
IMAGES Assessment of haemoptysis Images
Figure 4: Right upper lobe metastatic renal cell carcinoma

IMAGES
Figure 5: Endobronchial metastatic melanoma
51
IMAGES Assessment of haemoptysis Images
Figure 6: Endobronchial signs of coagulopathy in a patient taking clopidogrel and aspirin

IMAGES
Figure 7: Loquat seed completely occluding the bronchus intermedius
From the collection of Dr Septimiu Murgu and Dr Henri Colt; used with permission
53
Assessment of haemoptysis Disclaimer
Disclaimer
This content is meant for medical professionals situated outside of the United States and Canada. The BMJ
Publishing Group Ltd ("BMJ Group") tries to ensure that the information provided is accurate and up-to-
date, but we do not warrant that it is nor do our licensors who supply certain content linked to or otherwise
accessible from our content. The BMJ Group does not advocate or endorse the use of any drug or therapy
contained within nor does it diagnose patients. Medical professionals should use their own professional
judgement in using this information and caring for their patients and the information herein should not be
considered a substitute for that.
This information is not intended to cover all possible diagnosis methods, treatments, follow up, drugs and
any contraindications or side effects. In addition such standards and practices in medicine change as new
data become available, and you should consult a variety of sources. We strongly recommend that users
independently verify specified diagnosis, treatments and follow up and ensure it is appropriate for your
patient within your region. In addition, with respect to prescription medication, you are advised to check the
product information sheet accompanying each drug to verify conditions of use and identify any changes
in dosage schedule or contraindications, particularly if the agent to be administered is new, infrequently
used, or has a narrow therapeutic range. You must always check that drugs referenced are licensed for the
specified use and at the specified doses in your region. This information is provided on an "as is" basis and
to the fullest extent permitted by law the BMJ Group and its licensors assume no responsibility for any aspect
of healthcare administered with the aid of this information or any other use of this information.
View our full Website Terms and Conditions.
Contact us
+ 44 (0) 207 111 1105

support@bmj.com
BMJ
BMA House
Tavistock Square
London
WC1H 9JR
DISCLAIMER
UK
Contributors:
// Authors:
Irawan Susanto, MD, FACP, FCCP

Professor of Medicine
Interventional Pulmonology, David Geffen School of Medicine, University of California, Los Angeles, CA
DISCLOSURES: IS has received past support from Cook Medical for tracheostomy education and
workshops.
Joanne M. Bando, MD
Associate Professor of Medicine
David Geffen School of Medicine, University of California, Los Angeles, CA
DISCLOSURES: JMB declares that she has no competing interests.
// Acknowledgements:
Dr Irawan Susanto and Dr Joanne Bando would like to gratefully acknowledge Dr Erik Folch and Professor
James K. Stoller, previous contributors to this topic.
DISCLOSURES: EF and JKS are authors of references cited in this topic.
// Peer Reviewers:
Francis Thien, MD, FRACP, FCCP

Professor
Box Hill Hospital and Monash University, Victoria, Australia
DISCLOSURES: FT declares that he has no competing interests.
Miguel Angel de Gregorio, MD, PhD

Interventional Radiologist and Pulmonologist
Full Professor and Chief of Interventional Radiology, University of Zaragoza, Zaragoza, Spain
DISCLOSURES: MAdG has been reimbursed by Cook Medical and Abbott Vascular for attending several
conferences; by Cook Medical and UCB Pharma for speaking; by Cook Medical and St Jude Medical for
running educational programs.
Harman Singh Paintal, MBBS

Staff Physician
Division of Pulmonary & Critical Care Medicine, US Department of Veterans Affairs, Palo Alto Health Care
System, Clinical Assistant Professor of Medicine, Stanford University School of Medicine, Palo Alto, CA
DISCLOSURES: HSP declares that he has no competing interests.
Guy W. Soo Hoo, MD, MPH

Director
Medical Intensive Care Unit, West Los Angeles VA Healthcare Center, Los Angeles, CA
DISCLOSURES: GWSH declares that he has no competing interests.

Approach 2 PDF

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Approach 2 PDF

Uploaded by

Copyright:

Available Formats

Assessment of

The right clinical information, right where it's needed

Last updated: Jan 24, 2019

◊ Pseudohaemoptysis versus haemoptysis :

Pulmonary vascular anatomy

• Bronchial arteries (systemic circulation)

Experts recommend a stepwise approach to treat massive haemoptysis:

2. Protection of the non-bleeding lung

3. Airway intervention and control of bleeding

Step-by-step diagnostic approach

• Mild haemoptysis: <30 mL over 24 hours

Pathophysiologically, it is intuitive to consider >150 mL haemoptysis as life-threatening, as this volume of

The initial diagnostic assessment should aim to:

• Differentiate between haematemesis (the vomiting of blood), pseudohaemoptysis (the coughing of

History and physical examination

Key features of the history include the following points.

• The presence of ecchymoses and/or petechiae suggests haematological diseases.

Chest x-ray and chest computed tomography scan

Other imaging techniques

ECG and echocardiogram

[VIDEO: How to perform an ECG animated demonstration ]

Differential diagnosis overview

Primary lung cancer

Anticoagulants, thrombolytic agents

Mitral valve stenosis

Left ventricular failure

Disseminated intravascular coagulation

Aspiration of foreign body

Aspiration of gastric contents

Pulmonary artery aneurysm

Pulmonary haemorrhagic syndromes

Granulomatosis with polyangiitis (formerly Wegener's granulomatosis)

Congenital heart disease

History Exam 1st Test Other tests

This is not an initial test

History Exam 1st Test Other tests

history of travel to cachexia, fever, »chest x-ray: primary »bronchoscopy:

History Exam 1st Test Other tests

History Exam 1st Test Other tests

A positive test only

This is not an initial test

PPD and interferon-

History Exam 1st Test Other tests

high fever (>38.5°C fever, cardiac murmur, »FBC: leukocytosis, »contrast-enhanced

History Exam 1st Test Other tests

History Exam 1st Test Other tests

fever, cough, dyspnoea, dullness to percussion, »chest x-ray: lobar or

History Exam 1st Test Other tests

Primary lung cancer

History Exam 1st Test Other tests

new cough, dyspnoea clubbing, focal »chest x-ray: »PET-

recumbent position), breath sounds in show segmental scan: positive

Primary lung cancer

History Exam 1st Test Other tests

History Exam 1st Test Other tests

symptoms related to clubbing, focal »chest CT scan: one »PET-

History Exam 1st Test Other tests

Anticoagulants, thrombolytic agents

History Exam 1st Test Other tests

exposure to ecchymosis, petechiae, »INR: may be »bronchoscopy:

Anticoagulants, thrombolytic agents

History Exam 1st Test Other tests

History Exam 1st Test Other tests