By

Prof. Mohammad Khairy El-

Badrawy
Professor of Thoracic Medicine
Mansoura University
2009
Cardinal symptoms of chest
diseases
1. Cough
2. Hemoptysis
3. Chest wheezes
4. Dyspnea
5. Chest pain

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 1. Cough
• Cough reflex is almost
essential for life and by
which the airways are
maintained free of foreign
matter.
• Cough is the commonest
symptom in chest
diseases.

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 Cough
• Cough is considered
chronic when lasts >
3 weeks.
• It is an explosive
expiratory
maneuver, which
may be a voluntary
act, involuntary
(reflex) or both to
clear the airways.

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Components of the larnx
reflex arc:

1. Receptor sites:
trachea
• Larynx, trachea and
bronchi: (stretch or
irritant receptors).
• Terminal bronchioles and
alveoli are: receptors
sensitive to chemical bronchi
stimuli, as inhalation or
irritant gases.
• Pleura & mediastinum. TB

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Components of the reflex arc:
1. Extrathoracic receptor
sites:
• Vagal branches as:
• Meningeal.
• Auricular.
• Buccal.
• Cardiac.
• Gastric.

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2. Stimuli:
• Mechanical and chemical: irritation at
receptor sites or irritation of the cough
center by lesions in its locality.
3. Afferent nerves:
a) Vagus nerve.
b) Glossopharyngeal nerve.
c) Trigeminal.
4. Center:
• Cough center is present in the medulla
oblongata.
5. Efferent:
a) Vagus nerves: larynx.
b) Intercostal nerves: intercostal respiratory
muscles.
c) Phrenic nerve: diaphragm.
d) Pelvic nerves: pelvic muscles.
Components of cough maneuver:

• Deep inspiration.
• Closure of the glottis tightly to
entrap air within the lungs.
• Forceful contraction of
expiratory muscles (including
abdominal muscles)
consequently the pressure in
the lungs rise.
• Sudden opening of the glottis
widely so that air under
pressure in the lungs explodes
outward with very high
velocities carrying with it
secretion and foreign matter.
Cough reflex is decreased by:
• Laryngeal disorders: vocal cord paralysis,
tracheostomy, laryngeal tumors and bulbar palsy.
• Receptor site affection: Accommodation of cough
receptors to repeated stimuli, as in the smoker who
only coughs after his first cigarette of the day.
• CNS depression:
• General anaesthesia.
• Alcohol or addict drug over dose.
• Elderly.
• Respiratory muscle disorders:
• Chest pain.
• Muscle weakness: myasthenia gravis.
• Muscle paralysis: quadriplegia.
 Hazards of cough
I. To the patient:
a) Thoracic:
• Emphysema.
• Rupture bullae or blebs
leading to spontaneous
pneumothorax and
pneumomediastinum.
• Haemothorax from tearing
of adhesions.
• Stress fracture of a rib.
• Rupture of an aneurysm.
b) Extra thoracic:
• Increased intraabdominal
pressure: hernias, prolapse and
stress incontinence.
• Increased intraocular pressure:
subconjunctival and retinal
hemorrhage and retinal
detachment.
• Increased intracranial pressure:
rupture of mycotic aneurysm.
• Post-tussive emesis, syncope
and convulsions.
c) General:
• Insomnia.
• Exhaustion and possibly
neurosis.
II. To the community: transmission of infections.
Cough may be classified into: dry and
productive:
• Dry cough: it may be initiated by respiratory and
non respiratory diseases; it is useless cough and
should be suppressed.
• Productive: it is initiated only from airway
disease.
 Causes of dry cough
A) Respiratory causes:
1- Acute upper and lower respiratory tract
infections:
• Common cold.
• Acute rhinitis and sinusitis.
• Acute pharyngitis.
• Acute bronchitis, tracheitis and
tracehobronchitis.
• Pneumonias.
1. Allergy:
• Bronchial asthma.
• Allergic rhinitis.
2. Pulmonary edema:
• Cadiogenic.
• ARDS
• Pulmonary embolism.
• Tumors:
– Bronchial adenoma
– Bronchial carcinoma.
• FB inhalation.
• Pleural diseases.
• IPF and EAA.
• Mediastinal masses.
B) Non respiratory causes:
• Gastroesophageal reflux disease (GERD).
• Central causes: irritation of the cough center by
lesions in its locality.
• Reflex: due to irritation of vagus branches:
– Meningeal branches: meningitis.
– Auricular branches: otitis media.
– Buccal branches: pharyngitis.
– Cardiac branches: cardiac arrhythmias.
– Gastric branches.
4. Drug induced: Use of ACE inhibitors.
5. Psychogenic cough.
 Causes of productive cough
(expectoration)
Productive chough is initiated only
from airway disease.
1. Acute upper respiratory tract
infections.
2. Chronic sinusitis and allergic
rhinitis: postnasal drip
syndrome (PNDS).
3. Cigarette smoking.
4. Chronic bronchitis.
5. Pneumonia.
6. T.B.
7. Bronchial asthma.
1. Gastroesophageal reflux disease (GERD).
2. Suppurative lung disease.
3. Recurrent aspiration of eosophageal or
oropharyngeal contents.
4. Congenital tracheoesophageal fistulae.
5. Inhaled foreign bodies.
6. Bronchial carcinoma.
7. Pulmonary edema.
• Special characters of cough:
• Painful cough
• Whooping cough
• Bovine cough non explosive cough
• Brassy cough
• Barking cough
• Emetic cough
2. Special time of cough ocurrence:
• Nocturnal cough
– Left- sided heart failure and pulmonary edema.
– Bronchial asthma.
– Aspiration.
• After exertion (15min from start of
exercise) exercise-induced asthma or
cardiac aetiology.
• Occupational asthma.
• Early morning.
• Emetic cough.

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 Expectoration (productive cough)
• Expectoration entails the
passage of sputum out of
the respiratory tract.
• Sputum is composed of
expectorated or swallowed
mucus contaminated by
saliva, transudations from
serum, exfoliated epithelial
cells, glycoproteins and
serum proteins (mainly
albumin) and bacteriostatic
proteins (lysozymes,
lactoferrin, interferon,
secretory IgA).
 Differentiation of Sputum
1. Onset, course, duration.
2. Amount.
3. Color.
4. Consistency.
5. Smell.
6. Relation to day- time.
7. Relation to posture.
8. Associated haemoptysis.
 Onset, course, duration
2.Onset:
Acute:
• Acute bronchitis.
• Pneumonia.
• Acute abscess.
• Empyema with bronchopleural fistula.
Gradual:
• T.B.
• Chronic bronchitis.
• Bronchiectasis.
2. Course:
• Progressive:
– Infection uncontrolled by antibiotics.
• Regressive course:
– Spontaneous improvement.
– Good response to antibiotics.
• Intermittent course:
– Chronic bronchitis.
– Bronchiectasis.
3. Duration:
• Long duration:
– Chronic bronchitis
– Chronic lung abscess.
• Short duration:
– Acute bronchitis.
– Pneumonia.
– Acute lung abscess.
 Amount
A patient may swallow large amounts of
sputum unconsciously.
Volumes of more than 100ml sputum /day are
defined as bronchorrhoea.
Causes:
1. Suppurative lung disease.
2. Chronic bronchitis.
3. Asthma.
4. Alveolar cell carcinoma.
5. Acute organophosphorous poisoning.
 Relation to day -time
1. Chronic morning expectoration over
years: as in chronic bronchitis.
2. Excessive amounts of sputum production
mainly in the morning: suppurative lung
diseases.
3. Variable morning or nocturnal
expectoration: bronchial asthma.
4. Recent onset of sputum production:
bronchopulmonary infections.
Relation to posture
Only in suppurative lung
diseases.

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Color of the sputum: (it may be diagnostic):
1. Green or thick yellow sputum usually means
infection (the color and increased viscosity are
due to its content of leucocytes).
• Sputum stagnation containing leucocytes will turn
green. It is due to liberation of the green enzyme
verdoperoxidase or (myeloperoxidase) from the
broken-down cells.
• The first sputum produced in the morning in many
patients with chronic bronchitis will be green, while
that produced later in the day reverts to a clear
color.
• Asthmatic sputum laden with eosinophils: yellow or
green color.
1. Rusty sputum (brownish yellow).
2. Red current jelly sputum.
3. Haemoptysis.
4. Anchovy sauce sputum.
5. Black sputum.
6. Reddish tinge of sputum mistaken as
haemoptysis.
7. Blue sputum.
8. Watery sputum.
9. Trichoptysis.
10. Expectoration of chalky materials or small
stones is characteristic of broncholithiasis.
 Consistency of sputum
• Thick sticky sputum difficult to expectorate
occur in infections and bronchial asthma
• Extremely thick tenacious sputum: occur in
asthma.
• Expectoration of intrabronchial tumors may
occur, this is particularly important in
metastatic renal carcinoma.
 Smell of sputum
• Offensive putrid odour: suppurative lung
disease due to anaerobic infections.
• G-ve infection: distinctive odour to sputum,
similar to E-coli on a culture medium.
These odors can be used as an initial guide
for initial chemotherapy while a waiting the
culture results.
 Management of cough
1- Investigations:
• Since most coughs are transient and related to U.R.T
infection, it is normally appropriate to treat such a
suspected infection and/or to wait for 2-3w before
investigating further.
• History will give clues to diagnosis.
• ENT examination.
• Chest X-ray.
• X-ray sinuses if needed.
• Sputum examination
Sputum examination
a- Differentiation of sputum from saliva
b- Bacteriological examination including gram
stain and culture, and ZN stain and culture
for TB.
c- Examinations for fungi or parasites
d- Cytological examination
1- Investigations (Cont):
• Pulmonary function tests: spirometry.
• Barium esophogography and/or 24-hour
esophageal pH to monitor for silent gastro-
esophageal reflux disease (GERD).
• Bronchoscopy (in certain cases).
• HRCT chest (in cases with suspected
bronchiectasis).
• Non invasive cardiac studies as
echocardiogram and ECG.
2- Treatment of the primary
disease
 3- Symptomatic treatment of cough

a) Dry cough: cough sedatives

b) Productive cough:
• Expectorants
• Mucolytics
 Wheezes
• Wheezes are musical
adventitious lung sounds.
• It occurs due to airway
narrowing either to spasm or
endoluminal or extraluminal
obstruction.
• It is a common complaint in
patient with airway
obstruction.
• Wheezes can be heard
without stethoscope.
• Wheezes do not always
indicate bronchial asthma.
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Mechanism:

Fluttering of the airway wall is the mechanism

responsible for production of wheezes and
rhonchi. It occurs when air flows rapidly
through a narrow airway (bronchospasm,
thick secretions, edema), causing fluttering of
the airway wall at one or more sites.
 Causes of wheezy chest
Generalized chest wheeze
1. Bronchial asthma.
2. COPD.
3. Bronchitis, tracheobronchitis.
4. Bronchiolitis.
5. Bronchiectasis.
6. Cystic fibrosis.
7. Allergic bronchopulmonary aspergillsis.
8. Carcinoid tumor.
9. Left sided heart failure (cardiac asthma).
10. Uremia (renal asthma).
11. Anaphylaxis.
Localized chest wheeze
Localized bronchial obstruction:
a) Intralumenal:
• FB inhalation.
• Mucus plugs
• Bronchial carcinoma.
• Carcinoid tumor.
• Endobronchial TB.

b) Lumenal.
• Bronchial stenosis, stricture.

c) Extralumenal.
• Compression by enlarged lymph node or a mediastinal mass.
 Stridor
• Stridor is a particularly
loud musical sound of
constant pitch

• Most prominent during

inspiration,

• Heard at a distance
from the patient.

• Stridor indicates partial

central and upper
airway obstruction.
 Causes of Stridor

1. In children
– Viral croup
– Inhaled foreign body
– Acute epiglottitis
– Diphtheria
2. In adult
– Chronic laryngitis
– Vocal cord paralysis
– Neoplasm of the larynx
or trachea
 Hoarseness of voice
• Hoarseness is a rough, coarse quality of
voice, occurring when a normal, smooth
vocal cord is not brought into contact with its
fellow.

• It indicates:
– Irregularities on the surface of one or both cords
– Disorder of nerves and muscles responsible for
vocal cord movement.

• Any patient with more than three weeks of

hoarseness should be examined by indirect
laryngoscopy.
 2. Dyspnea
Dyspnea is subjective complaint by
the patient that can be expressed as:
• Difficulty of breathing.
• Difficult or laboured breathing.
• Undue awareness of breathing.
• Need to breath more.
• Uncomfortable or unpleasant breathing.
Mechanism of dyspnea:
The concept of unbalanced demand
for ventilation and ventilatory reserve
(supply) demonstrates how dyspnea
occurs.
(A) Increased demand: Increase drive for
respiration through stimulation of
peripheral and central chemoreceptors
by: fever, acidosis, anemia, hypoxemia,
and hypercapnea.
(B) Reduced reserve of:
• Airways: increased airway resistance that
interfere with ventilation.
• Lung parenchyma and pleura: decreased
compliance that impair diffusion.
• Pulmonary circulation: decreased perfusion.
• Chest wall:
• Respiratory muscle dysfunction (weakness,
fatigue).
• Kyphoscoliosis and obesity (extrathoracic
restriction).
 Demand

•Normal
Demand Reserve

Reserve
•Dyspnea

Mechanism of dyspnea: when there is

no balance between demand and
respiratory reserve
 Causes of dyspnea

A) Pulmonary causes:
1- Airway diseases:
• Upper airway obstruction.
• Bronchial asthma.
• COPD.
• Localized bronchial
obstruction either due to:
• Extraluminal obstruction: as
in mediastinal syndrome.
• Intraluminal obstruction: as
in foreign body or thick
viscid secretions.
• Lesions in the wall itself: as
in tumors or stenosis.
2- Lung parenchyma diseases:
• Pulmonary edema.
• Consolidation.
• Collapse.
• Interstitial pulmonary fibrosis.
• Post TB fibrosis.
• Sarcoidosis.
• Pneumoconiosis.
• Resection of a lobe or lung.
3- Pleural diseases:
• Pneumothorax.
• Pleural effusion.
• Pleurisy.
• Pleural tumors.
4- Pulmonary
circulation diseases:
• Pulmonary
hypertension.
• Pulmonary embolism.
• Intrapulmonary shunt.
5- Chest wall
diseases:
• Kyphoscoliosis and
other chest wall
deformities.
• Respiratory muscles
disorders.
• Weakness and fatigue.
• Diaphragmatic paralysis
and eventration.
• Myopathies, myasthenia
gravis and myotonia.
• Obesity.
• Thoracoplasty.
B) Cardiac causes:
Left sided heart failure due to:
• Increase preload:
• Right to left shunt (Eisenminger's
syndrome)
• Mitral and aortic regurge.
• Increase afterload: mitral stenosis,
aortic stenosis, systemic
hypertension.
• Muscle disorders: cardiomyopathy -
myocardial infarction.
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 Chest Pain .3
• One of the commonest and important
symptoms in cardiopulmonary
practice.
• Chest It is pain carries unique property
as it may be just trivial due to myositis
or catastrophic due to acute MI.
• To know the etiology and to reach the
anatomical origin of chest pain
 Causes of chest pain
• Thoracic causes: Extrathoracic causes:
2. Chest wall. • Abdominal causes.
3. Pleura. Pancreatitis.
Cholycystitis.
4. Mediastinum:
• Cardiac causes. Peptic ulcer.
• Vascular causes. • Functional chest pain.
• Oesophageal causes.
• Tracheal causes.
• Mediastinitus.
• Mediastinal tumors

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 Management of chest pain:
• Treatment of the cause.
• Pleuritic pain:
• Analgesics.
• Local anaesthetic nerve block.
• Anginal pain: nitroglycerine.
• Myocardial infarction: morphia and nitroglycerine.
• Oesophageal pain: antispasmadics and antacids.
• Mediastinitis: analgesics and antibiotics even
exploration thoracotomy may be indicated for
aetiological treatment.
 4. Haemoptysis
• Haemoptysis is expectoration or coughing
up of blood, or blood-tinged sputum from
the lungs or tracheobroncheal tree below
the level of vocal cords.
• Spurious haemoptysis (false): it is that
bleeding from sites above the level of VC.
(nose, mouth, pharynx, larynx and must
be examined carefully and investigated for
any cause of bleeding).
Haemoptysis may be confused
with haematemesis
Haemoptysis Haematemesis
History Previous chest Previous history of heart
symptoms as cough burn, esophageal varices
and expectoration. or peptic ulcer.
Color of blood Blood is red, frothy with Coffee-brown color, acidic
alkaline pH and mixed pH and mixed with food.
with sputum. Sputum
contains
haemosiderin-laden
macrophages.
On examination Crepitation is heard over Chest examination is free
the affected side.
After attack Many days after the After the attack, melena will
attack, sputum will be follow it.
mixed or stained with
blood.
 Classification of hemoptysis
1) Based on anatomical basis:
• True-haemoptysis: bleeding from
tracheobronchial tree or the pulmonary
parenchyma.
• Pseudohaemoptysis or false haemoptysis:
expectoration of blood aspirated into the
respiratory tract from supraglottic region or
gastroentistinal tract.
• Factitious or simulated haemoptysis
(voluntary induced by trauma): it is rare but
should not be overlooked as a possible
explanation of sudden episode of bleeding.
It has been described for neurotic and
aggressive young women.
2) According to severity:
• Fatal haemoptysis.
• Non fatal haemoptysis.

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3) According to amount:
• Blood streaked sputum.
• Mild haemoptysis < 20ml blood per 24 hours.
• Moderate haemoptysis 20 - 200ml blood/24
hours.
• Massive haemoptysis or life threatening
haemoptysis:
– Coughing up ≥ 150ml of blood in a single attack,
which may fill the dead space of the bronchial tree
(the patient may suffocate).
– or 400ml blood within 3 hours.
– or 500ml blood within 12 hours.
– or 600ml blood within 24 hours.
 Tuberculosis
Bacterial
Neoplasms
pneumonia
Miscellaneous

Bronchiectasis

Cryptogenic

Bronchitis

Common causes of hemoptysis.

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Less common causes of hemoptysis
• Mitral valve disease • Haemosiderosis.
• Good-pasture syndrome. • Aspergilloma.
• Foreign body aspiration • A-V malformation.
• Primary hemorrhagic • Acute left ventricular
disease. failure.
• Systemic hypertension. • Hematogenous
amoebiasis.
• Lung abscess. • False hemoptysis (nose,
mouth, pharynx, larynx).
 Most common causes of
massive haemotpysis
• Bronchiectasis.
• Cavitating lung diseases 2ry to
necrotizing infections as TB or
fungus (mycetoma) cavity.
• Bronchial carcinoma.
• Mitral valve disease.
 Fatal or exsanguinating
haemoptysis
• ≥ 150ml / attack.
• ≥ 1000ml total loss.
• It is the severe form of hemoptysis
that may lead to death if not
vigorously treated.
Most common causes of fatal
hemoptysis:
• Rupture of a bronchial artery in a TB or aspergilloma
cavities.
• Following iatrogenic trauma to vascular tumors by
biopsy forceps.
• Iatrogenic trauma to fibrotic lung with drill or needle.
• Rupture of aortic even pulmonary artery aneurysm.
 Mechanisms of hemoptysis
1. Intra-alveolar hemorrhage and diapedesis of the
RBCs from pulmonary microvasculature into the
alveoli (acute pulmonary edema).

3. Necrosis of lung tissue with hemorrhage into the

alveolar spaces (infarction).

5. Rupture of distended endobronchial blood vessels

(bronchial varices) as in mitral stenosis.

7. Ulceration or erosion of the bronchial epithelium

(bronchitis, brocholithiasis).

9. Sloughing of a caseous lesion into the

tracheobronchial tree (TB).
• Rupture of intrapulmonary collaterals:
– Pulmonary A-V fistula (Osler- Weber- Rendu disease).
– Bronchial artery -pulmonary venous collateral channels
(bronchiectasis).
– Systemic blood vessel -pulmonary venous collateral channels
(sequestration).

• Invasion of blood vessels (bronchial carcinoma or

adenoma).

• Necrosis of lung tissue associated with

inflammation and rupture of blood vessels
(necrotizing pneumonias and some parasitic
infestations).
• Rupture of an aortic aneurysm into the
tracheobronchial tree (weeping
aneurysm).
• Anticoagulants and
immunosuppressive drugs causing
intrapulmonary bleeding.
• With menstruation due to presence of
endobronchial endometriosis
(catamanial hemoptysis).
• Malingering.

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Clinical points in patients with hemoptysis
• Repeated small hemoptysis: bronchial
carcinoma, bronchiectasis or pulmonary
emboli.
• Repeated large hemoptysis: bronchiectasis,
aspergilloma, lung abscess, TB.
• Single or frequent hemoptysis with purulent
sputum: acute bronchitis or acute
exacerbation of chronic bronchitis.
• Single or infrequent hemoptysis: bronchial
carcinoma.
• Pleuritic pain or chest wall pain: pulmonary
emboli, chest trauma or spontaneous
pneumothorax.
• With dyspnea: pulmonary emboli, central
bronchial carcinoma or endobronchial tumor.
• With wheezes: chronic bronchitis, bronchial
carcinoma or adenoma or foreign body
aspiration.
• Heart disease: mitral stenosis.
• Bleeding from other sites: haemostatic
failure.
Examination:
• Finger clubbing: bronchiectasis or bronchial
carcinoma.
• Wheezes: unilateral or bilateral.
• Signs of consolidation or collapse.
• Heart examination and signs of DVT.
 Management of haemotysis
Investigations:
• ENT examination, bleeding time, clotting time
and platelet count.
• Chest X- ray.
• Bronchoscopy is usually advisable unless a
non-malignant cause is obvious. It should be
carried out in other individuals in whom the
hemoptysis is recurrent after an interval of
observation.
• Sputum cytology for malignant cells.
• ZN for acid- fast bacilli may diagnose
endobronchial TB.
• Iron-containing macrophages in patients with
hemosiderosis and Good-Pasture syndrome.
• Other special investigations:
– Bronchiectasis: HRCT.
– A- V fistula or pulmonary embolism:
• Pulmonary or bronchial arteriogram
• Spiral CT.
• If the history and physical examination
are characteristic of acute bronchitis,
the haemoptysis is mild, no further
investigations will be required unless
the symptoms of cough persist or the
bleeding recurs.
• If no cause is evident it is called
idiopathic hemoptysis.
• If pulmonary embolism is suspected
with normal CXR:
– ECG.
– Chest X-ray.
– Ventilation / perfusion scanning.
– Spiral CT of the chest.
– Pulmonary angiogram.

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 Treatment of hemoptysis
It depends on diagnosis and treatment of the
1ry condition after control of hemoptysis.
1) Mild and moderate haemoptysis:
• Rest, cough suppressants and haemostatic drugs.
• Specific treatment:
– TB: anti TB.
– Abscess or pneumonia or infective exacerbation of
chronic bronchitis: antibiotics.
– Bronchial carcinoma:
• External irradiation.
• Laser beam through rigid bronchoscope or through FOB.
• Argon- plasma coagulation.
• Electrotherapy.
• If controlled, the patient must be investigated later on by the
investigations mentioned above and elective surgery will be
done if the patient is fit for surgery.
2) Massive haemoptysis:
Emergency treatment is life saving:
– Positioning: the bleeder side of the chest is the
lower most to prevent the expected aspiration of
blood to the healthy side and hence drowning.
– Sedation: diamorphine is the drug of choice.
Diazepam can be used.
– Set up IV line and collect blood for grouping and
possible cross- matching for tranfusion.
– Endotracheal tube for aspiration of blood.
5. Emergency rigid bronchoscope on theater
while preparing for resection in certain cases.
The bleeding will be controlled through the
rigid bronchoscope by:
– Aspiration of blood and cold saline lavage through
concomitant FOB.
– Fogartey balloon catheter inserted into and
inflated in the affected main bronchus or lobar
bronchus to isolate the affected site with lavage of
the other bronchi and trachea from blood.
– Gauze packing by the forceps through the rigid
bronchoscope.
– Double lumen-tracheal catheter.
6. FOB:
It may be used and is considered the
procedure of choice in experienced hands
since it can be performed rapidly, requires
only light sedation, and allow excellent airway
visualization.
• All patients should be intubated prior to FOB.
This optimize airway control, allows effective
suctioning and permits the bronchoscope to
be removed easily and reinserted if the
suction channel become occluded.
• A balloon catheter may be used to occlude a
segmental or lobar airway alternatively the
FOB can be used to intubate selectively and
ventilate the non bleeding lung.
7. Emergency lung resection of the bleeding
lobe or lung.
8. Induction of artificial pneumothorax on the
affected side to collapse the lung.

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3) Bronchial artery embolism by gel foam
embolization in cases of bronchiectasis
and cystic fibrosis.
4) If no cause can be detected follow up
with chest X- ray of the patient for 3-6
months. If no cause can be detected no
follow is recommended after that
period.
Causes of haemoptysis with normal CXR
• Acute bronchitis.
• Chronic bronchitis.
• Bronchiectasis.
• Endobronchial TB.
• Tracheal trauma from endotracheal
intubation or suction.
• Hemorrhagic disorders.
• Anticoagulants over dosage.
• Tracheal tumors.
• Bronchial tumor.
• Pulmonary embolism.
• Idiopathic.
Chest Signs

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