THE RESPIRATORY SYSTEM

CONTENTS
I. GENERM4TIES
1.1.History
1.2.Family and social history
1.3.Occupation and other enviromental hazards
n. SYMPTOMS OF RESPIRATORY DISEASES 2.
l.Thoracic pain
2.2. Dyspnoea
2.3. Wheeze
2.4. Cough
2.5. Sputum
2.6. Haemoptysis
ffl. THE PHYSICAL EXAMINATION OF RESPIRATORY SYSTEM
3.1. The external feature of respiratory disease
3.2. General inspection
3.3. Examination of the chest:
- inspection
-palpation
-percussion
- auscultation
IV. RESPIRATORY SYNDROMES
4.1. Bronchial syndromes
4.2. Consolidation syndromes
4.3. Pulmonary tuberculosis syndrome
4.4. Pulmonary suppurative syndrome
4.5. Airways obstruction syndrome
4.6. Pleural syndromes
4.7. Chronic obstructive pulmonary disease
4.8. Pulmonary insufficiency
V. FURTHER INVESTIGATIONS OF THE RESPIRATORY SYSTEM
5.1. Radiological examination
- radiography
- tomography
- pulmonary angiography
- fluoroscopy
5.2.Examination of the sputum
5.3.Examination of the blood
5.4.Intradermal tests
5.5.Tests of respiratory function
5.6. Bronchoscopy
5.7.Bronchoalveolar lavage
5.8. Bronchography
5.9.Pleural aspiration and biopsy
5.10. Lymph node biopsy
5. ll.Lung biopsy

111. GENERALITIES
1.1. HISTORY
The approach to history taking in patients thought to have respiratory disease differs according to the nature of the
illness, the main distinction being between an acute or subacute illness and a chronic respiratory disorder.
In an acute respiratory illness it is always important to enquire carefully about the onset of the illness which may
provide a valuable clue to its nature. In pneumococcal pneumonia, for example, systemic disturbance (rigor, pyrexia,
malaise) seldom precedes the first respiratory symptom (often pleural pain) by few hours, while in viral pneumonia the
patient may be generally unwell for several days before there are any symptoms or signs to suggest pulmonary involvement.
Acute dyspnoea represents a symptom of particular importance since it often demands urgent treatment, and an error
in diagnosis between, let's say, tension pneumothorax, an acute attack of bronchial asthma, and left heart failure may have
catastrophic consequences.
In chronic disorders history-taking is always a complex and time consuming procedure. In the case of acute
episodes, such as exacerbations of chronic bronchitis, an enquiry should be made into the events which preceded them on the
course of the disease.
The course of disease may be adversely influenced by treatment of coexisting disorders, for example, a betaadrenoreceptor blocking drug for hypertension or angina in a patient with chronic asthma. The influence of environmental
factors, such as weather and time of year, changes of temperature and exposure to smoke and dust, should always be
recorded.
1.1 FAMILY AND SOCIAL HISTORY
The family history of patients with respiratory disease may be singnificant in three ways:
1.certain infections, notably tuberculosis, may be transmitted from one person to another. In such cases a
history of contact with an infected person is, of course, more important than the family relationship.
2.in allergic disorders, such as some bronchial forms of asthma, there is often an inherited predisposition,
and a family history is not uncommon.
3.in chronic bronchitis, although an inherited predisposition cannot be excluded, the liability of several
members of one family to develop the disease is more likely to be related to the conditions under which they all live. Social
problems, such as housing, finance and employment, loom large in the management of patients with all types of chronic
respiratory disease and should be fully documented in every case.
Cigarette smoking is now accepted as the most important cause of bronchial carcinoma and chronic bronchitis. A
smoking history should include details such as the time when regular smoking started, the average consumption of tobacco
and the age when cough started being productive.
1.3. OCCUPATION AND OTHER ENVIROMENTAL HAZARDS
Since both acute and chronic respiratory disease may be caused by the inhalation of certain inorganic and dust and
chemical substances, it is important to record a complete occupational history, covering both present and previous
employment.
Such hazards may be encountered by workers in the coal, iron and steel, and pottery industries, by stonemasons and
farm workers, and by those who are liable to inhale asbestos dust and chemical substances, such as isocyanates, in the course
of their work. Whenever such an occupational history is obtained detailed information should be obtained regarding the
degree and duration of exposure, and its time relationship at the onset of symptoms. This may establish a diagnosis of
occupational asthma or allergic alveolitis.
Persons in close contract with pigeons, parrots, buderigars or canaries may develop allergic alveolitis or psittacosis,
while atopic subjects may develop allergic rhinitis or bronchial asthma when exposed to allergens such as pollen, house dust
or certain types of fungal spores.
fill. SYMPTOMS OF RESPIRATORY DISEASES
The six principal symptoms of respiratory disease are:
2.1. thoracic pain 2.2. dyspnoea 2.3.
wheeze 2.4. cough 2.5. sputum 2.6.
haemoptysis
2.1. THORACIC PAIN
GENERALITIES

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In practice, by far the most common cause of severe thoracic pain in the middle-aged or elderly is ischaemic heart disease.
Pain worsening on breathing is almost always pleuritic in origin, and in a woman on the oestrogen containing contraceptive
pill or in a post-operative patient it should suggest a pulmonary embolus. Trauma is a likely cause in the young whilst extrathoracic causes increase in frequency with advancing age. In any case, by anamnesis we must precise: the type of onset of
the pain location radiation character duration incidence
aggravating and relieving factors
associated symptoms TYPE OF ONSET can
be:
- acute in pneumonia, pleuresy, pneumothorax, pulmonary embolism
- chronic: bronchial cancer, pleuresy
LOCATION AND RADIATION
- retrosternal: if the pain radiates to shoulder, arm, it orients you to cardiac disease; if it does not radiate it
can suggest an acute tracheitis, laryngotracheitis, esophagities, cancer of the oesophagus
- anterior pain suggests sufferance of anterior mediastinum
- apexian pain usually appears in tuberculosis, neoplasm
DURA TIONAND INCIDENCE
The time and circumstance of the first appearance of the pain should be ascertained and whether the incidence is
sudden, diurnal, episodic or constant. A sudden onset is seen in such major disorders as myocardial infarction, pulmonary
embolism, pneumothorax, or vertebral collapse.
AGGRA VA TING OR RELIEVING FACTORS
In cardiac diseases pain is often aggravated by exertion or emotional stress. It is relieved by rest and in case of
angina, it dramatically ceases by the administration of trimtroglycerin.
Pleuritic pain is increased by coughing and deep inspiration whilst pain arising from the spine is often increased by
sneezing, blowing the nose and movement. Changes of posture such as lying down or bending encourage oesophageal reflux,
and the pain of reflux oesophagitis is usually relieved by milk or antacids.
ASSOCIA TED SYMPTOMS
Cardiac disorders are often associated with dyspnoea, palpitations and oedema of the lower limbs. Cough, especially
if there is purulent or bloody sputum, points to a pulmonary cause, whilst dysphagia is almost always of oesophageal origin.
Anorexia and rapid weight loss are ominous symptoms which may suggest an underlying carcinoma of the oesophagus or
bronchus. Both are known to be commoner in the heavy smoker.
CAUSES OF THE THORACIC PAIN
Thoracic pain has been classified as having intrathoracic, thoracic wall and extrathoracic causes. The most frequent
of these causes are those which lie within the chest The intrathoracic pain can have respiratory, cardiovascular and
oesophageal causes.
/. INTRATHORACIC CAUSES
A. RESPIRATORY CAUSES:
pneumonia
pleurisy
pulmonary embolism
pneumothorax
neoplasm
tracheitis
B. CARDIOVASCULAR CAUSES:
angina pectoris
myocardial infarction
pericarditis
cardiomyopathy
aortic aneurysm
C. ESOPHAGEAL CAUSES:
esophagitis
esophageal spasm
esophageal carcinoma
//. THORACIC WALL CAUSES:
A. NON-INFLAMMATORY CAUSES:
trauma
Tietze's disease

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ostheo-arthritis
osteoporosis
osteomalacia
Paget's disease
neoplasm
B. INFLAMMATORY CAUSES:
herpes Zoster
Bomholm disease
tuberculosis of the bones
ankylosing spondylitis ///.
EXTRATHORACIC CAUSES
cervical spondylosis
gall stones
hepatic abscess
subphrenic abscess
splenic disease
psychogenic causes.
DIAGNOSTIC APPROACH
Three types of chest pain are directly due to respiratory disease:
l.upper retrosternal pain of the type experienced in acute tracheitis;
2.retrosternal pain associated with lesions of the mediastinum, e.g. tumors, acute mediastinitis and
mediastinal emphysema. This type of pain, which is an uncommon but important symptom, has a constrictive or oppresive
character similar to that of cardiac pain and may radiate into the arms or neck, but is seldom severe and is not related to
exertion.
3.pleural pain caused by stretching of an inflamed parietal pleura, can occur in all forms of pleurisy.
Identical pain is produced by fractures of ribs. Pleural pain is recognised by its sharp, stabbing character and its relationship
to breathing and coughing. It may be present only at the end of a deep inspiration or during cough; in a more severe status
-even a shallow breathing may produce intense pain. The pain is aggravated by exertion and occasionally by movements of
the thoracic spine. Pleural pain often, but not invariably, subsides when an effusion develops.
In spontaneous pneumothorax pleural pain may be present, particularly if the amount of air in the pleural space is
small. More often, however, after a brief mitral episode of severe unilateral pain the patient complains mainly of tightness
across the front of the chest, which may later become localised to the affected side. Rarely, there may be central retrosternal
pain resembling that of myocardial infarction, with radiation into the neck and upper limbs. This type of pain may be due to
mediastinal emphysema and spontaneous pneumothorax which associates with it occasionally. Other intrathoracic disease
may produce central chest pain, e.g. lesion of the heart arid great vessels or/of the oesophagus. Piercing unilateral chest pain
may be due to involvement of a spinal nerve root by a vertebral lesion or by herpes zoster.
Pain caused by invasion of the chest wall by a malignant pulmonary tumor or by a metastatic deposit in a rib is
constant, severe, aching and usually unrelated to breathing, while that produced by simple rib fractures or Coxsackie B
infection (Bornholm's disease) resembles pleural pain. Chest pain in the absence of organic disease may be a manifestation
of anxiety.
2.2. DYSPNOEA
DEFINITION
Dyspnoea is a subjective complaint and represents the patient's perception that breathing is excessive, difficult or
uncomfortable.
It is described like: breathlessness, shortness of breath, the sensation of difficult, labored or uncomfortable
breathing.
CAUSES OF DYSPNOEA
A. RESPIRATORY CAUSES:
obstruction - foreign body
- anaphylactic reaction
-tetanus
- poliomyelitis
- invasive thyroid cancer
bronchial asthma
bronchitis
emphysema
bronchial/lung carcinoma
pneumonia
pneumothorax
pleural effusion
pneumoconiosis

5
extrinsec fibrosing alveolitis
cryptogenic fibrosing alveolitis
sarcoidosis
pulmonary embolism
B. CARDIAC CAUSES:
heart failure - especially left heart failure
coronary heart disease
myocardial infarction
valvular disease: aortic stenosis, mitral stenosis
congenital heart disease
pericarditis
C GENERAL CAUSES:
drugs: aspirin, p-blockers
hyperthyroidism
Addison's disease
terminal renal failure
anxiety state
TYPES OF DYSPNOEA
L PHYSIOLOGIC DYSPNOEA
- the most common type of dyspnoea is that associated with physical exertion
- also common during acute hypoxia, as at high altitude
2. PULMONARY DYSPNOEA
a. Restrictive dyspnoea - due to low compliance of the lungs or chest wall (e.g. pulmonary fibrosis or chest
deformities). These patients are ussually comfortable at rest but become intensely dyspneic when exertion causes pulmonary
ventilation to approach their greatly limited breathing capacity.
b. Obstructive dyspnoea - due to high airway resistance (e.g. obstructive emphysema or asthma).
In this type increased ventilatory effort induces dyspnoea even at rest and breathing is labored and retarded,
especially during expiration.
3. CARDIAC DYSPNOEA
a* Cardiac asthma is a state of acute respiratory insufficiency accompanied by severe breathlesness. Its
manifestations may be indistinguishable from other types of asthma, but it originates in failure of the left ventricle.
b. Periodic or Cheyne-Stokes respiration is characterized by alternate periodes of apnea and hyperpnea, often
including both neurologic and cardiologic componente. In heart failure, slowing of the circulation is the predominant cause;
acidosis, and hypoxia in the respiratory centres contribute importantly.
a Orthopnea is the respiratory discomfort that occurs while the patient is supine (thus impelling him to set up). It is
precipitated by an increase in venous return of blood to left ventricle. Orthopnea, usually a manifestation of left ventricular
failure, sometimes occurs in other cardiovascular disorders (e.g. pericardial effusion).
d. Paroxysmal nocturnal dyspnoea - (which may be dramatic and terrifying) the patient awakens gasping for
breath. It may occur in mitral stenosis, aortic insufficiency, hypertension, or other conditions affecting the left ventricle.
4. CIRCULATORY DYSPNOEA
- "air hunger" (acute dyspnoea occuring in the terminal stages of exsanguinating haemorrhage)
- also occurs with chronic anemia, coming on only during exertion.
5. CHEMICAL DYSPNOEA could be:
- KussmauTs breathing, diabetic acidosis (blood pH 7,2~6,95) induces a distinctive pattern of slow, deep respiration
in fburtimes: deep inspiration - apnee, deep expiration - apnee
- in uremia the patient may complain of dyspnoea because of severe panting brought about by a combination of
acidosis, heart failure, pulmonary edema and anemia.
6. CENTRAL DYSPNOEA
- Biot's respiration: central lesions such as haemorrhage are often associated with intense hyperventilation that is
sometimes noisy and stertorrous and occasionaly irregulary periodic. It is also called agonic respiration.
7. PSYCHOGENIC DYSPNOEA. Hie hysterical types of overbreathing are the most common:
in one type there is continous hyperventilation, sometimes leading to acute alkalosis from "blowing of
C02, and positive Trousseau's and Chvostek's signs from lowered senium calcium ion levels.
. other type is characterized by deep, sighing respirations, the patient breathing at .naxin^ depth until
respiration "is satisfactory", at which time hyperventilatory impulse subsides. DIAGNOSTIC APPROACH
This will vary with the type of onset and age of the patient.
Sudden breathlessness may tesult from:
- spontaneous pneumothorax
- pulmonary embolus
- myocardial infarction
- rapiddly forming pleural effusion
- obstruction by a foreign body in the air passages.

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Paroxysmal bouts of dyspnoea are ussually due to asthma and may be precipitated by an upper
respiratory infection, exertion, emotional upsets or exposure to a potential allergen.
Progressive dyspnoea at first only at exertion, at the beginning, is commonly due to:
- chronic bronchitis
- emphysema
- diffuse pulmonary fibrosis
- ischemic heart disease.
In childhood acute respiratory infections and asthma are the the most common causes of
expiratory dyspnoea.
In the very young age a very frequent cause of inspiratory dyspnoea it is an inhaled foreign body. When
taking a history in adults it is very important to enquire about previous illnesses, drugs recently taken, smoking
habits, hobbies and occupations.
a sudden onset with chest pain in a healthy young man is probably caused by a spontaneous pneumothorax, but
similar symptoms in a woman on the contraceptive pill or during the last trimester of pregnancy are more likely
to be due to pulmonary embolism;
the inhalation of fumes or dust at work in susceptible individuals may provoke attacks of occupational asthma or the
insidious pulmonary fibrosis of extrinsic fibrosing alveolitis. Farm workers and bird founder are obvious victims but many
others work in enviroments where exposure to industrial dusts is common place. Miners, stonemasons, foundrymen,
sandblasters and those who work with asbestos, in one form or another are liable to develop pneumoconiosis and massive
fibrosis may occur long after they have moved to safer occupations. Cigarette smoking may exacerbate these dust
diseases quite apart from its role in causing chronic bronchitis and emphysema. With advancing age cardiovascular
causes assume increasing importance.
Associated symptoms must be noted for they will often point to the most probable cause (e.g. chest pain will, as a rule, be
prominent on myocardial infarction, pulmonary embolism, pleurisy and pneumothorax). Cough, haemoptysis and fever may
be present in both respiratory and cardiac disorders.
The extent of the physical examination will obviously depend upon the circumstance but should always involve a
thorough examination of chest and the cardiovascular system. Clubbing of the fingers is seen in congenital heart disease,
bacterial endocarditis, bronchiectasis, bronchial carcinoma, tuberculosis and disorders which give rise to progressive
pulmonary fibrosis.
2.3. WHEEZE
When a patient complains of wheeze it is important first to discover what this term means:
Some patients use it merely to describe noisy and laboured breathing while others apply it to rattling of secretions in
the upper air passages. Wheeze should, however, be applied only to the musical sounds produced by the passage of air
through narrowed bronchi. It is invariably louder during expiration and is often confined to that phase of the respiratory
cycle. It is always more conspicuous during deep breathing and sometimes may become audible only when the depth of
respiration is increased. Many patients become too accustomed to wheeze that they cease to be aware of its presence until a
relative or friend draws attention to it.
Another sound is stridor.
Patients with stridor may describe it as wheeze. Care must be taken to distinquish between these two sounds because
stridor is usually caused by local obstruction of a major airway, a tumor or an inhaled foreign body, and thus demands urgent
investigation and treatment
2.4. COUGH
DEFINITION: an explosive expiration required for the self-cleaning of the lungs. It is a reflex act generaly arising from
stimulation of the mucosa of the airways. CAUSES OF COUGH
A. CAUSES IN RESPIRATORY TRACT:
laringo-tracheo-bronchitis (croup)
whooping cough
laryngitis
laryngeal neoplasm
acute bronchitis
chronic bronchitis
bronchiectasis
asthma
bronchial neoplasm
B. CAUSES IN THE LUNGS:
pneumonia
abscess
tuberculosis

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fibrosis
embolism C.
CARDIAC CAUSES:
cardiac failure - left ventricular failure
TYPES OF COUGH
The frequency, severity and character of cough are dependent on several factors including:
- the situation and nature of the lesion responsible for the cough
- the presence or absence of sputum
- coexisting abnormalities such as vocal cord paralysis, impairment ventilatory function and pleural pain
COUGH produced by stimuli arising in the pharyngeal mucosa occurs in pharingitis or may be caused by
secretion trickling down the posterior pharyngeal wall from the nasal sinuses. It is typically a persistent cough, but may be
paroxysmal.
COUGH arising in the larinx has a harsh barking quality and may be painful, especially in acute laryngitis. If a
vocal cord is paralysed, a cough, whatever its site of origin will cease to be as effective in clearing the respiratory tract of
secretion.
WHOOPING-COUGH is characterized by prolonged severe paroxysms culminating in a long, stridulous
inspiratory whoop produced by laryngeal spasm.
COUGH arising in the trachea is usually caused by tracheitis in which it is harsh, dry and painful at first,
becoming loose, productive and painless later.
COUGH caused by a malignant tumor partially obstructing the trachea is associated with stridor, persistent and at
times severe and suffocating. Such patients may become deeply cyanosed and even unconscious during paroxysms of
coughing.
COUGH of several different types may be produced by stimulation of nerve endings in the bronchial mucosa.
COUGH in acute bronchitis in the early stages sounds dry; later it becomes
loose and productive usually of purulent sputum.
COUGH in chronic bronchitis has other typical features: it is particularly
frequent and severe when the patient retires to bed at night and, even more so, on getting up in
the morning, because of sudden changes in posture and in the temperature and humidity of the
inspired air. Sleep is seldom disturbed by coughing, but most patients with chronic bronchitis
wake up in the morning with a wheeze and a sensation of tightness in the chest.
a chronic, non-productive COUGH occurs in bronchial asthma and diffuse
pulmonary fibrosis. The presence of other diseases such as rheumatoid arthritis, lupus
erytematosus or systemic sclerosis should remind one of the possibilities of cryptogenic
fibrosing alveolitis.
COUGH in bronchial carcinoma may be an early and persistent symptom. At
first it is frequent short dry cough, but later it may become more severe and distressing.
COUGH in bronchiectasis, uncomplicated by chronic bronchitis or asthma, is
characteristically loose and readily productive of sputum. Large amounts of sputum are
coughed up, particulary on rising in the morning. It may be brought on by changes in posture
-postural cough.
COUGH in pneumonia is dry and irritant at first, later becaming loose and
productive, frequent haemoptysis.
COUGH in acute pulmonary edema sedondary to left heart failure is generally
short, paroxysmal, persistent and exhausting. A paroxysm of coughing in an elderly patient
which wakes him from sleep may herald the onset of pulmonary edema.
DIAGNOSTIC APPROACH
Healthy individuals seldom cough unless exposed to noxious fumes or a dusty environment A persistent cough is
abnormal and enquiry should be made about its character, duration and any accompanying symptoms. An acute nonproductive cough, particulary if it is associated with sore throat or nasal discharge, is likely to be due to an upper respiratory
infection. In pneumonia the cough may be dry at first but it most cases it will eventually produce some purulent sputum.
Paroxysms of coughing ending in the high-pitched sound of inspiratory stridor due to laryngeal spasm is virtually
diagnostic of whooping cough.
A chronic non-productive cough occurs in asthma and diffuse pulmonary fibrosis.
A dry cough accompanied by hoarseness in a middle-aged adult is commonly due to chronic lanyngitis from
excessive smoking or overuse of the voice. Hoarseness persisting for more than a month should be investigated further, for it
may be due to laryngeal carcinoma or to involvment of the recurrent laryngeal nerve by a bronchial neoplasm.
A chronic productive cough is seen in chronic bronchitis, bronchiectasis, pulmonary tuberculosis and neoplasms of
the bronchus. In bronchiectasis large volumes of purulent sputum are coughed up, particularly on rising in the morning.
The timing of cough may throw some light on its probable cause. A persistent cough at night is commonly due to
obstructive airways disease but a paroxysm of coughing in an elderly patient which wakes him from sleep may also herald
the onset of pulmonary edema.
Associated symptoms such as fever and sweating would point to infection, whilst loss of weight would bring
tuberculosis or neoplasm on mind.

8 The
extent of the physical examination will obviously depend upon the age of the patient, the history and the likely pathology.
Finger clubbing is an important sign and should be sought. Common pulmonary causes include bronchiectasis, bronchial
neoplasm, tuberculosis, lung abscess and fibrosing alveolitis.
2.5. SPUTUM
DEFINITION
It is a result of expectoration. Expectoration represents elimination of the sputum from the tracheo-broncho-alveolar
territory by the act of coughing.
GENERALITIES
When a patient has sputum, information should be obtained as to amount, character, viscosity and taste or odour. If
it is important to obtain precise information about the amount of sputum, the patient should be given a graded container and a
24-hour collection is measured. Some patients deny cough while admitting to the presence of sputum, saving that they bring
it up merely by clearing the throat.
CHARACTER OF THE SPUTUM
This is seldom described accurately by the patient and, wherever possible, a specimen should be inspected by the
doctor. Apart from haemoptysis, there are four types of sputum: serous, mucoid, purulent and mucopurulent
Serous sputum - which is usually described by the patients as clear frothy, is seen in acute pulmonary edema, in
which it may acquire a pink colour through mixture with red blood cells, and in the rare condition of alveolar-cell carcinoma;
Mucoid sputum - which is a characteristic feature of chronic bronchitis, is usually described by patients as grey,
clear, or sometimes black (when it contains soot particles);
Purulent and mucopurulent sputum is usually described as yellow or green, but occasionally white sputum
proves on inspection to be purulent. The term "dirty spit" used by many patients is misleading as it may refer either to
purulent sputum or to mucoid sputum containing soot particles. Mucoid sputum may be copious and frothy in some cases of
chronic bronchitis and asthma
Hysterical patients may spit out large amounts of saliva which they claim to be sputum.
Viscosity - mucoid sputum is often more viscous than purulent sputum and for that reason is more difficult to cough
up. Sputum is particularly viscous in the early stages of pneumococcal pneumonia and in severe asthma. Serous sputum is
watery with a low viscosity;
TASTE OR ODOUR
When described as "nasty" the patient may merely be referring to the normal taste of purulent sputum only when
terms such as offensive, nauseating or putrid are used can it be assumed that sputum is fetid (as in bronchiectasis or lung
abscess with anaerobic bacterial infection). The observer's own sense should be used to assess odour.
2.6. HAEMOPTYSIS
DEFINITION: coughing up of blood as a result of bleeding from the respiratory tract
GENERALITIES
Haemoptysis, particularly if an appreciable quantity of blood or if recurrent, is a frightening and potentially fatal
event and all diagnostic resources must be used to establish the etiology. More than two tea spoons of bright red blood is
omnious because it suggests severe hemorrhage. Not only the quantity but the precise location of the bleeding must be
determined. Haemoptysis must be differentiated from hematemesis and from blood or hemorrhagic exudate dripping into the
tracheobronchial passage from the nose, mouth or nasopharynx. Although most patients realise whether blood has been
coughed up or vomited, haemoptysis is occasionally confused with hematemesis.
The history, physical examination, and chest X-ray usually define the more obvious causes of hemoptysis such as
trauma, tumor, tuberculosis, bronchiectasis, heart failure, or pulmonary infarction (embolism).
A. Laringeal causes of haemoptysis and pharingeal:
- lymphoma
- carcinoma
- tuberculous ulceration
B. Tracheal and in the large bronchi:
- benign or malignant primary tumor
- teleangiectasia
- erosion by an aortic aneurysm
- brochogenic cyst
- broncholithiasis
- erosion by a caseocalcific node
- erosion by a tumor from nodes, esophagus or other mediastinal structures
- severe acute bronchitis
-trauma
C. Smaller bronchial structures:
- carcinoma
- adenoma (carcinoid or cylindromatous)
- acute bronchitis

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- bronchiectasis
- bronchopulmonary sequestration
- chronic bronchitis
D. Pulmonary parenchyma:
- primary or metastatic tumor
-infarct
- abscess
- active granulomatous disease (tuberculosis, funga, parasitic, luetic)
- fungus ball (aspergillus) in an old cavity
- acute pneumonia
- idiopathic hemosiderosis
- Good Pasture's syndrome
E. Cardiovascular:
- left ventricular failure
- mitral stenosis
- pulmonary embolism/infarct
- primary pulmonary hypertension
- pulmonary arteriovenous fistula
- atrial myxoma
- fibrous mediastinals with pulmonary vein obstruction
- aortic aneurysm with leakage into the pulmonary parenchyma
F. Clotting defects:
- thrombocytopenia
- vitamin K - dependent factors: prothrombin (II), Stuart factor (X), factor (VH), Christmas factor
(IX)

- diffuse intravascular coagulation

- heparin therapy
- fibrinolytic therapy: urokinase, streptokinase

- miscellaneous congenital coagulation defects.

The most important causes of haemoptysis are:
pulmonary tuberculosis
broncho-pulmonary neoplasm
pulmonary abscess pneumonia
acute pulmonary edema mitral
stenosis pulmonary infarction
thoracic traumatism haemorrhagic
syndrome periarteritis nodosa
TYPES OF HAEMOPTYSIS
FRANK HAEMOPTYSIS, in which the material coughed up consists wholly of blood, occurs most commonly in
bronchiectasis, pulmonary infarction and tuberculosis. A rough estimation should be made of the amount of blood lost,
bearing in mind that most patients tent to overestimate this.
BLOOD-STAINED SPUTUM, in which the blood and sputum are intimately mixed in various proportions, occurs
in bronchial infections and suppurative pneumonia.
BLOOD-STREAKED SPUTUM, in which streaks or specks of blood are present in mucoid or purulent sputum, is
a fairly frequent symptom in bronchial carcinoma and chronic bronchitis.
RUSTY SPUTUM, in which degraded products of haemoptysis give the sputum a colour varying between rust and goldenyellow, is a common feature of pneumococcal pneumonia and occurs in few other coditions. DIAGNOSTIC APPROACH
This will depend to some extent upon the severity of the blood loss. Profuse haemorhage is uncommon and the
patient may die rapidly of asphyxiation, before a diagnosis can be made. In such cases immediate bronchoscopy is vital for
this will enable the airways to be cleared of blood and the source of bleeding to be identified.
In young adults the most likely cause of massive haemoptysis is acute pulmonary tuberculosis; less commonly it is
due to a lung abscess or bronchiectasis.
In older patients it may arise from a bronchial neoplasm, chronic cavitated pulmonary tuberculosis or a mycetoma. Rarely, it
may be due to a necrotising vasculitis, as in Goodpasture's syndrome, or to a haemorrhagic pneumonia where the infection is
accompanied by some gross disturbance of the clotting mechanism such as occurs with disseminated intravascular
coagulation.
Fortunately the haemoptysis is less severe in most patients and may only amount to the expectation of some bloodtinged sputum. There is time to take a careful history of past illnesses, smoking habits, current state of health and any
accompanying symptoms.

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In the young, tuberculosis remains the most likely cause but this one and bronchiectasis may both present with
malaise, fever, loss of weight and a productive cough. There is often a history of previous respiratory illnesses, or of a contact
with a known case of tuberculosis at work or in the iamily.
During pregnancy and in femals on the contraceptive pill the possibility of pulmonary embolism should always be
kept in mind.
The same applies to all post-operative patients and those who have been confined to bed with major illnesses. The
haemoptysis is likely to have been preceded or accompanied by pleuritic pain and some shortness of breath. Similar
symptoms will be seen in pneumonia but frank haemoptysis will favour embolism.
A small haemoptysis in a middle aged or elderly subject with a smoker's cough may be the first indication of the
presence of a squamos cell carcinoma or pulmonary tuberculosis; chronic bronchitis should never be accepted as an adequate
explanation without further investigation.
Examination of the patient is essential for the diagnosis procedures.
mil THE PHYSICAL EXAMINATION OF RESPIRATORY SYSTEM
3.1. THE EXTERNAL FEATURE OF RESPIRATORY DISEASE
Initial impression: there are a number of features which may have become evident during the course of history-taking and
should immediately cause the observer to suspect respiratory disease. There are some important elements: -cough
- wheeze and stridor
- laboured breathing
- abnormality of the voice
- to foetor of the breath (which can suggest an anaerobic infection of the lung)
-state of nutrition
3.2. GENERAL INSPECTION
Cyanosis
Central cyanosis of respiratory origin is most frequntefy seen in chronic obstructive airways disease. In such cases peripheral
vasodilatation leads to warm blue hands, but the colour of the tongue is a more reliable indicator of central cyanosis.
It may also he present in:
- pneumonia
- bronchial asthma
- pulmonary infarction
- fibrosing alveolitis
- sarcoidosis
Peripheral cyanosis affecting the face and the neck, and in some cases the upper limbs also, is one of the features of
superior vena cava obstruction.
Edema
The detection of peripheral edema in patients with chronic obstructive airways suggests the development of right
ventricular failure.
Edema of a different distribution is seen in obstruction of the superior vena cava.
This condition is a fairly common complication of bronchial carcinoma, but may also occasionally be caused by a
large benign tumor. Obstruction of superior vena cava is manifested by:
- grossly external jugular veins without venous pulsation
- dilated veins and venules on the anterior and lateral aspects of the chest wall
- swollen face and neck
- conjunctival edema (chemosis)
Clubbing of the fingers
The phenomenon occurs in a variety of respiratory, cardiovascular and alimentary diseases, including: 1.bronchial carcinoma and certain other intrathoracic tumors
- bronchiectasis
- pulmonary abscess and empyema
- fibrosing alveolitis
2.- cyanotic congenital heart disease
- infective endocarditis
3.- the malabsorbtion syndrome 4.
- Crohn's disease
- ulcerative colitis
- hepatic cirrhosis

11
It has also been observed as a familial trait and may occur unilaterally in association with an aneurysm of the
subclavian artery.
Examination of the eves:
- Horner's syndrome, phlyctenular keratoconjunctivitis which may be a manifestation of primary
tuberculosis
- iridocyclitis which may be seen in tuberculosis or sarcoidosis
- chemosis and dilatation of the conjunctival and retinal veins are very common in secondary hypercapnia
to chronic obstructive airways disease
Examination of the scalene lymph nodes
These nodes are often involved when a pathological process, such as carcinoma, lymphoma, sarcoidosis or
tuberculosis affects the mediastinal nodes, and aspiration or biopsy of enlarged scalene node may provide information of
conclusive diagnostic value.
Nodes which are greather then 0,5cm in diameter, firm in consistence and round in shape are usually of pathological
signifiance, many of them containing metastatic deposits from a bronchial carcinoma.
Large, fixed masses are present in some of these cases. Hard, crraggy nodes may be caused by healed and calcified
tuberculosis.
3.3. EXAM1NA TION OF THE CHEST
Physical examination of the chest makes use of the tehniques of inspection, palpation, percussion and auscultation.
3.3.1. INSPECTION AND PALPATION
1. Abnormalities in the shape of the chest. Those of clinical importance are as follows:
The anteroposterior diameter may be increased as compared to the lateral diameter. In normal subjects the ratio is
usually about 5:7, and in flat-chested patients without respiratory disease, it may be as low as 1:2.
In some patients with emphysema, however the two measurements may approximate - barrel-chest. Chest deformity
in emphysema is not a reliable clue to the severity of the functional defect. It is seen most frequently in patients who have
developed chronic respiratory disease (bronchitis or asthma) relatively early in life.
-Pectus carinatum (pigeon chest) is a common sequel to chronic respiratory disease in childhood. It
consists of a localised prominence of the sternum and adjacent costal cartilages, often accompanied, by indrawing
symmetrical horizontal grooves above the margins, which are themselves everted. These deformities are though to result
from lung hyperinflation with repeated strong contractions of the diaphragm while the bony thorax is still in a pliable state.
- Pectus excavatum (funnel-chest) is a developmental defect in which there is either a localised
depression of the lower end of the sternum, or, less commonly, depression of the whole length of the body of the sternum and
of the costal cartilages attached to it. This produces displacement of the apex beat to the left, and the ventilatory capacity of
the lungs may be restricted when there is a very marked degree of depression of the sternum.
- Thoracic kyphoscoliosis ranges in degree from the minor changes in spinal curvature seen in may
otherwise healry subjects to grossly disfiguring and disabling deformities. Severe kyphoscoliosis may have profound effects
on pulmonary function as the chest deformity reduces ventilatory capacity of the lungs and increases the work of breathing.
Many such patients develop hypoxaemia, hypercapnia and heart failure at an early age.
- Thoracic operation, particularly thoracoplasty, may result in a considerable degree of chest deformity, of
which scoliosis may be an important secondary failure.
2. Lesion of the chest wall. Combined inspection and palpation of the whole chest wall is essential for the detection
of abnormalities which may include:
- cutaneous lesion, e.g. skin eruption, sarcoid or other nodules, purpuric spots, bruises, scars, discharging
sinuses.
- subcutaneous lesion, e.g. inflammatory swellings, metastatic tumor, nodules, neurofibromas, lipomas
- subcutaneous emphysema (air in the subcutaneous tissues) may cause diffuse swelling of the chest wall,
the neck and in some cases the face. The condition is recognised by the characteristic crackling elicited by palpation of the air
containing tissues.
- vascular abnormalities, e.g. spider teleangiectasis, enlarged vascular channels
- localised preeminences and deformitis involving clavicles, scapulae, sternum, ribs, costochondral
junctions and spinous processes
- localised tenderness on palpation, e.g. from a fractured rib, from tumors invading the chest wall, from
spinal injury or in association with pleural or nerve root pain
- lesions of the breasts and enlargement of the axilary lymph nodes.
3. The observation of respiration movements
a. Respiratory frequency
The number of breaths is counted by surreptitiously observing the movements of the chest wall, with the fingers
held on the pulse to avoid drawing the patient's attention to breathing.
The normal frequency at rest in a healthy adult is about 14 respirations per minute. The rate is increased in a variety
of pathological states, including pyrexia from any cause, acute pulmonary infections, particularly those accompanied by

12
pleural pain, and conditions in which there is a sudden increase in the work of breathing: bronchial asthma and acute
pulmonary edema.
b. Respiratory depth
In massive pulmonary embolism and in metabolic acidosis, usually due to diabetic ketosis, or uremia, pulmonary
ventilation at rest may be considerably raised. This can be recognised clinically by an increase in the depth of respiration
which may give rise to the subjective of dyspnoea.
In periodic or Cheyne-Stokes breathing there is a clinical variation in the depth of respiration, with periods of
overventilation alternating with complete apnoea. This occurs in left ventricular failure and in certain neurological
conditions.
Overventilation may also occur in patients who are unconscious as a result of severe brain caused by trauma,
haemorrhage or infarction.
c. Maximum chest expansion
This is estimated by placing a tape measure round the lower third of the chest and recording the maximum
inspiratory/expiratory difference in the chest circumference.
Chest expansion is diminished in almost every type of diffuse, broncho-pulmonary disease, e.g. bronchial asthma,
emphysema and pulmonary fibrosis, and in conditions which restrict movement of die ribs, such as ankylosing spondylitis.
d. Mode of breathing
Women make more use of the intercostal muscles then of the diafragm and their respiratory movements are
predominantly thoracic.
Men, on the other hand, rely more on the diaphragm and their respiratory movements at rest are abdominal. Babies
of both sexes are also diaphragmatic breathers.
If respiratory movements are exclusively thoracic this indicates that diaphragmatic movement is inhibited by pain
caused, for example, by peritoneal irritation, or restricted by increased intraabdominal pressure in conditions such as ascities,
gazeous distension of the bowel, a large ovarian cyst or pregnancy.
If respiratory movements are exclusively abdominal, ankylosing spondylitis, intercostal paralysis or pleural pain
may be responsable for the lack of chest expansion.
c Methods of comparing range of movement of the chest wall
The object of these procedures is to detect differences in the range of movement on the two sides of the chest.
1. Respiratory movement in the infraclavicular regions is compared by inspecting the chest with
the patient supine and the head resting on a pillow. The observer views the infraclavicular regions tangentially and asks the
patient to take steady deep breaths. By this techique unilateral impairement of chest wall movement can usually be
recognised. Breathless patients should not be examined in this way because their distress is increased if they lie flat.
2. Respiratory movement at the costal margins can also be accurately gauged by inspection if the
patient is thin. In other cases, however, palpation in the only tehnique avaible for this purpose. The sides of the chest are
grasped with the fingers in such a way as to approximate the tips of the outstreched thumbs in the region of the xiphoid
process. The hand should be adjusted to ensure that there is a loose fold of skin between the two thumbs so that they can
move apart as the chest expends. The movement of the two thumbs with deep breathing can then be used to estimate the
relative degree of movement on the sides.
3. Respiratory movement of the lower ribs posteriorly, where inspection is seldom helpful, have to
be estimated by a similar technique. With the patient sitting erect the chest is grasped from behind with the two hands and the
tips of the outstretched thumbs are brought together in the region of the tenth thoracic spine.
f. The significance of reduced movement
Unilateral reduction of chest wall movement occurs in many types of respiratory disease.
In pleural effusion and emphysema, movement may be absent, and if the lesion has persisted for some weeks
retraction of the ribs and intercostal spaces may produce flattening of the affected side of the chest. Less marked reduction
of movement occurs in pulmonary consolidation and collapse.
- in pneumothorax the limitation of movement is related to the amount of air in the pleural space; in tension
pneumothorax the affected side of the chest may be immobilised in a position of almost full inspiration.
- in bronchial asthma, emphysema and diffuse pulmonary fibrosis movements of the chest wall are
symmetrically reduced.
g. Vocal fremitus
This crude test provides no information that is not obtained by vocal resonance. It is perfomed by placing the palm of the
hand on equivalent areas of the chest wall and asking the patient to say "one, one, one" or "33, 33, 33". h. Palpable
accompaniments
The vibrations from a low pitched rhonchus or a coarse pleural rub can occasionally be detected by a hand placed on
the chest wall.
In such cases an unusually loud rhonchus or rub is invaribly present on auscultation and there is seldom any
difficulty in distinquishing between the two.
A palpable rhonchus generally has its origin in a large bronchus and, if persistent and unilateral, it suggests partial
bronchial obstruction by a tumor or a foreign body.
3.3.2. PERCUSSION

13
The object of percussion is to compare the degree of resonance over equivalent areas on the two sides of the chest,
and to map out any area in which the percussion note is abnormal.
Fig. 18/8 116
The percussion note has normal resonance whenever aerated lung tissue is separated from the chest wall by pleural
fluid or thickening, or when lung tissue is rendered airless by consolidation, collapse or fibrosis. Over such lesions the
percussion note is impaired or dull. The most marked degree of dullness on percussion is found over a large pleural effusion.
Fig. 22a/23/24 p 118/119
Percussion over a solid organ such as the heart or the liver will elicit a dull note, but the area of dullness is always
less extensive than would be expected from anatomical surface marking since aerated lung is interposed between part of the
organ and the chest wall.
A hyperresonant percussion note may be found over a large thin walled pulmonary cavity, over a pneumothorax,
particulary if the pleural pressure is above atmospheric level, and also over lung wich is markedly emphysematous. An
apparent finding of generalised hyperresonance must, however, be accepted with reserve since a change in the absolute pitch
of percussion note is always difficult to recognise and may depend mainly upon the thickness of the chest wall. For that reson
it is not usually advisable to attempt to distinguish between normal resonance and hyperresonance when the percussion note
is equally resonant on the two sides. The sound produced by percussion over a hollow organ is described as tympanitic.
TECHNIQUE OF PERCUSSION
The basic technique of percussion is as follows:
1. the left hand is placed on the chest wall, palm downwards and with the fingers slightly separated, so that
the second phalanx of the middle finger is precisely over the area to be percussed.
2. the middle finger of the left hand is then pressed firmly against the chest wall and the centre of its second
phalanx is struck shapfy with the tip of the right middle finger. In order to produce a satisfactory percussion note the right
middle finger must be held at a right angle (to produce a "hammer" effect) and the entire movement must come from the wrist
joint.
The positions in which the percussion note on the two sides should be compared are as follows:
Fig. 9/117
ANTERIOR CHEST WALL
Clavicle infraclavicular region
Second to sixth intercostal spaces.
Fig. 22b/118
LATERAL CHEST WALL
Fourth to seventh intercostal spaces.
Fig. 21/117
POSTERIOR CHEST WALL
Trapezius, percussing downwards on lung apex. Above spine of scapula. At intevals of 4 to 5 cm from below spine
of scapula down to eleventh rib.
The technique of clavicular percussion which may be of value in detecting lesions of the upper lobes, differs from
that used elsewhere in the clavicles can be percussed directly with the right middle finger or if preferred, with the right index,
middle and ring fingers held closely together.
The lung apices are percussed by placing the left middle finger across the anterior border of the trapezius,
overlapping the supraclavicular fossa, and directing the percussion downwards.
3.3.3. AUSCULTATION
Auscultation of the lungs has an important place in the diagnosis of certain respiratory diseases but is of little or no
value in others. In bronchial asthma and pleuresy, for example, the stethoscope provides information of positive diagnostic
value which can not be obtained in any other way. In contrast, auscultation is unhelpful in the early diagnosis of pulmonary
tuberculosis, which may reach an advanced stage before any abnormality can be detected.
TECHNIQUE OF AUSCULTATION
Auscultation should be carried out with the patient relaxed, breathing deeply and fairly rapidly. The mouth should be
kept wide open and the patient should be specifically asked not to purse the lips during expiration. It should be borne in mind
by the beginner that prolonged deep breathing may cause giddiness or even tetany.
The following information can be obtained from auscultation:
1. the type and amplitude of the breath sounds
2. the type and number of any added sounds and their position in the respiratory cycle
3. the quality and amplitude of the conducted voice sounds. A.
BREATH SOUNDS AND VOICE SOUNDS
Breath sounds are produced by vibration of the vocal cords caused by the turbulent flow of air through the larynx
during inspiration and expiration. The sounds so produced are transmitted along the trachea and bronchi and through the
lungs to the chest wall.
Diseases of the bronchi, lungs and pleura may alter the breath sounds in three main ways: 1.
Diminished vesicular breath sounds

14 If the
conduction of the breath sounds to the chest wall is attenuated by airflow limitation (as in bronchial asthma, or local, as
when a large bronchus is obstructed by a tumor) or by a shallow pneumothorax, a small pleural effusion or pleural thickening,
they remain vesicular but are diminished in amplitude.
2. Bronchial breath sounds
If the lung tissue through which the breath sounds are transmitted from the air passages to the chest wall has lost its
normal spongy consistence and has become firm or solid e.g. in consolidation of fibrosis, the sounds picked up by the
stethoscope resemble more closely those produced at the larynx than those heard over normal lung.
Voice sounds (vocal resonance) conducted through consolidated lung tissue also resemble more closely those
produced at the larynx than those heard over normal lungs, or that they are louder and more distinct In some cases the
whisperead voice may be transmitted almost without distorsion, so that individual syllables can be clearly recognised
(whispering pectoriloquy).
High-frequency sounds are selectively conducted throught consolidated lung tissue, high-pitched bronchial breath
sounds are heard in lobar or segmental pneumonia.
Fibrotic lung tissue, on the other hand transmits sounds of lower frequency and thus produces low-pitched bronchial
breath sounds.
When bronchial breath sounds traverse air-containing cavities in their passage to the chest wall, they may
occasionally acquire a resonating amphoric quality, resembling the sound produced by blowing across the top of bottle.
3. Intermediate breath sounds
Breath sounds may be intermediate in type between vesicular and bronchial, for example, vesicular with prolonged
expiration.
This type is heard commonly in the presence of diffuse pulmonary fibrosis, chronic bronchitis and emphysema.
B. ADDED SOUNDS
Added sounds heard on auscultation of the chest are therefore of three types: rhonchi, crepitations and pleural
sounds.
1. Rhonchi. These are musical, high, medium or low pitch sounds produced by the passage of air through
narrowed bronchi. Rhonchi caused by mucosal edema or spasm of the bronchial musculature are usually superimposed upon
the expiratory phase of the respiratory murmur, which is always prolonged when rhonchi are present.
Rhonchi heard during inspiration are more often due to secretion in the large bronchi and may disappear, or at least
become less numerous after coughing. A constant low-pitched rhonchus (fixed rhonchus) usually indicates partial obstruction
of a major bronchus by a local lesion in a large bronchus, such as a tumor or an inhaled foreign body.
2. Crepitations. These are non-musical sounds, called crackles by some clinicians, mainly audible during
inspiration.
A frequent cause of crepitations in lung disease is the explosive reopening, during inspiration of peripheral small
airways which have become occluded, during expiration. These crepitations are most numerous during the second half of
inspiration and in some cases confined to the last part of the breath (in end-inspiratory crepitations). Such crepitations are not
influenced by coughing, and are more conspicuous over the lower parts of the lungs because in the upright position small
airway closure is more liable to occur mere than in the upper lobes.
Another distinct type of crepitation may be heard or heard over a pneumothorax when fluid is present in the pleural
space. These sounds, which have a thickling quality usually indicate that the air in the pneumothorax is under tension and are
often audible only during coughing, which creates the sounds by agitating the fluid in the pleural space.
3. Pleural sounds. A pleural rub is a leathery or cracking sound produced by movement of the visceral
pleura over the parietal pleura, when both surfaces are roughened as by fibrinous exudate. It is usually heard at two separate
stages in the respiratory cycle, towards the end of inspiration and just after the beginning of expiration. A pleural rub may be
inaudible during normal breathing but can be heard when the patient is asked to breathe deeply.
It is sometimes, difficult to distinguish between a low-pitched rhonchus, coarse crepitations and a pleural rub. If
there is any doubt as to the nature of sound auscultation it should be repeated after a forceful cough, when rhonchi or
crepitations will usually alter in character or disappear, while a pleural rub will remain unchanged.
THE INTERPRET A TION OF A VSCUL TA TORY FINDINGS
1. high-pitched bronchial breath sounds are heard in areas of pneumonic consolidation, over a collapsed
lung or lobe when the large bronchi are patent, over some large superficial pulmonary cavities, and sometimes over a lung
compressed by a large pleural effusion or a tension pneumothorax. In all these conditions when bronchial breath sounds are
audible the voice sounds are louder than normal and whispering pectoriloquy is present.
2. low-pitched bronchial breath sounds are heard over localised areas of pulmonary fibrosis, e.g. in chronic
pulmonary tuberculosis, chronic suppurative pneumonia or bronchiectasis. In all these conditions the vocal resonance is
louder and more distinct, and whispering pectoriloquy usually present.
3. breath sounds are diminished or absent over a pleural effusion thickened pleura, a pneumothorax or a
collapsed lung, lobe or segment where the major bronchus supplying it is obstructed. The breath sounds are symmetrically
diminished over both lungs in emphysema in these conditions the vocal resonance is decreased in amplitude to the same
degree as the breath sounds are diminished.
4. rhonchi are heard diffusely over both lungs in bronchial asthma and in most cases of acute and chronic
bronchitis. In asthma the rhonchi are typically expiratory and medium or high pitched and are mainly heard during expiration
which is prolonged. In bronchitis they are usually low and expiratory. A localised rhonchus may be heard over a partially
obstructed large bronchus. If the obstruction is caused by a fixed lesion, such as a tumour or foreign body in large bronchus,

15
the rhonchus is usually louder during inspiration, is not altered by coughing and is often accompanied by stridor. If due to
secretions, these are usually removed by coughing, which causes the rhonchus to disappear.
5. crepitations caused by secretions within the larger bronchi in acute or chronic bronchitis, or in resolving
bronchopneumonia, are widespread and bilateral, while those audible over resolving lobar or segmental pneumonic
consolidation, dilated bronchi (bronchiectasis), lung abscesses or tuberculous cavities are localised to the site of the lesions.
In all these conditions they are audible throughout inspiration, and alter after coughing. Crepitations in other parenchymal
lung conditions, such as interstitial pulmonary edema, allergic and fibrosing alveolitis and perhaps early pneumonic
consolidation and miliary tuberculosis, are in contrast audible mainly during the second half of inspiration, and are
uninfluenced by coughing.
6. a pleural rub is heard over areas of pleurisy. It disappears as soon as the visceral and parietal pleura are
separated by fluid, but often remains audible above an effusion. If pleurisy involves the pleura adjacent to the pericardium, a
pleuro-pericardial rub may also be heard. This is a rather misleading term since the pericardial element in the sound is not due
to pericarditis. It is caused merely by roughened pleural surface adjacent to the pericardium being moved across one another
by cardiac pulsation. A pleuro-pericardial rub may, in some cases, be impossible to be distinguished from a pericardial rub.
IIV1. RESPIRATORY SYNDROMES
4.1. BRONCHIAL SYNDROMES
4.1.1.ACUTE BRONCHITIS
DEFINITION
It is an acute inflammation of the tracheobronchial tree, generally self limited and with eventual complete healing and return
of function. ETIOLOGY
- acute infectious bronchitis, most prevalent in winter
- acute irritative bronchitis may be caused by various mineral and vegetable dusts
SYMPTOMS AND SIGNS
Acute infectious bronchitis is often preceded by symptoms of upper respiratory infection: coryza, malaise,
chilliness, slight fever, back and muscle pain, and sore throat.
Onset of cough usually signals onset of bronchitis.
The cough is initially dry and nonproductive, but small amounts of viscoid sputum are raised after a few hours or
days.
The sputum later becomes more abundant and mucoid or mucopurulent Obvious, purulent sputum suggests
superimposed bacterial infection.
In a severe uncomplicated case, fever to 38,3 or 38,9 C may be present for up to 3 or 5 days, following which acute
symptoms subside (though cough may continue for 2 to 3 weeks). Persistent fever suggests complicating pneumonia.
Dyspnoea may be noted secondary to the airways obstruction.
Pulmonary signs are few in uncomplicated acute bronchitis.
Scattered sibilant or sonorous rhonchi may be heard, as well as occasional crackling or moist rales at the bases.
Wheezing, especially after cough, is commonly noted.
Persistent localized signs suggest development of bronchopneumonia. Serious complications are usually seen only in
patients with an underlying chronic respiratory disorder. In such patients, acute bronchitis may lead to severe blood gas
abnormalities (acute respiratory failure).
DIAGNOSIS
Diagnosis is usually possible on the basis of the symptoms and signs, but a chest X-ray is to rule out. Other diseases
or complications are suspected, if symptoms are serious or prolonged. Arterial blood gases should be monitored when serious
underlying chronic respiratory disease is present. In cases that do not respond to antibiotic therapy, or in special
circumstances such as immunosuppresion, Gram stain and culture of sputum should be done for specific etiologic diagnosis.
4.1.2.CHRONIC BRONCHITIS
DEFINITION
Chronic bronchitis represents a progressive and unspecific chronic inflammation of the bronchi and bronchioles, which is
clinically manifest by cough with expectoration at least 3 months per year, two years successively. ETIOLOGY In this
etiology are involved many factors, but none of them can explain all the clinical manifestations:
- irritant factors (tobacco), industrial factors, physical, chemical factors, infectious factors and allergic
factors.
CLINICAL FEATURES
The chief symptom is a persistent cough with the expectoration of mucoid or mucopurulent sputum. Cough in
chronic bronchitis tends to occur in prolonged paroxysms, which usually culminates in the production of sputum. Bouts of
coughing in these patients often produce severe dyspnoea, frequently accompanied by wheezing, and might be very

16
distressing. Cough is particularly frequent and severe when the patient retires to bed at night and, even more so on getting up
in the morning. Most patients with chronic bronchities waken in the morning with a wheeze and a sensation of tightness in the
chest
Mucoid sputum, which is a characteristic feature of chronic bronchitis, is usually described by patients as grey,
clear, or sometimes black (when it contains soot particles). Blood-streaked purulent sputum is occasionally seen in chronic
bronchitis.
Dyspnoea may be denied but the capacity for exertion is progressively impaired. With the development of
emphysema this becomes more prominent than the cough except during acute exacerbations.
On examination the chest may appear barrel - shaped and respiratory movements are poor.
Rhonchi will be audible throughout the lung and fields and may be accompanied by wheezing.
In an advanced case cyanosis and finger clubbing are present.
DIAGNOSIS is usually based on the clinical features but examination of the sputum, a chest X-ray, spirometry and
in particulary cases bronchoscopy are also helpful.
4.2. CONSOLIDATION SYNDROMES
The consolidation syndromes can be divided into two categories:
A. CONSOLIDATION SYNDROMES WITH FREE BRONCHI
a. consolidation by inflammatory processes - pneumonia
b. consolidation by tumoral process - tumors of the lung
c. unretractable consolidation syndrome - thromboembolism and infarction
B. CONSOLIDATION SYNDROMES WITH OBSTRUCTED BRONCHI - ATELECTASIS.
A. CONSOLIDATION SYNDROMES WITH FREE BRONCHI
The most common cause is lobar pneumonia, which may be the result of a variety of bacterial infections. The signs
of consolidations may occasionally be found over a lung abscess or a large area of pulmonary embolization. Consolidation is
infrequent in viral infections. Signs of consolidations may be found at times over areas of confluent bronchopneumonia,
which is as usual characterized by one or more patches of pneumonia.
The signs of consolidation are:
- limitation of lung expansion of the side involved, often palpable limitation of expansion
- increase of vocal fremitus
- dull percussion note
- bronchial breath sounds with fine or medium rales at the end of inspiration. Bronchophony and
pectoriloquy may be heard, and occasionally egophony is present. A friction rub is occasionally audible.
a. Consolidation by inflammatory processes - pneumonia
Pneumonia is an acute infection of the parenchyma (alveolar spaces and/or interstitial tissue) of the lung.
Pneumonia can be bacterial or viral.
Pneumococcal pneumonia, the most common bacterial pneumonia, is usually lobar but it may be segmental.
SYMPTOMS AND SIGNS
- onset is usually sudden, with a shaking chill, sharp pain in the involved hemitorax (pleurisy), cough with
early sputum production, fever and headache.
- dyspnoea is frequent, respiration is rapid (25 to 45/min)
- delirium may occur, especially in alcoholic patients, when fever is high or cyanosis is marked
- the patients are cyanotic and sweating profusely
- the temperature rises rapidly to 38 to 40,5 C. The pulse accelerates to between 100 and 130.
Signs of consolidation involving part of one or more lobes are found.
The cough, initially dry, usually occurs in extremely rjainful paroxysms.
The sputum, pinkish or blood-flecked at first, becomes rusty at the height of the illness, then yellow and
mucopurulent during resolution.
Herpes infection is often present, usually in the lips and face.
Physical signs are moist rales initially, with evidence of consolidation later.
Streptococcal pneumonia
ETIOLOGY
Hemolytic streptococci of Lancefield's group A are the most common organisms, though other streptococci are
occasionally responsible. The disease is now infrequently seen except as a complication of measles or influenza.
SYMPTOMS, SIGNS AND DIAGNOSIS
The disease, which occured in epidemics in military camps in both world wars, usually begins with a sore throat,
accompanied or followed by laryngitis and tracheobronchitis with presternal soreness and pain on coughing.
It spreads by way of the bronchial and pleural lymphatics, producing bronchopneumonic lesions and pleural
effusion. Toxemia is often pronounced.
Early in the course of the pneumonia, presence of a large pleural effusion, frequently bloody, suggests a
streptococcal pneumonia.
A history of recent pharingitis, measles, or influenza, with early development of emphysema is suggestive.

17
Diagnosis is confirmed by demonstration of streptococci in sputum, blood, and pleural exudate. The gross appearance
of sputum is not of diagnostic significance, but stained smears may show chains of Gram-positive cocci that can be identified
by culture on blood AGAR.
Staphylococcal pneumonia
ETIOLOGY
Staphylococcal pneumonia is usually caused by coagulase-positive Staphylococcus Aureus. It is often a
complication of influenza, but may be primary, particularly in infants and the aged.
SYMPTOMS AND SIGNS
Some or all of the symptoms of Pneumococcal pneumonia (pleural pain, dyspnoea, cyanosis, productive cough) may
be present in varying degres of severity and in cases complicating influenza, may appear at any stage of the illness.
Sputum may be copious and salmon-colored. Prostration may be often marked.
Physical examination of the lungs frequently demonstrates patchy involvment of several pulmonary segments, but
lobar involvment may also occur. Pneumatoceles from <lcm to several cm in diameter, though common, may be difficult to
detect by physical examination. Leukocytosis is usually present
Furuncles are seen occasionally, and, if bacteremia occurs, metastatic abscesses may be found in the liver, kidneys,
brain, or elsewhere.
DIAGNOSIS
The symptoms and signs of pneumonia and a positive sputum or blood culture are of diagnostic value. Gram stain of
the sputum provides the earliest diagnostic clue.
X-ray early in the disease shows many small round areas of densities that later enlarge and coalesce to form abcesses
and leave evidence of multiple cavities or pneumatoceles during resolution.
Pneumonia caused by Klebsiella and by gram-negative intestinal bacili
ETIOLOGY AND PATOLOGY
Any of the more than 70 types of Klebsiella pneumonia (Friedlander's bacillus) may cause pneumonia, though
infection with type 1 or 2 is most common.
SYMPTOMS AND SIGNS
The findings are similar to those of Pneumococcal pneumonia, as above, though onset may be gradual and
bronchopneumonia is the usual type of pulmonary involvement. Pleural involvement is common and the course often is
fulminant. Signs of cavitation may develop and persist if the illness becomes chronic.
DIAGNOSIS
Patients with pneumonia caused by Klebsiella or other Enterobacteria usually are critically ill. The disease is
suspected in any patient with unusually rapid spread of consolidation from one lobe to another. Predisposing conditions
include alcoholism, diabetes mellitus, aspiration or immunosuppresive therapy.
In Friedlander's pneumonia, the sputum is viscid and "ropy", and may be "bricked' in colour, stain smears typically
show many encapsulated Gram-negative bacili. Blood culture is frequentiy positive.
Pneumonia caused by Hemophilus influenza
ETIOLOGY
Hemophilus influenza was one of the principal bacterial causes of the pneumonias complicating the influenza
pandemics of 1889 and 1918. H. influenzae is now an infrequent cause of pneumonia.
SYMPTOMS, SIGNS AND DIA GNOSIS
H. influenzae pneumonia usually follows common viral upper respiratory infections and is characterised by
bronchopneumonia, bronchitis and broncheolitis (almost never by lobar pneumonia with corresponding physical and X-ray
findings).
Symptoms include fever, cough that may be croupy, malaise, myalgias, arthralgia (in adults), and increase in
sputum, which may become yellow or greenish. Cyanosis may be marked, especially in infants and young children.
The characteristic small pleomorphic Gram-negative bacillus is usually seen in large numbers in Gram-stained
smears of sputum. Positive blood cultures confirm the diagnosis in some cases.
Viral pneumonia
ETIOLOGY: may be caused by various agents: Influenza and Parainfluenza viruses, adenoviruses.
SYMPTOMS AND SIGNS
Most cases of viral pneumonia are mild, and pulmonary involvment is often undetected.
Severe and even fatal illness may result especially in influenza.
Constitutional symptoms may be pronounced, with severe headache, anorexia, fever and myalgia. Sputum is usually
mucopurulent, occasionally bloody, and often contains many mononuclear cells.
Cough is common. Most viral lung infections are bronchopncumonic, frequently involving more than one
pulmonary segment.
b. Consolidation by tumoral processes
Tumors of the lung
ETIOLOGY AND INCIDENCE
The lungs are the site of origin of primary benign and malignant tumors and receive metastases from many other
organs and tissues.
SYMPTOMS AND SIGNS
Manifestations depend on the tumor's location and type of spread.

18 COUGH
usually is present in patient with chronic bronchitis, increased intensity and intractabihty of preexisting cough sugests a
neoplasm.
THE SPUTUM arising from an ulcerated bronchial tumor usually is not excessive.
COPIOUS BLEEDING strongly suggests invasion of large underlying blood vessels.
Bronchial narrowing may cause air trapping with localized wheezing, and commonly causes atelectasis with
mediastinal shift, diminished expansion, dullness to percussion, and loss of breath sounds.
INFECTION of obstructed lung produces fever, chest pain, and weight loss.
Persistent localized chest pain suggests neoplasic invasion of the chest wall.
Peripheral nodular tumors are asympthomatic until they invade the pleura or chest wall and cause pain or
metastasize to distant organs.
Late symptoms include weight loss and Horner's syndrome (due to invasion of the cervical thoracic sympathetic
nerves) and infiltration of the brachial plexus and the neighboring ribs and vertebrae occurs with apical tumors (Pancoast
syndrome).
A tumor may extend directly into the esophagus, producing obstruction, sometimes complicated by a fistula.
Phrenic nerve invasion may cause diaphragmatic paralysis (causing hoarseness). It is produced by extension of
tumor from neighboring lymph nodes.
In the superior vena cava syndrome (SVCS), obstruction of venous drainage leads to dilation of collateral veins of
the upper part of the chest and neck, edema and plethora of the face, neck and upper part of the thorax including breasts;
suffusion and edema of the conjunctiva; and CNS symptoms, such as headache, visual distortion, and disturbed states of
consciousness.
Intrapulmonary spread of primary and secondary cancer may cause lymphangitic carcinomatosis with subacute cor
pulmonale. Hematogenous nodular metastases within the lungs are common, but bronchial invasion by a secondary tumor is
rare. Hematogenous spread of primary lung neoplasm to the liver, brain, adrenals, and bone is common.
EXTRAPULMONARY MANIFESTATIONS of lung cancer are numerous. In hypertrophic pulmonary
osteoarhropathy, the best known, clubbing of the fingers and toes and periosteal elevation of the distal parts of the long bones
occur.
Other extrapulmonary manifestations (principally encephalopathy, subacute cerebellar degeneration,
encephalomyelitis, and peripheral neuropathy) occur at all levels of the syndromes due to production of substances.
Hormonal activity may develop.
OAT cell carcinomas may secrete ectopic ACTH or ADH and are associated with the carcinoid syndrome (flushing,
wheezing, diarrhoea, and cardiac valvular lesions).
Other endocrine syndromes associated with primary lung carcinomas include gynecomastia, hyperglicemia,
thyrotoxicosis, and skin pigmentation.
c. Unretractable consolidation syndrome
Thromboembolism and infarction syndrome
DEFINITION
Pulmonary embolism (thromboembolism) = lodgement of a blood clot in a pulmonary artery with subsequent
obstruction of blood suply to the lung parenchyma.
Pulmonary infarction: hemorrhagic consolidation (often followed by necrosis) of lung parenchyma resulting from
thromboembolic pulmonary arterial occlusion.
SYMPTOMS AND SIGNS
The clinical manifestations of pulmonary embolism are not specific. The symptoms and signs vary in frequency and
intensity depending on the extent of pulmonary vascular occlusion, the development of pulmonary infarction and the
patient's preembolic cardiopulmonary function.
Embolism without infarction is manifested by breathlessness.
Tachypnea is a consistent and striking feature. Anxiety and restlessness may be prominent. Cyanosis is usual in
patients with massive embolism. Wheezing may sometimes be heard, particularly if underlying bronchopulmonary or cardiac
disease is present.
The manifestations of pulmonary infarction include cough, haemoptysis, pleuritic chest pain , fever, and signs of
pulmonary consolidation or pleural fluid. A pleural friction rub may be heard.
B. CONSOLIDATION SYNDROMES WITH OBSTRUCTED BRONCHI
Atelectasis
DEFINITION
A shrunken and airless state of a part or of all of the lung; the disorder may be acute or chronic, complete or
incomplete.
Atelectasis is often accompanied by infection. The atelectatic lung is a complex mixture of airlessness, infection,
bronchiectasis, destruction, and fibrosis.
ETIOLOGY
- acute massive lung collapse is usually a postoperative complication
- in the middle lobe syndrome, a form of chronic atelectasis, middle lobe collapse usually results from
bronchial compression by surrounding lymph nodes
- partial bronchial obstruction in the presence of infection may also lead to chronic atelectasis.
CLINICAL FEATURES
Atelectasis may be either

19
- congenital
- functional
-acquired.
- Congenital atelectasis is the failure of the lungs to expand fully in the immediate neonatal period.
- Functional atelectasis results from the fact that the lungs may not completely inflate during ordinary quiet
respiration. Occasionally fine rales will be noted in the axilla and over the extreme lower margin of the lungs when the
patient breathes more deeply. These result from the inrush of air into small areas of unexpanded lung. After a few deep
breaths the involved areas will become fully expanded, and the rales will disappear. As a consequence these fine rales are
commonly called atelectatic rales. They are more frequently found in older patients or in those confined to bed.
- Acquired atelectasis may be either obstructive or compressive:
1. obstructive atelectasis is the result of some obstruction of the trachea or bronchi. It may be the result of
aspiration of a foreign body, tumor mass inside or outside the bronchi, or exudate. The fact that the bronchus or bronchi to
the affected area are obstructed will produce abnormal physical findings: diminished expansion over the area involved,
absence of vocal fremitus, dullness to percussion, absence of breath sounds, and absence of whispered and spoken voice
sounds. Rales will not be present since there is no significant flow of air to produce them.
When there is a large area of atelectasis, it is often termed massive collapse in which the heart may be displaced
toward the affected side.
2. compressive atelectasis is the result of compression of the lung by fluid or air in the pleural or
precordial space, a large intrathoracic tumor, or elevation of the diaphragm. In this instance where the bronchus is patent, the
physical findings will be limitation of expansion, decreased spoken voice sounds, and occasionally egophony. Rales may or
may not be heard. In some instances it will be noted that the heart will be displaced to the opposite side. Often the signs of
the condition producing the compression will predominate.
4.3. PULMONARY TUBERCULOUS SYNDROME
Its course is marked by gradual loss of weight, night sweats, fever, malaise and persistent cough with mucoid
sputum. Reccurrent small haemoptysis may be the first sign of the infection and such patients are fortunate for the alarm to
which this gives rise ensures prompt medical attention.
On the other hand the disease may be indolent with cough as the only prominent symptom.
Physical findings reveal a consolidation syndrome.
The condition is readily diagnosed on a chest X-ray which will show soft infiltrates in the apices of the lungs and
possibly cavitation in the upper lobes.
At least three specimens of sputum should be examined for tubercle bacilli and set for culture on Lowenstein-Jensen
media.
4.4. PULMONARY SUPPURATIVE SYNDROME
A. PRIMARY SUPPURATIVE SYNDROME: LUNG ABSCESS
B. SECONDARY SUPPURATIVE SYNDROME: BRONCfflECTASIA
A. PRIMARY SUPPURATIVE SYNDROME
Lune abscess
DEFINITION: a localized inflammatory lesion with necrosis of lung tissue and surrounding pneumonitis. The term
"gangrene of the lung" denotes a similar though more diffuse and extensive process in which necrosis predominantes.
A lung abscess may be putrid (due to anaerobic bacteria) or nonputrid (due to anaerobes or aerobes).
SYMPTOMS AND SIGNS
Onset may be acute or insidious.
Early symptoms are often those of pneumonia: malaise, anorexia, sputum - producing cough, sweats, chills, and
fever.
The sputum is purulent unless the abscess is completely walled off and it is frequently blood - streaked and
sometimes foul - smelling (putrid).
Severe prostration and a temperature of 39,4C or higher may be present.
Chest pain, if present, indicates pleural involvement.
Repeated chills in a patient with pneumonia suggest abscess formation.
Physical signs include a small area of dullness indicating localized pneumonic consolidation, and usually,
suppressed rather than bronchial breath sounds. Fine or medium moist rales may be present Though unusual with current
therapy there may be tympany and amphoric breathing if the cavity is large. An abscess may remain unsuspected until it
perforates a bronchus, when a large amount of purulent sputum, fetid or nonfetid, may be expectorated over a few hours or
several days.
The sputum may contain, gangrenous lung tissue; fever, anorexia, weakness, and debility are usually present but are
sometimes minimal if the disease is limited.
Dyspnoea occurs when the involvment is massive.
Failure of an area of pneumonia to resolve always suggests abscess formation, bronchial neoplasm or both.
B.SECONDARY SUPPURATIVE SYNDROME
Bronchiectasis

20
DEFINITION: a chronic congenital or acquired disease characterized by irreversible cylindrical, saccular, or
varicose dilation of the bronchi with secondary infection.
ETIOLOGY
Congenital bronchiectasis is a rare condition arising from agenesis of the alveoli with resultant cystic dilation of
the terminal bronchi.
Acquired bronchiectasis is often obscure. It can develop at any age but most often begins in early childhood.
KARTAGENER's syndrome (Situs inversus, sinusitis, and bronchiectasis), a condition in which an
abnormality in the cilial organelles results in defective mucociliary clearance that leads to suppurative bronchial infections
and bronchiectasis.
SYMPTOMS AND SIGNS
Vary widely from patient to patient, and in some patients from time to time, depending largely on the extent of the
disease and the amount of complicating chronic infection present.
Chronic cough and sputum production are the most characteristic and common symptoms. As the condition
progresses, the cough tends to become more productive and has a typical regularity, occurring in the morning on arising, late
in the afternoon, and on retiring.
Sputum may be abundant and may separate into three layers on standing: frothy in the top, greenish and turbid in the
middle, and thick with pus at the bottom.
Haemoptysis is common and may be the first and only symptom.
Recurrent acute pneumonia is a common complication and investigation may lead to the diagnosis of bronchiectasis.
Physical findings are clubbing of the fingers. Pulmonary functional changes are those of any associated disease or of
the pulmonary fibrosis that may complicate bronchiectasis.
4.5. AIRWAYS OBSTRUCTION SYNDROME
A. REVERSIBLE AIRWAYS OBSTRUCTION - BRONCHIAL ASTHMA
B. IRREVERSIBLE AIRWAYS OBSTRUCTION - EMPHYSEMA
A. BRONCHIAL ASTHMA
DEFINITION
It is a reversible airways obstruction due to a variable combination of bronchospasm, inflammation of the bronchial
walls and plugging of the distal air passages by intraluminal secretions and epithelial debris.
ETIOLOGY
Bronchial asthma can occur secondarily to a variety of stimuli. Although the underlying mechanisms responsible for
attacks of paroxysmal wheezing are unknown, inherited or acquired unbalance of adrenergic and cholinergic control of
airway diameter has been implicated. Persons manifesting such imbalance have been shown to have hyperreactive bronchi. In
these individuals, bronchoconstriction may persist at subclinical levels even when they are asymptomatic. When individuals
with hyperreactive bronchial tree are subjected to stresses of different kinds, overt asthma attacks may occur. Among the
known stresses are viral respiratory infection, exercise, emotional upset nonspecific factors, inhalation of cold air or such
irritants as gasoline fumes, fresh paint and other noxious odors, or cigarette smoke, and exposure to specific allergens.
Psychologic factors may aggravate an asthmatic attack but are not assigned a primary etiologic role.
Persons whose asthma is precipitated by allergenic exposure (most commonly airborne pollens and molds, house
dust, animal danders), and whose symptoms are IgE mediated are said to have allergic or "extrinsic asthma". They account
for only about 10 to 20% of the adult asthmatic population.
In perhaps 30 to 50% of asthmatic adults, symptomatic episodes appear to be triggered by nonallergic factors
(infection, irritants, emotional factors). These patients are said to have nonallergic or "intrinsic asthma".
In many individuals, both allergic and nonallergic factors appear to play signficant triggering roles. Allergy is said
to be more important in the etiology of the asthma in infants and children than in adults, but the evidence is not entirely
conclusive.
SYMPTOMS AND SIGNS
Individuals with asthma differ greatly in the frequency and degree of their symptoms. Some have only an occasional
symptomatic episode, mild in degree and of brief duration, and otherwise are entirely free of symptoms.
Others have mild coughing and wheezing much of the time, punctuated by severe exarcerbations of symptoms
following exposure to known allergens, viral infection, exercise, or nonspecific irritants.
Psychosocial stress alone may precipitate an attack or may be additive with these noxious exposures.
An asthma attack may begin acutely with paroxysms of wheezing, coughing and shortness of breath, or insidiously
with slowly increasing symptoms and signs of respiratory distress.
In either cases, the patient usually first notices the onset of dyspnoea, tachypnea, cough and tightness or presure in
the chest, and may even notice audible wheezes. All of this may subside quickly or persist for hours to days. Pulmonary
function abnormalities, may persist for weeks to months after an acute attack, even in asymptomatic patients.
The cough during an acute attack sounds "tight" and is generally nonproductive of mucus. Except in young children,
who rarely expectorate, tenacious mucoid sputum is produced as the attack subsides.
On physical examination during the acute asthmatic attack the patients exhibit varying degrees of respiratory
distress depending on the severity and duration of the episode.
Tachypnea, anxiety and audible wheezes are frequently present. Tachycardia and elevation of systolic BP are also
common and are related to the primary disease, the effects of recent therapy, or both.

21
Variable degrees of dehydration may be present in a patient with more prolonged episodes because of sweating and
increased insensible water loss from the lungs secondary to tachypnea.
The patient prefers to sit upright or even leans forward. Accessory muscles of respiration are used and the patient
may appear to be struggling for air. Examination of the chest shows a prolonged expiratory phase with relatively highpitched
wheezes throughout most of expiration and through inspiration. Although wheezes may be accompanied by coarse rhonchi.
fine "wet" rales are not heard unless pneumonia, atelectasis, or cardiac decompensation is also present.
In more severe episodes, the patient may not be able to speak more than a few words at a time without having to stop
for breath. Fatigue and severe distress are evident in the rapid, shallow, ineffectual respiratory movements. Cyanosis becomes
evident as the attack worseness. Confusion and lethargy may indicate the onset of progressive respiratory failure. In such
individuals, it is unusual to hear less wheezing in auscultation. The chest may sound quiet because the combination of
extensive mucous plugging of airways and patient fatique has resulted in marked reduction of air flow and gas exchange.
The presence, absence, or prominence of wheezes does not correlate precisely with the severity of an asthma attack.
The most reliable signs indicating a severe asthma attack include assessment of the degree of dyspnoea at rest,
difficulty in talking, pulsus paradoxus of > 20 to 30 mm, and the use of accessory muscles of respiration. The severity of an
attack can be most precisely assessed by blood gas determinations.
Between acute attacks, physical examination may be normal during quiet respiration. However, sonorous or sibilant
rales or fine wheezes may be heard during forced expiration or after the patient exercises.
DIAGNOSTIC TESTS
- examination of the blood and the sputum
- chest X-ray
- pulmonary function tests
- static lung volumes and capacities
- dynamic lung volumes and capacities
OTHER DIAGNOSTIC TESTS
- allergy skin tests
- radioallergosorbent test (RAST)
- exercise testing
- arterial blood gases and pH
B. EMPHYSEMA
DEFINITION
It is the distension of the air sacs that produces considerable increase in the volume of the lungs.
ETIOLOGY
Pulmonary emphysema may occur as primary condition but a mixed picture of chronic bronchitis and emphysema is
much more common than the occurrence of the either condition alone.
It probably results from the destructive effect of proteolytic enzymes such as neutrophil elastase on lung tissue and is
much more prevalent in cigarette smokers, particularly those with a homozygous alpha-antitrypsin deficiency. Destruction of
the alveolar walls leads to a reduced number of enlarged air spaces with progressive obliteration of the vascular bed.
CLINICAL FEA TVRES
In primary emphysema there is but one symptom, dyspnoea, coming at first on exertion and ultimately at rest In the
commoner variety associated with chronic bronchitis this will be accompanied by wheezing and a productive cough.
The physical findings that accompany the emphysema are increased in anteroposterior diameter of the chest, fixation
of the chest with the ribs in a more nearly horinzotal plane, obvious participation of accessory muscles, normal or decreased
vocal fremitus, hyperresonance, depressed diaphragms with decreased respiratory excursion, and decreased or absent breath
sounds with diminished transmission of the whispered and spoken voice. Breath sounds are usually definitely prolonged
during expiration and often accompanied by sibilant rhonchi.
4.6. PLEURAL SYNDROMES
A. PLEURISY
B. PNEUMOTHORAX
A. PLEURISY DEFINITION:
inflammation of the pleura ETIOLOGY Pleurisy
may occur as a result of:
1. pleural injury by a process in the underlying lung (e.g. pneumonia, pulmonary infarction);
2. entry of an infectious agent or irritating substance into the pleural space (e.g. as in amebic empyema or
pancreatic pleurisy);
3. transport of an infectious or noxious agent or neoplasic cells directly to the pleura by the blood stream or
lymphatics (e.g. as in tuberculous pleural effusion, uremic pleurisy, or collagen vascular diseases such as SLE);
4. pleural trauma;
5. asbestos - related pleural disease in which the noxious agent (asbestos particles) reaches the pleura by
traversing the conducting airways and respiratory tissues of the lungs;
6. rarely, pleural effusion related to longstanding ingestion of dantrolene sodium.
SYMPTOMS AND SIGNS

22
Onset is usually sudden.
Pain, the symptom of fibrinous pleurisy, may vary from vague discomfort to an intense stabbing sensation. The pain
is aggravated by breathing and coughing, or may be present only when the patient breathes deeply or coughs.
The visceral pleura is insensitively, painful result from inflammation of the parietal pleura.
Pain is usually felt over the site of the pleuritis, but pain may be reffered to distant regions.
Respiration is usually rapid. Motion of the affected side may be limited. Breath sounds may be diminished. A pleural
friction rub is the characteristic physical sign. The friction rub varies from a few intermittent sounds which may simulate
crakles to a fully developed harsh grating.
When pleural effusion develops, pleuritic pain usually subsides. Fluid in the pleural space may be an inflammatory effusion,
congestive hydrothorax, or empyema. Although the fluid may be the result of a variety of causes, the physical findings will
be the same - decreased respiratory excursion on the side involved, decreased or absent vocal fremitus, dullness to flatness,
depending on the amount of fluid present, and decreased or absent breath sounds and vocal transmission; egophony at the
upper border of the fluid are then noticeable. B. PNEUMOTHORAX
DEFINITION: free air in the pleural cavity, between the visceral and parietal pleura.
ETIOLOGY AND PATHOPHYSIOLOGY
- traumatic pneumothorax;
- open pneumothorax occurs when a penetrating chest wound creates a communication between the outside
air and the pleural space;
- closed pneumothorax;
- pulmonary barotrauma;
- spontaneous pneumothorax.
The most common cause is emphysema in which air escapes into the pleural cavity because of rupture of a distended
bula on the surface of the lung.
The lung is an elastic structure, expansion of which is maintained by the negative intrapleural pressure. With the
entrance of air into the pleural space, the lung will collapse.
SYMPTOMS AND SIGNS
Symptoms vary greatly according to the size of the pneumothorax and the extent of disease in the lung. They range
from minimal disturbance to severe dyspnoea, shock, and life-threatening circulatory collapse. Sudden sharp chest pain,
dyspnoea, and occasionaly, a dry, hacking cough occur at onset
The pain may be referred to the corresponding shoulder, across the chest, or over the abdomen; it may simulate an
acute coronary oclusion or an "acute abdomen". Symptoms tend to be less severe in a slowly developing pneumothorax and
usually subside as accommodation to the altered physiologic state occurs.
Physical findings depend on the size of the pneumothorax. With a small collection of air there may be no detectable
signs, or diminution of voice and breath sounds may be the only abnormality.
With large or tension pneumothoraces, tympany on percussion, diminished or absent tactile fremitus and diminished motion
on the affected side occur. Shift of the mediastinum may be detectable as displacement of the cardiac dullness and apex beat
away from the affected side.
Hypoxemia is minimal or absent in a previously well young person with spontaneous pneumothorax, but may be severe and
associated with hypercapnia in a patient with diffuse underlying lung disease.
4.7. CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
DEFINITION: clinically significant irreversible, generalized airways obstruction associated with varying degrees of
chronic bronchitis, abnormalities in small airways, and emphysema.
The designation was introduced because chronic bronchitis, small airways abnormalities, and emphysema often
coexist and it may be difficult in an individual case to decide which is the major factor producing the airways obstruction.
When it is clear that the patient's entire disease can be explained by emphysematous changes in the lung, the
diagnosis "chronic obstructive emphysema" is preferred to the more general designation COPD. Similarly, the diagnosis
"chronic obstructive bronchitis" should be used when the obstructive abnormality is a direct result of an inflammatory process
in the airways. To avoid the semantic confusion often encountered in discussions of these disorders, the following definitions
are to be taken into account:
Chronic bronchitis, when unqualified, is defined as a condition associated with prolonged exposure to nonspecific
bronchial irritants in the bronchi. Clinically, it is characterized by chronic productive cough and is usually associated with
cigarette smoking.
Pulmonary emphysema is defined as enlargement of the air spaces distal to the terminal nonrespiratory
bronchioles, accompanied by destructive changes of the alveolar walls.
Airways obstruction is defined as increased resistance to the air flow during forced expiration. It may result from
narrowing or obliteration of the airways secondary to intrinsic bronchial disease or from excessive collapse of airways during
forced expiration secondary to pulmonary emphysema.
SYMPTOMS, SIGNS AND X-RAY FINDINGS
COPD is thought to begin early in life, though significant symptoms and disability, usually do not occur until middle
age. Mild ventilatory abnormalities may be discernible long before the onset of significant clinical symptoms. A mild
"smoker's cough" is often present many years before onset of exertional dyspnoea.

23
Gradually progressive exertional dyspnoea is the most common presenting complaint. Patients may date the onset of
dyspnoea to an acute respiratory illness, but the acute infection may only unmask preexisting subclinical chronic respiratory
disorder.
Cough, wheezing, recurrent respiratory infections, or occasionally, weakness, weight loss, or lack of libido may also
be initial manifestations. Rarely, initial complaint are related to congestive heart failure secondary to cor pulmonale, patients
with such complaints apparently ignoring their cough and dyspnoea prior to the onset of dependent edema and severe
cyanosis.
Cough and sputum production are extremely variable. The patient may admit only to "clearing his chest" on
awakening in the morning or after smoking the first cigarrete of the day. Other patients may have severe disabling cough.
Sputum varies from a few ml to clear viscid mucus to large bronchiectasis - like quantities of purulent material.
Wheezing also varies in character and intensity. Asthma - like episodes may occur with acute infections. A mild
chronic wheeze that is most obvious on reclining may be noted. Many patients deny having any wheeze.
THE PHYSICAL FINDINGS in COPD are notoriously variable, epecially in early cases. A consistent abnormality is
obstruction to expiratory air flow manifested by a slowing of forced expiration. To demonstrate this, the patient is asked to
take a deep breath and then empty his lungs as quickly and completely as possible. Forced expiration is normally virtually
complete in <4 seconds.
Other findings, including rhonchi, diminished vesicular breath sounds, tachycardia, distant hearttones, and decreased
diaphragmatic motion, are not consistently present. The typical findings of gross pulmonary hyperinflation, prolonged
expiration during quiet breathing, depressed diaphragm, pursed-lip breathing, stooped posture, calloused elbows from
repeated assumption of the "tripod position", and marked use of accesory muscles of respiration are seen only in later stages
of COPD.
A barrel-chested appearance is an unreliable finding since it is often noted in elderly patients without significant
respiratory problems.
Late in the disease, there may be frank cyanosis from hypoxemia, a plethoric appearance associated with secondary
erythrocytosis, and in patients with severe cor pulmonale, signs of congestive heart failure.
X-ray findings are also variable.
DIAGNOSIS
COPD should be suspected in any patient with chronic productive cough or exertional dyspnoea of uncertain
etiology, or whose physical examination reveals evidence of slowing of forced expiration.
Definite diagnosis depends on:
1. demonstration of physiologic evidence of airways obstruction which persists despite intensive and
maximum medical management;
2. exclusion of any specific disease (e.g. silicosis, tuberculosis, or upper airways neoplasm)as a cause of this
physiologic abnormality.
3. spirometric testing.
4.8. PULMONARY INSUFFICIENCY. RESPIRATORYFAILURE
Pulmonary insufficiency or some degree of respiratory failure occurs when the exchange of respiratory gases
between the circulatory blood and the ambient atmosphere is impaired.
The terms are used synonymously though the term respiratory failure generally refers to more severe lung
dysfunction. The gases composition of generally arterial blood with respect to 0 2 and C02 pressures is normally maintained
within restricted limits; pulmonary insufficiency occurs when the Pa02 is <60mm Hg and the PaCC2 is >50mm Hg, but
pulmonary insufficiency or respiratory failure may be manifested by a reduced Pa02, with a normal, low or elevated PaC02.
There are 3 pathogenic categories of diseases of the respiratory apparatus.
1. those manifested mainly by airways obstruction;
2. those largely affecting the lung parenchyma but not the bronchi;
3. those in which the lungs may be anatomically intact but the regulation of ventilation is defective because
of abnormal musculoskeletal structure and function of the chest wall or primary disfunction of the CNS respiratory center.
The etiology and mechanisms of disease leading to the physiologic disturbances in each of these categories may
differ, but the pattern of physiologic disturbance of lung function is quite similar.
22. FURTHER EXAMINATION OF THE RESPIRATORY SYSTEM
Beside the clinical examination, which has, in most of the cases, its fundamental value in determining a diagnosis
concerning respiratory or extra-respiratory affections (diseases) with pleuro-pulmonary implications, there is a need of
corroboration with other paraclinic exploration methods in order to obtain decisive data to formulate a correct and complete
diagnosis.
The complementary examinations related to respiratory diseases can be classified as follows: A.
1. Morphologically
citologic and bacteriologic exams of the sputum;
complete examination of pleural fluid;
image exploration and interpretation (X-ray slides, scintigraphic or sonographic records);
direct microscopic examinations (bronchoscopic, mediastinoscopic etc);

24
microscopical exams (anatomo-pathological): pleuro-pulmonary and lymph nodes biopsies. 2. Functionally:
ventilatory tests; alveolocapillary tests;
intra-pulmonary and intrapleural pressure check up. B. 1. External
(non invading the inner part of respiratory system): X-ray and
scintigraphic exams etc; the lab exams of sputum; ventilatory
tests etc. 2. Internal:
bronchoscopic and bronchographic investigations; pleural fluid
sampling; pleural or pulmonary biopsy; mediastinoscopy
etc. These exploratory methods vary a great deal, as required
by:
the value level and specifity of a certain diagnosis; the degree of comfort or risk related to a certain medical
subject. Hence the caution in choosing the most suitable methods of investigation there are to be used, at first, the less
risky and unpleasant ones to the patient and only in well justified cases, one should consider using the methods that imply a
higher risk for the patient
22.1. THE SPUTUM EXAMINATION
It is a rapid and harmless exam. One should make sure that the sputum sample is saliva free (not being contamined
by), paying attention to the right procedures of sputum sampling scenario (in the morning, with storage in highly sterile petri
boxes, after a thorough hygene of oral cavity and pharynx).
22.1.1. MICROSCOPICAL EXAMINATION
(cito-bacteriologic)
Microscopical examination sheds lights on guide lines elements or comes with conclusive and specific data to a
certain pulmonary deficiency as:
cilindrical epithelial cells - catarrhal inflamation (tracheo-bronchitis);
macrophages - acute catarrhal pneumonias;
macrophages with hemosiderin ("cardiac" cells) in mitral stenosis, pulmonary infarction,
Goodpasture's syndrome;
macrophages with fat inclusions ("fat" cells) as side effects of suppuration in chronical infections;
granulocytes - in inflamations;
eosinophiles - in reduced number: TB, pulmonary helminthiasis;
- in great number (20-60%) - bronchial asthma;
lymphocytes - whooping cough, pulmonary TB;
erythrocytes (if found in great number it bears the name of microscopical hemoptysis); in pneumonias,
bronchopneumonias, catarrhal bronchitis, minor pulmonary infarctions, tumors etc; tumoral cells - in
malign tumors; Curschmann spirals - in allergic bronchial asthma; elastic fibres - in acute
pulmonary leakage; crystals of different patterns:
Characot-Leiden crystals - in bronchial asthma;
cholrsterol crystals - in slow or occasional supurations;
hematoidin crystals - in hemoptysis;
fat-acids crystals - in suppurations;
pulmonary mycosis - candidosis, actinomycosis;
parasites - scolecses - in "hidatic" cyst;
microbian flora - deverse (including Koch bacillus in pulmonary TB).
22.1.2. BACTERIOLOGICAL EXAMINATION
- antibiograme Expectorated sputum (spontaneous or induced) is inseminated in a breeding culture, thus enabling the identification
of incriminating pathogen agent against antibiotics compatibility and conclusive tests.
Due to numerous irrelevant test results (caused by contaminations of sputum with saliva and other liquids resident in
oral cavity and pharynx), this method is recommended only in identifying the Koch bacillus or fungi/mycosis infections.

25 There
are four generally accepted methods of proper bacteriological exam consisting in lab techniques and avoiding the
contamination caused by oral cavity and pharynx, allowing access to a truly representative sample extracted directly from
disabled area:
direct sampling with a brush cateter' transtracheal aspiration; pulmonary trans-bronchial
biopsy; aspiratory biopsy of the pulmonary
secretions.
22.2. PLEURAL FLUID SAMPLING
It takes place while the patient is sitting on a chair, with the sternum slightly bended towards the chair back, while
the dorsal part of the thorax is facing the exairuning doctor.
In very severe patients the sampling of the pleural fluid can be performed in lateral decubitus. The sampling of pleural fluid
is to be performed on dorsal axillary line, in full dullness, on the upper edge of the subadjacent rib (to avoid the lower
edge line of the superiacente rib).
As premedication, we use 1 milligramme of atropine subcutaneous (s.c.) or intravenous (i.v.), to avoid
vagal reflexes.
For a successful puncture one must take all the needed aseptic measures of the area that has to be punctured.
Xilina may be used for a local anaestesia.
Pleural puncture will be performed with a hypodermic/hollow needle attached to a syringe, in a single movement,
steady, but not abrupt.
As soon as you feel that the hypodermic/hollow needle has passed the outer layer of the pleural membrane, one may start the
suction of the pleural fluid sucking the amount requested by a specific purpose: a few millilitres in exploratory
cases; up to 500 millilitres when evacuation is needed. It is not allowed to evacuate more than 500 ml in one go, as this
may cause a cardio-respiratory arrest and therefore, when larger evacuations are needed, the task can be achived by repeating
the evacuation for a number of days.
Great care should be taken in order to avoid any pumping of air into the pleural cavity, particularly in cases of
exploratory punctures.
The pleural exploratory puncture is aimed at:
diagnosticating the cases of pleura effusions and pleural air,
reaching the right diagnosis whenever the amount of pleural fluid is less than 200-300 ml and any
medical evaluation can't be achieved even by radioscopy;
diagnosing the major Grancher pneumonia and pleural syndromes that can be mistaken for pleuresy; defining more
accurately the macroscopical aspect of pleural fluid, providing this way a great etiological value.
Contraindications for pleural puncture are:
very poor general state of health, hypertoxicity state, hyperthermia;
severe cardiac disorders as in cases of major arrhythmias;
presence of an inflammation of the thoracic wall as in cases of cellulites, erysipelas, folliculitis etc;
assumption of pulmonary cyst, especially in hidatic cyst located near the pleuras (because of the risk of
anaphylactic shock).
Accidents that may occur during the pleural puncture include: breakage of the hollow
needle-eithe due to a faulty technique or due to a sudden change in the position of the patient, cases,
that require an immediate surgical intervention; acute pain;
damage of interribs vessels - in this case the pleural puncture must be stopped; appearance of
hemoptysis is a clear sign of pulmonary injury; acute pneumothorax, the most frequent complication
that involves acute asphyxia; acute pulmonary edema - "ex vacuo" - when more than 800 ml of fluid has
been extracted; sudden death due to pleuro-cardiac or pleurocentral reflex. LATE ACCIDENTS
subcutaneous emphysema; turning of the fluid into a purulent one. Pleural puncture can be positive when liquid is
extracted and nagetive or "white" when no liquid can be obtained. There are manifold reasons responsible for a white pleural
puncture: a technical mistake; lack of permeability of the hollow needle (the inner pipeline hole of the needle has been
obturated by a tissue fragment); the thickening of pleura membrane does not allow needle penetration; the absence of
pleura liquid, the puncture needle has been pushed too deep.
22.3. PLEURAL FLUID EXAMINATION
It is done either in a macroscopic or microscopic way in order to establish a few major guide lines elements, as
helpful hints from the etiological point of view.

22.3.1.

26

Judging by macroscopic aspect, one can evaluate cases of: serous pleuresy, sero-fibrous, purulent, hemorrhagic,
"chiliform".
Orientative etiological elements:
serous fluid is typical for transsudation;
serofibrous fluid occurs in TB pleuresy, but also in: neoplasms, collagenosis and allergy cases;
purulent fluid revealed by bacillary etiology when pleural fluid has been already infected or after a
major acute pneumonia;
hemorrhagic fluid occurs after pulmonary infarction being typical for broncho-pulmonary neoplasm
with pleural implication;
chillous (milky aspect) is observed after thoracic duct compresion, generally being of a neoplasm
origin as etiology.
22.3.2.

Taking into consideration the transsudate or exudate character one can make a very important differentiation that
may lead to a good etiological orientation.
To help differentiate those two types one has to identify and quantify the following elements: the aspect, density,
albumine, Rivalta reaction, etiological aspects, as follows:
a. in transsudate: the macroscopic aspect is colour less, pale, the fluid density is small, less than 1015, with negative
Rivalta reaction, the protein amount is under 3 g% (Rivalta reaction after adding a few drops of acetic acid into the
pleural liquid there is no trace of any precipitate) and with very poor citology where endotelial cells prevail)
b. in exudate: the general aspect is citriu (alongside with all the other already described, macroscopical aspects), density
exceeds 1018, protein amount exceeds 3 g% Rivalta reaction is positive and has a very rich reaction is positive and has a
very rich citology which can be etiologicalry differentiated as follows:
lymphocitary predominance, warms on bacillary etiology at values exceeding 95%;
neutrophile predominance opens the case of inflammatory and infectious etiology;
eosinophile predominance rise the problem of allergic and parasitic etiology;
hematine and atypical cells predominance leads to neoplasm etiology.
22.3.3.

after the bacteriological test has been completed one can distinguish two types of pleurisy: the infectious one and the
noninfectious one.
This exam serves to reveal the involved bactoria or virus and, after the results of antibiogramme have been
evaluated, to properly choose the treatment and monitor the evolution of the patient placed in medical care.
22.3.4.

After chemical exam, one can evaluate a great deal of data related to: the
fibrous amount as an end results in Rivalta reaction; the
protein and albumine ratio, considered as individual values;
the cholesterol percentage into the sampled fluid (under 0,25 g% in transsudates and over 0,60 g% in
exudates);
the glucose ratio/percentage into the sampled liquid which is higher than average in neoplasical
etiology;
the amylase ratio-typical for pancreatic pleurisy;
the lacto-dehydrogenase ratio/percentage etc.
22.4. RADIOLOGICAL EXAMINATION OF THE RESPIRATORY SYSTEM
22.4.1. GENERAL OVERVIEW
The radiological image is a mixture of shadows and transparencies that enables to reveal, the shape, the size, the
situation, the structure and sometimes even the chemical composition of involved anatomical elements, the features of
functional movements either normal or induced by the radiologist during the examination time Rontgen rays (X-rays) are
produced into Rontgen rays duct by abrupt deceleration of electrons being in a state of accelerated movement They have a
wavelenght of 0,06-135L.
The human body is a nonhomogenous one when it comes to X-ray absorption, because the human tissue is of
different density and its organs varies in thickness.
X-rays are unevenly absorbed by different components of a nonhomogenous body hence the amount of X-rays that
penetrates those parts varies according to the absorbing ratio of each component

27
Total absorbtion is regarded as a summing up of layer/component power of absorbtion; hence the created X-ray
image is as well an overlay of plans with different absorption power.
If we place a radioscopic screen or a radiologic film at the end way of a flux of X-rays that penetrates a
nonhomogenous body we shall be able to notice muniniscent effect on radioscopic screen or obtain a photochemical effect on
photographic emulsion. The effect/impression on screen or film varies with the power of X-ray flux that has managed to pass
through the surveyed body.
A rich X-ray flux at the other side of surveyed body means that we had a low absorption of X-rays.
A weak X-ray flux at the other side of surveyed body means that we had a high absoption of X-rays.
This is how we get the final image on radioscopic screen or the image on radiologic film. As each screen or film
points is differently impressed we finally obtain the X-ray image of a surveyed body.
The luminiscent (white) section of the radioscopic screen has been caused by the powerful end flux of X-rays that
has passed through layers with very low absorption power of X-rays and this section is generally known as transparency.
Whatever is dark (black) on radioscopical screen (due to a very weak flux of X-rays, as most of them have been
absorbed on the way to the screen) turns into white on film and this feature is known as shadow, opacity or fogginess.
Features of radiological images worth mentioning:
radiological image is larger than the surveyed object;
radiological image is distorted;
the same body can produce many radiological images, according to the spining angle of the surveyed
body.
Methods of radiological examination of the respiratory system.
Thoracical radioscopy (fluoroscopy) is the simplest method as this does not involve a beforehand preparation. It
offers morphological information but mainly dynamical ones regarding intra-thoracical structures (pulsatile injuries,
diaphragmatic movements, pulmonary modifications during inspiration and expiration and allows the radiologist to get a
large range of specialized images.
The main disavantage of this method consists in the lack of facilities to record the image, depriving the radiologist
of an objective document needed for comparing of the surveyed subject.
Thoracical radioscopy allows a fine analysis being detailed and interdiciplinary (radiologist and clinician), while
time monitoring of an injured organ is a common feature (shape, size and structural changes).
It does not need any beforehand preparation. This method provides only morphological information upon intrathoracical structures.
X-ray microphotograph (MRF - micro-radiophotograph) is a mass screening method, greatly used in revealing cases
of pulmonary TB or professional lung diseases (silicosis).
A sensitive photographic camera fitted to a radiological system (apparatus) can stock the radiological images on
film that, in the end, is developed and examined.
Thoracical radioscopy, radiography and MRF countable for two major functions:
a. the detection feature (reveals a pulmonary affection that is asymptomatic or other connected affection);
b. the guide feature (based upon the image source one can get conclusive hints leading to a specific affection or drives the
image evaluation towards other investigations needed for the final diagnosis).
Tomography (stratigraphy, planography, lamelography) allows an X-ray photography of a single plan, situated at a
selected depth, being as relevant as an anatomico-pathological section at the chosen level.
This way the overlaying effect is avoided. The method is employed in revealing cavities, mediastinal adenopathy or
tumors present at a certain level.
Computerized tomography (CT) provides in depth information regarding pleural (heping to differentiate fluid and
tumour), mediastinal (lymph nodes, tumours, vascular structures) and pulmonary diseases.
Bronchography consists of introduction of certain radio absorbent fluid into the broncho-tracheal tree with the help
of a catheter or a bronchoscope.
Changing the position of the patient and of the instrument involved (catheter or bronchoscope), one can spray evenly
the inner part of the broncho-tracheal tree with a special substance (also known) as the contrast agent that will stay for a
period of time (long-enough to allow us to complete the thoracic radiography. The contrast agent will take the shape of a
certain involved segment and it will be cast on radiological film as an opaque/foggy shape. This method is
suitable for the following purposes: to diagnosticate bronchiectasis; to identify (locate certain bronchial
obstructions (distal);
to reveal certain cases of broncho-tracheal malformations either congenital or acquired, before a surgical interven is
to be decided. Bronchography may induce bronchial spasm and the unpleasant irritative effect of the contrast substance can
last for a couple of days.
22.4.2. THE NORMAL RADIOLOGICAL IMAGE OF THE LUNGS
The normal healthy lungs appear on radiological screens/films as two translucid zones outlined on the outside by the pleuras
on the medial-vertical axis by the mediastinum and on inferior side by the diaphragm. For each lung one can describe the
following zones:
the apical (the tip), located over-clavicularly;