R e s p ir a t o r y

D is o r d e r s

f o r DP HC & CP H C
Faculty of Health Sciences
MCHE

R
Reessppiirraattoorryy D
Diissoorrddeerrss ...................................................................................................... 1
ffoorr D
P
H
C
&
C
DPHC & CP
PH
HC
C ........................................................................................................... 1
INTRODUCTION .............................................................................................................. 5
ANATOMY AND PHYSIOLOGY .................................................................................... 5
UPPER RESPIRATORY TRACT INFECTIONS ............................................................. 6
VIRAL RHINITIS .............................................................................................................. 6
Definition .................................................................................................................... 6
Aetiology..................................................................................................................... 6
Transmission ............................................................................................................... 7
Incubation period ........................................................................................................ 7
Clinical features .......................................................................................................... 7
Complications ............................................................................................................. 7
Diagnosis..................................................................................................................... 7
Management ................................................................................................................ 7
Prevention ................................................................................................................... 8
ALLERGIC RHINITIS ....................................................................................................... 8
Definition .................................................................................................................... 8
Types ........................................................................................................................... 8
Aetiology..................................................................................................................... 8
Transmission ............................................................................................................... 8
Clinical features .......................................................................................................... 8
Complications ............................................................................................................. 9
Diagnosis..................................................................................................................... 9
Management ................................................................................................................ 9
Prevention ................................................................................................................. 10
PNEUMONIA................................................................................................................... 10
Definition .................................................................................................................. 10
Community-Acquired Pneumonia ................................................................................ 10
Aetiology................................................................................................................... 10
Transmission ............................................................................................................. 11
Risk factors ............................................................................................................... 11
Clinical features ........................................................................................................ 11
Complications ........................................................................................................... 12
Diagnosis................................................................................................................... 12
Management .............................................................................................................. 12
Prevention ................................................................................................................. 13
BRONCHIAL ASTHMA ................................................................................................. 13
Definition .................................................................................................................. 13
Asthma is classified as early onset (atopic) asthma and late onset (non-atopic)
asthma. ...................................................................................................................... 13
Aetiology/predisposing factors ................................................................................. 13
Clinical features ........................................................................................................ 14
Complications ........................................................................................................... 14
Investigations ............................................................................................................ 14
Management .............................................................................................................. 14
Prevention ................................................................................................................. 15

ACUTE ASTHMA ........................................................................................................... 15

Definition .................................................................................................................. 15
Aetiology................................................................................................................... 15
Clinical features ........................................................................................................ 15
Complication ............................................................................................................. 16
Investigation .............................................................................................................. 16
Management .............................................................................................................. 16
TENSION PNEUMOTHORAX ....................................................................................... 17
Definition .................................................................................................................. 17
Aetiology................................................................................................................... 17
Clinical features ........................................................................................................ 17
Complication ............................................................................................................. 17
Investigations ............................................................................................................ 17
Management .............................................................................................................. 17
CHRONIC OBSTRUCTIVE PULMONARY DISEASES .............................................. 18
Definition .................................................................................................................. 18
Importance of COPD ................................................................................................ 18
CHRONIC BRONCHITIS ............................................................................................... 18
Definition .................................................................................................................. 18
Aetiology................................................................................................................... 18
Clinical features ........................................................................................................ 19
Complications ........................................................................................................... 19
Investigations ............................................................................................................ 19
Management .............................................................................................................. 20
Management of acute COPD exacerbation ............................................................... 20
Prevention ................................................................................................................. 21
BRONCHIECTASIS ........................................................................................................ 21
Definition .................................................................................................................. 21
Aetiology................................................................................................................... 21
Clinical features ........................................................................................................ 21
Complications ........................................................................................................... 22
Investigation .............................................................................................................. 22
Management .............................................................................................................. 22
Prevention ................................................................................................................. 22
LUNG ABSCESS ............................................................................................................. 23
Definition .................................................................................................................. 23
Aetiology................................................................................................................... 23
Clinical features ........................................................................................................ 23
Complications ........................................................................................................... 23
Investigations ............................................................................................................ 23
Management .............................................................................................................. 23
RESPIRATORY FAILURE ............................................................................................. 24
Aetiology................................................................................................................... 24
Clinical features ........................................................................................................ 24
Investigations ............................................................................................................ 25
Management .............................................................................................................. 25

BRONCHIAL CARCINOMA .......................................................................................... 25

Aetiology................................................................................................................... 25
Clinical features ........................................................................................................ 25

Respiratory disorders for DPHC & CPHC

INTRODUCTION
The human cells need a constant supply of oxygen to live and grow. In the process of
metabolism they use this oxygen and produce carbon dioxide as a waste product.
Accumulation of this in the body produces harmful effects. The respiratory system is
designed to exchange carbon dioxide accumulated in the blood for oxygen in the airways
which enters the lungs from the surrounding atmosphere. This air is breathed into the
airways via the nose, pharynx, larynx, trachea and bronchi.
The lungs have a combined surface area of greater than 500m2 which are directly exposed
to the environment. Thus structural, functional and microbiological changes in the lungs
can be closely related to epidemiological, environmental, occupational, personal and
social factors. Respiratory symptoms are the most common cause of presentation to the
doctor. Respiratory diseases are responsible for a major burden of morbidity and
untimely deaths, and the lungs are often affected in multi system diseases.

ANATOMY AND PHYSIOLOGY

The respiratory system forms an interconnecting tree of tubular conducting airways
joining the alveoli via terminal bronchioles to form the acini. It begins at the nose and
mouth through which air enters with each breath. The air then flows to the back of the
throat and down the trachea or windpipe. Inhaled air then passes the larynx or voice box
to reach the left and right bronchi which are formed by the division of the trachea and
reaches the left and right lungs respectively. In the lungs the bronchi branch into small
tubules called bronchioles.
The bronchioles carry air into the thousands of tiny sacs called alveoli, which make up
the lungs. Each group of alveoli is surrounded by numerous tiny capillaries. Oxygen
passes through wall of alveoli into the blood in the capillaries where it attaches to the
hemoglobin in the red blood cells. Red blood cells carry oxygen to the cells of the body.
The cells use up oxygen and release carbon dioxide. Red blood cells pick up the carbon
dioxide and travel back to lungs. Red blood cells release carbon dioxide through the
capillaries to the alveoli. Breathing out removes carbon dioxide from the blood and
breathing in brings in air filled with fresh oxygen into the body.
The cells lining the respiratory system ensure that the air that reaches the lungs is warm,
clean and moist. The nose and mouth along with epithelial cells of the respiratory tract
warms the air. The mucous secreted by the glands of the respiratory tract moistens the air.
Tiny hair like structures in the trachea, bronchi and bronchioles push up mucous and dirt
particles out of the airway towards the nose and mouth. Coughing, sneezing or blowing
the nose forces out the mucous and dirt particles.
When a respiratory system infection develops the trachea, bronchi and bronchioles
produces more mucous to fight the infection. The mucous may become thick and cloudy
or it may contain blood. This thick mucous is called sputum.

Page 5 of 26

Respiratory disorders for DPHC & CPHC

The respiratory system is divided into upper and lower respiratory tracts. The upper
respiratory tract includes the nose, nasopharynx and larynx. It is lined by vascular
mucous membranes with ciliated epithelium on their surfaces. The lower respiratory tract
includes the trachea and bronchi. The lower respiratory tract is lined with ciliated
epithelium up to the terminal bronchiole.
Diaphragm is the main muscle of respiration (breathing) and normal quiet breathing is
accomplished almost entirely by movement of the diaphragm. During inspiration,
contraction of the diaphragm pulls the lower surface of the lungs downwards. During
expiration it simply relaxes and the elastic recoil of the lungs, chest wall and abdominal
structures compresses the lungs. During heavy breathing this is not powerful enough to
cause necessary rapid expiration, so that the abdominal muscles come to action. Other
important muscles of respiration are the intercostals, sternocleidomastoid, anterior serrati
and the scaleni. During respiratory distress of dyspnoea these muscles become more
prominent and should be looked for when examining a dyspnoic patient.
The acini are supplied with a rich network of capillaries for the exchange of gases. Gas
exchange in the lungs is suboptimal unless there is sufficient ventilation. Ventilationperfusion mismatch result in varying degrees of respiratory distress and it sequelae.

UPPER RESPIRATORY TRACT INFECTIONS

Infection of upper respiratory tract is very common throughout the world. Viruses are the
most frequent causative agents with secondary bacterial invasion in many cases. Most
cases of upper respiratory infections are self limiting and recover rapidly. Specific
investigations and treatment is needed in very few and in more serious cases.

VIRAL RHINITIS (Common Cold/Coryza)

Definition
This is an acute catarrhal inflammation of the nasal mucosa due to infection by
respiratory viruses and accompanied by profuse nasal discharge. The nonspecific
symptoms of common cold are present in the early phase of many diseases that affect the
upper aerodigestive tract. Because there are numerous serological types of these viruses,
patients remain susceptible throughout life.
Aetiology
Several viruses are responsible
Adenovirus
Picorna virus
Rhino virus
Coxsackie virus

Page 6 of 26

Respiratory disorders for DPHC & CPHC

ECHO virus, etc

Transmission
Usually airborne-droplets
Incubation period
1 to 4 days. May lasts for 2 to 3 weeks.
Clinical features
Burning sensation at the back nose (usually the 1st symptom)
Nasal stuffiness
Rhinorrhoea
Sneezing
Feels chilly
Scratchy throat
Low grade fever
General malaise
Nasal discharge is watery and profuse at first, may become purulent due to
secondary bacterial invaders like: Streptococcus haemolyiticus, Pneumococcus,
Klebsiella pneumoniae, M. catarrhalis
Complications
Sinusitis
Pharyngitis
Tonsillitis
Bronchitis
Pneumonia
Otitis media
Diagnosis
Largely a clinical diagnosis
Nasal examination shows reddened, edematous mucosa and a watery discharge
The presence of purulent discharge suggest bacterial infection
Management
There is no curative treatment for common cold however, there is a common
misperception among many people that antibiotics are helpful.
Bed rest, essential to cut down the course of illness
Plenty of fluids
Anti histamines such as cetrizine 10 mg once a day
Analgesics to relieve headache, paracetamol or panadine one tab every 4 to 6
hours
Antibiotics when secondary infection is present

Page 7 of 26

Respiratory disorders for DPHC & CPHC

Nasal decongestants should not be used for more than a few days at a time, since
chronic use leads to rebound congestion that is often worse than the original
symptoms. This chronic nasal stuffiness is known as rhinitis medicamentosa.

Prevention
Avoiding close contact with those affected

ALLERGIC RHINITIS
Definition
This is an IgE mediated immunological response of nasal mucosa to airborne allergens.
This is also known as hay fever and the symptoms are similar to those of viral rhinitis but
are usually persistent and show seasonal variation.
Types
Seasonal: symptoms appear in or around a particular season
Perennial: present throughout the year
Aetiology
Inhalant allergens
Pollens from trees and grasses
Mould spores
Home dust
Debris from insects
Home mite
Genetic predisposition: chance of children developing allergy are 29 to 47%
respectively if one or both parents suffer
Transmission
Via airborne route
Clinical features
Cardinal symptoms in seasonal types
Paroxysmal sneezing (10 to 20 sneezes at a time)
Nasal obstruction
Watery nasal discharge
Itching in the nose
Some patients may get bronchospasm
Cardinal symptoms in perennial types
Not as severe as seasonal type
Frequent colds
Persistently stuffy nose
Loss of sense of smell (due to mucosal oedema)

Page 8 of 26

Respiratory disorders for DPHC & CPHC

Chronic cough
Hearing impairment (due to Eustachian tube blockade or fluid in the middle ear)

Signs (common to both types)

Nasal
Nasal mucosa is pale and oedematous, may appear bluish or violaceous due to
venous congestion. This is in contrast to the erythema of viral rhinitis
Swollen turbinates
Thin watery or mucoid discharge
Ocular
Lid oedema
Congestion
Otologic
Retracted tympanic membrane
Serous otitis media (due to Eustachian tube blockade)
Laryngeal
Hoarseness of voice
Pharyngeal
Granular pharyngitis
Complications
Recurrent sinusitis (due to obstruction of sinus ostia)
Nasal polypi
Orthodontic problems, especially in children as a result of prolonged mouth
breathing
Bronchial asthma
Diagnosis
Largely clinical
Blood routine: Eosinphilia
Nasal smear: Increased IgE
Management
Antihistamines: cetrizine or loratadine 10 mg orally once daily or fexofenadine 60
mg orally twice daily or 120 mg once daily. Fexofenadine is non-sedating while
the other two are minimally sedating
Intranasal corticosteroid spray: beclomethasone (42 g/spray twice daily in each
nostril), mometasone furoate (200 g once daily per nostril) or fluticasone
propionate (200 g once daily per nostril). The latter two have higher topical

Page 9 of 26

Respiratory disorders for DPHC & CPHC

potencies and lipid solubility and reduced systemic bioavailability, suggesting

possible practical advantages
Sympathomimetic nasal decongestants (topical) e.g. phenylepherine,
oxymetazoline
Sodium chromoglycate (mast cell stabilizer)

Prevention
Maintaining an allergen free environment by
Covering pillows and mattresses with plastic covers
Substituting synthetic materials (foam, mattress, acrylics) for animal products
(wool, horse hair, feather)
Removing dust collecting household fixtures (carpets, drapes, bedspreads, wicker)
Air purifiers and dust filters may also aid in maintaining an allergen-free
environment
Removal of a pet from the house
Change in place of work
Elimination of a particular food from diet
When symptoms are extremely troublesome, a search for offending allergens may
prove helpful. This can either be done by skin testing or by serum RAST
(radioallergosorbent test) testing. Desensitization to identified allergens may be
tried in selected patients, but with variable results.

PNEUMONIA
Definition
It is an acute lower respiratory tract infection associated with recently developed
radiological shadowing which is either segmental or affecting more than one lobe. Two
major types of pneumonias are community-acquired and hospital-acquired (nosocomial)
pneumonias.

Community-Acquired Pneumonia
Community acquired pneumonia begins outside of the hospital or is diagnosed within 48
hours after admission to the hospital in a patient who has not resided in a long-term care
facility for 14 days or more before the onset of symptoms. This could be either lobar
pneumonia affecting one or more lung lobes or bronchopneumonia where there is a more
widespread involvement often affecting both lower lobes. This is one of the most deadly
infectious diseases worldwide.
Aetiology
Common organisms include
Streptococcus pneumoniae

Page 10 of 26

Respiratory disorders for DPHC & CPHC

Chlamydia pneumoniae
Haemophilus pneumoniae
Mycoplasma pneumoniae
Neisseria meningitidis
Staphylococcus aureus
Klebsiella pneumoniae
Legionella pneumoniae

Transmission
Via droplet inhalation
Aspiration of oropharyngeal secretions containing bacteria
Risk factors
Cigarette smoking
Alcoholics
Corticosteroid therapy
Old age
Recent influenza infection
Preexisting lung diseases
Clinical features
Prodrome of cough, fever, malaise pleuritic chest pain which may be referred to
shoulder or anterior abdominal wall
Cough is short, painful and non-productive at first but later become productive
and may become rust-coloured or even frankly blood stained
High fever with rigors
Breathing difficulty
Headache
Loss of appetite
In severe pneumonia patients may be confused
Physical signs
High fever or hypothermia
Tachycardia
Tachypnoea
Hypoxaemia
Hypotension and confusion in sever cases
Decreased chest movement and a pleural rub on the affected side
Impairment of percussion note
Bronchial breath sounds
Numerous coarse crepitations
Parapneumonic pleural effusion
Important risk factors for increased morbidity and mortality
Advanced age

Page 11 of 26

Respiratory disorders for DPHC & CPHC

Comorbid medical conditions

Altered mental status
Respiratory rate 30 breaths/min
Hypotension: systolic blood pressure of < 90 mmHg or diastolic blood pressure of
< 60 mmHg
BUN > 30 mg/dL

Complications
Parapneumonic effusion
Empyema
Lobar collapse
Thromboembolism
Lung abscess
ARDS, renal failure, multi-organ failure
Hepatitis, myocarditis, meningoencephalitis
Diagnosis
Chest x-ray: homogenous opacity localized to the affected lobe or segment
Sputum for Gram and Ziehl-Neelson staining
Sputum culture and drug sensitivity testing
Blood culture
Total and differential lymphocyte count
Arterial blood gas measurements
Management
Antibiotics: if possible culture specimens should be sent before starting
antibiotics. Oral cephalosporins should not be used in the management of
community-acquired pneumonia as they do not penetrate well into sputum or
bronchial fluids and do not cover likely organisms.
Treatment of outpatients
Amoxicillin 500 mg 8 hourly orally
Azithromycin 500 mg as first dose then 250 mg once daily for 4 days
Doxycycline 100 mg orally twice a day
Augmentin 375 mg or 625 mg orally three times a day
Cefuroxime axetil 250-500 mg orally twice a day
Therapy until the patient is afebrile for 72 hours is usually sufficient for
pneumonia due to S. pneumoniae. A minimum of 2 weeks of therapy is
appropriate for pneumonia due to other organisms
Analgesics and antipyretics if necessary
Treatment of hospitalized patients
These patients are usually treated with intravenous antibiotics
Ceftriaxone 1-2 gm IV daily or Cefotaxime 1 gm IV twice a day. A macrolide
such as Erythromycin, Azithromycin of Roxithromycin may need to be added to
cover the atypical organisms.

Page 12 of 26

Respiratory disorders for DPHC & CPHC

Duration of antibiotic treatment is the same as for outpatients with communityacquired pneumonia
Oxygen: should be administered to all hypoxemic patients and high concentration
should be used in all patients who do not have hypercapnia or advanced airway
obstruction
With appropriate interventions most patients respond promptly to antibiotic therapy.
Delayed recovery suggests either that some complications such as empyema has
developed or that the diagnosis is incorrect. Alternatively, the pneumonia may be
secondary to a proximal bronchial obstruction or recurrent aspiration which delays
recovery.
Prevention
Pneumococcal and influenza vaccine in high risk groups

BRONCHIAL ASTHMA
Definition
Asthma is a chronic inflammatory disorder of the airways, characterized by reversible
airflow obstruction causing cough, wheeze, chest tightness and shortness of breath. There
is hypertrophy of bronchial smooth muscles and hypertrophy of mucous glands with
increased mucous production and plugging of the small airways with thick mucous can
occur. Also there is airway hyper-responsiveness so that they narrow more readily in
response to a wide range of stimuli.
Asthma is classified as early onset (atopic) asthma and late onset (non-atopic) asthma.
Aetiology/predisposing factors
Atopy
Early exposure to aero-allergens: common aero-allergens include house dust
mites (often found in pillows, mattress, carpets and drapes), cockroaches, cats,
and seasonal pollens.
Early viral infections
Diet
Precipitants of asthma
Exercise
Upper respiratory tract infections
Postnasal drip
Gastro-oesophageal reflux
Changes in weather
Stress
Exposure to environmental tobacco smoke
Dust and acrid fumes
Drugs: adrenoceptor antagonists, aspirin and other NSAIDs

Page 13 of 26

Respiratory disorders for DPHC & CPHC

Clinical features
The frequency of asthma symptoms is highly variable. Some patients may have a
chronic dry cough while others have a productive cough. Some patients have
infrequent, brief attacks and others may suffer nearly continuous symptoms.
Asthma symptoms may occur spontaneously or may be precipitated or
exacerbated by many different triggers given above. Asthma symptoms are
frequently worse at night.
Episodic wheezing
Difficulty in breathing
Chest tightness
Cough (often nocturnal)
Tachypnoea
Audible wheeze
Hyperinflated chest
Hyperresonant percussion note
Diminished air entry
Widespread polyphonic wheeze
Complications
Exhaustion
Dehydration
Airway infection
Cor-pulmonale
Tussive syncope
Pneumothorax (rarely)
Acute hypercapnic and hypoxic respiratory failure occur in severe diseases
Investigations
Diagnosis is made on the basis of a compatible clinical history and demonstration
of variable airflow obstruction
Pulmonary function tests: FEV1 and FVC are decreased
Radiological examination: lungs appear hyperinflated in acute attacks. Between
episodes chest x-ray is normal. In longstanding chronic cases the chest x-ray may
be difficult to distinguish from emphysema. Chest x-ray is not necessary
pneumonia, another disorder mimicking asthma, or a complication of asthma such
as pneumothorax is suspected.
Arterial blood gas analysis: acidaemia and hypoxaemia may be present
In more difficult cases when such tests are negative, an exercise test or histamine
bronchial provocation test, occupational exposure test, or a trial or oral
corticosteroids mar be required
Management
Salbutamol nebulization (1.25-5 mg in 2-3 ml of normal saline) every 4-8 hours
Ipratropium bromide nebulization (0.25-0.5 mg) every 6 hours
Steroids

Page 14 of 26

Respiratory disorders for DPHC & CPHC

Beclomethasone (beclate) inhaler 200 mcg/metered dose three times per day
Prednisolone 40-60 mg per day as a single dose or in two divided doses for 3-10
days
Antibiotics can be given during asthma exacerbation if bacterial respiratory tract
infections are thought to contribute
Oxygen supplementation in all dyspnoic patients
Long-term control medications
Inhaled corticosteroids
Oral sustained release 2 agonist (deriphyllin retard)
Mast cell stabilizers (ketotifen)
Management of chronic persisting asthma (step-up concept)
Occasional inhaled 2 agonists
Low dose inhaled steroids or other anti-inflammatory agents
High dose inhaled steroids or low dose inhaled steroids plus 2 agonists SOS
oral Deriphyllin
High dose inhaled steroids plus Deriphyllin and/or inhaled Ipratropium bromide
Addition of regular oral steroids
Prevention
Avoidance of allergens and predisposing/triggering factors are important
whenever possible
Patients should be taught to recognize symptoms and an action plan be given to
guide treatment and getting expert help when needed
Periodic assessments and ongoing monitoring of patients

ACUTE ASTHMA
Definition
Severe acute asthma (previously know as status asthmaticus) is a persistent and
intractable form of asthma and a medical emergency which if not treated properly could
endanger life.
Aetiology
Failure to take medications adequately and properly
Severe respiratory tract infections
All the causes in aetiology of asthma
Clinical features
Patient usually adopts an upright position, fixing the shoulder girdle to assist the
accessory muscles of respiration
During the attack the chest is held near the position of full inspiration
Percussion note may be hyper-resonant
Breath sounds vesicular in nature with prolonged expiration

Page 15 of 26

Respiratory disorders for DPHC & CPHC

Numerous high pitched polymorphic inspiratory and expiratory rhonchi

Often there is a cough which aggravates respiratory distress
Tachycardia
Pulsus paradoxus
Sweating
Central cyanosis and bradycardia in very severe asthma
Airflow may be so restricted in very severe asthma resulting in a silent chest
which is an ominous sign
Signs of severe asthma
Inability to complete sentences
Pulse rate more than 110/minute
Respiratory rate more than 25 per minute
Signs of life-threatening asthma
Silent chest
Cyanosis
Bradycardia
Exhaustion
Confusion
Feeble respiratory effort
Complication
Same as in asthma
Investigation
Same as in asthma
Management
High concentration oxygen
Inhaled 2 agonists along with oxygen: e.g. salbutamol 2.5-5mg nebulization
repeated with in 30 min if needed
Systemic steroids
If still not improving
Ipratropium 0.5mg added to the inhaled 2 agonists
Aminophylline infusion, 500g/kg/min
Continue nebulized 2 agonists every 15-30 min as needed, decrease to 4 hourly
once clear
Mechanical ventilation if the above measures fail
Indications for mechanical ventilation
Coma
Respiratory arrest
Deterioration of ABG
Exhaustion, confusion, drowsiness

Page 16 of 26

Respiratory disorders for DPHC & CPHC

TENSION PNEUMOTHORAX
Definition
This is accumulation of air in the pleural space with the pressure of air in the pleural
space exceeds ambient pressure throughout the respiratory cycle. A check-valve
mechanism allows air to enter the pleural space on inspiration and prevents the air to go
out during expiration.
The mediastinum is pushed over into the opposite hemithorax, kinking and compressing
the great veins, impairing venous return.
Aetiology
Penetrating trauma
Lung infection
Cardiopulmonary resuscitation
Positive pressure mechanical ventilation
Clinical features
Respiratory distress
Tachycardia
Hypotension
Distended neck veins
Trachea pushed towards the opposite side
Increased percussion note
Reduced air entry/breath sounds on the affected side
Complication
Tension pneumothorax may be life-threatening
Hypotension and shock
Cardiorespiratory arrest
Investigations
Chest x-ray: large amount of air in the affected hemithorax and shift of
mediastinum to the opposite side
Arterial blood gas analysis: hypoxaemia and respiratory alkalosis
Management
Spontaneous pneumothorax is an acute emergency and patient may collapse and
die if management is delayed. Air should be removed with a large-bore (14-16 G)
needle with a syringe partially filled with 0.9% saline. The needle is inserted into
the second intercostals space in the midclavicular line on the side of
pneumothorax. The plunger can be removed to allow trapped air bubble through
the syringe with the saline in it as water seal until a chest tube can be placed.
Alternatively a large-bore IV cannula can be inserted in the same location.
A chest drain has to be inserted subsequently.

Page 17 of 26

Respiratory disorders for DPHC & CPHC

CHRONIC OBSTRUCTIVE PULMONARY DISEASES

(COPD/COAD/COLD)
Definition
Chronic obstructive pulmonary disease is a chronic progressive respiratory disorder
characterized by presence of airflow obstruction with little or no reversibility and which
does not change markedly over the months. Included in this are chronic bronchitis,
emphysema and certain cases of chronic asthma.
Importance of COPD
In recent years there has been an increasing prevalence of COPD in the Maldives and the
rest of the world. It is beyond doubt that cigarette smoking is a major factor in the
development of COPD, though it is also found in people who never smoked. COPD is
related to the number of cigarettes smoked per day. The risk of death from COPD in
patients smoking 30 cigarettes per day is 20 times greater than that of a non-smoker. It is
also related to heavy atmospheric pollution.
The socio-economic burden of COPD is considerable. It is an important cause of absence
from work and causes a significant loss of working days in middle and older age group.
The morbidity of COPD is significantly high with very frequent respiratory infections
and the need for repeated hospitalization. Patients gradually go into chronic respiratory
failure and secondary heart failure (cor-pulmonale), with progressively decreasing effort
tolerance and deteriorating quality of life. Ultimately they become oxygen dependant and
have to be put on home oxygen supplementation in order to achieve a reasonable level of
oxygen saturation.
There is a great deal of financial burden on the family and the country to support patients
with COPD. These patients have to be on lifelong medication and oxygen therapy which

CHRONIC BRONCHITIS
Definition
Chronic bronchitis is a condition associated with excessive tracheobronchial mucous
production sufficient to cause cough with sputum expectoration on most days of at least 3
consecutive months for more than 2 successive years in the absence of any other disease
that might account for this symptom.
Aetiology
Cigarette smoking is the single most important cause. A direct correlation exists
between the number of cigarettes smoked in pack years and the likelihood of
developing COPD. 1 pack year = 20 cigarettes smoked daily for 1 year. Smoking
induces persistent airway inflammation and causes direct imbalance in
oxidant/antioxidant capacity and proteinase/antiproteinase load in the lungs
Air pollution, especially with sulphur dioxide (SO2), (NO2) and particulate matter
Occupation: more common in workers who engage in occupations exposing them
to either inorganic or organic dust or to noxious agents
Infections: morbidity, mortality and frequency of exacerbations are increased

Page 18 of 26

Respiratory disorders for DPHC & CPHC

Familial and genetic factors: Alpha1-antitrypsin deficiency which is associated

with emphysema

Clinical features
Patients with COPD characteristically presents in the fifth or sixth decade of life.
Chronic cough
Recurrent respiratory infections
Exertional breathlessness
Regular and more severe morning cough
Wheeze and chest tightness
Production of sputum which may be scanty, mucoid, tenacious and occasionally
streaked with blood during infective exacerbation
Inspiratory and expiratory rhonchi
Crepitations which usually, but not always, disappear after coughing, mostly
audible over lower zones
Clinical abnormalities in patients with advanced airflow obstruction
Rhonchi, especially on forced expiration
A reduction in the length of trachea palpable above the sternal notch
Tracheal descent during inspiration (tracheal tug)
Contraction of the sternomastoid and scalene muscle on inspiration
Excavation of the suprasternal and supraclavicula fossae during inspiration,
together with indrawing of costal margins and intercostals spaces
Increased antero-posterior diameter of the chest relative to the lateral diameter;
loss of cardiac dullness (barrel chest)
Loss of weight
Pursed-lip breathing (physiological response to decrease air trapping
Central cyanosis
Flapping tremor and bounding pulse (due to hypercapnia)
Peripheral oedema cor-pulmonale
Right ventricular heave, loud pulmonary second sound, tricuspid regurgitation
Complications
Acute bronchitis
Pneumonia
Pulmonary embolization
Pulmonary hypertension
Cor-pulmonale
Chronic respiratory failure
Haemoptysis
Polycythaemia
Investigations
Full blood count: polycythaemia (venesection may be considered if PCV is >
50%), increased lymphocyte count if infection is present
Page 19 of 26

Respiratory disorders for DPHC & CPHC

Chest x-ray: hyperinflation (more than 6 anterior ribs seen above diaphragm in
mid-clavicular line), flat hemi diaphragms, large central pulmonary arteries,
reduced peripheral vascular markings
Arterial blood gas analysis: hypoxaemia with or without hypercapnia
Pulmonary function tests
Classification and diagnosis of COPD based on spirometry
Severity Spirometry
Mild
FEV1 60 79%predicterd
Moderate FEV1 40 59% predicted
Severe
FEV1 < 40% predicted

Management
Treatment of stable COPD patients
Non-pharmacological
Stop smoking
Encourage exercise
Treat poor nutrition or obesity
Pharmacological
Mild: short acting 2 agonists or ipratropium
Moderate: regular short acting 2 agonists and/or ipratropium. Corticosteroid trial
may be considered
Severe: combination therapy with regular short acting 2 agonists and ipratropium
Corticosteroid trial may be considered. Home nebulization if possible
In advanced cases patients have to be on home oxygen supplementation
Management of acute COPD exacerbation
Check ABG, chest radiograph, ECG, CBC, urea/electrolytes, send sputum for c/s
and blood c/s if febrile
Oxygen: controlled O2 therapy at the rate of 2 lit/min by nasal prongs
Nebulized bronchodilators: salbutamol 2.5-5 mg four hourly and sos and
ipratropium 0.5 mg six hourly. If no response with the nebulized bronchodilators,
consider intravenous aminophylline infusion
Antibiotics: to be considered if any two of the following are present. Increasing
expectoration, purulent sputum or increasing dyspnoea
Chest physiotherapy to aid sputum expectoration
Oral corticosteroids: if patient is already on steroids, if airflow obstruction fails to
respond to bronchodilator therapy or if patient is known to be steroid responsive
(prednisolone 30mg daily for 1 week)
Diuretics: if JVP elevated and oedema present
Non-invasive intermittent positive pressure ventilation (CPAP mask), if
respiratory rate remains more than 30 per minute or pH less than 7.35 even after
starting maximal therapy
Consider intubation and ventilation if pH less than 7.26 and PaCO2 is rising

Page 20 of 26

Respiratory disorders for DPHC & CPHC

Prevention
Quit smoking: COPD is largely preventable through elimination of chronic
exposure to tobacco smoke
Avoidance of dusty and smoke-laden atmosphere
Vaccination against influenza and Pneumococcal disease may also benefit

BRONCHIECTASIS
Definition
Bronchiectasis is a congenital or acquired disorder of the large bronchi characterized by
permanent, abnormal dilatation and destruction of bronchial walls. It may be localize or
diffused and may affect any part of the lungs, but the more efficient drainage by gravity
of the upper lobes produces less serious symptoms and complications.
Aetiology
Congenital
Ciliary dysfunction
Cystic fibrosis
Primary hypogammaglobulinaemia
Acquired (in children)
Primary pulmonary tuberculosis
Foreign body
Acquired (in adults)
Suppurative pneumonia
Pulmonary tuberculosis
Allergic bronchopulmonary aspergillosis
1-antiprotease deficiency with cigarette smoking
Bronchial tumors
Clinical features
Chronic productive cough, usually worse in the morning and often brought out by
changes in posture
Sputum often copious and persistently purulent in advanced diseases copious
foul smelling, purulent sputum is characteristic
Recurrent pneumonia: Fever, malaise, and increased sputum volume which is
frequently associated with pleurisy
Haemoptysis: can be slight or massive and often recurrent
Weight loss
Anorexia
Lassitude
Sleep sweating
Digital clubbing

Page 21 of 26

Respiratory disorders for DPHC & CPHC

Obstructive pulmonary dysfunction with hypoxaemia seen in moderate or severe

disease
Persistent crepitations at the lung bases are common

Complications
Pneumonia
Pleural effusion
Pneumothorax
Haemoptysis
Cor-pulmonale
Secondary visceral abscesses at distant sites (e.g. brain)
Amyloidosis
Investigation
Chest x-ray: crowded bronchial marking due to peribronchial fibrosis, and small
cystic spaces at the base of the lungs
CT scanning: high resolution CT is the diagnostic study of choice
Sputum examination
Management
Antibiotics selected on the basis of sputum culture and sensitivity. Empirical
therapy for 10-14 days with Amoxicillin 500 mg PO 8 hourly, Augmentin
375/625 mg PO 8 hourly, Septran 1 tab PO 12 hourly can be used
Postural drainage to keep dilated bronchi free from secretions is of great value in
reducing the amount of cough and sputum and in preventing recurrent episodes of
bronchopulmonary infection. In its simplest form this is done by adopting a
position in which the lobe to be drained is uppermost. This causes secretions to
gravitate towards trachea which can subsequently be cleared by vigorous cough.
Percussion of chest wall with cupped hands aids in dislodgement of sputum.
Mechanical devices that causes chest wall to oscillate and facilitate removal of
mucous are also available. Duration and frequency of postural drainage depends
on the amount of sputum. 5-10 min once or twice per day is the minimum. Forced
expiratory maneuvers (huffing and puffing) are of help in augmenting the
expectoration of sputum.
Bronchoscopy is sometimes necessary to evaluate haemoptysis, remove retained
secretions and rule out obstructing airway lesions.
Surgical treatment (only in certain selected cases) involves resection of areas of
bronchiectatic changes.
Prevention
The key to prevention of acquired bronchiectasis is adequate treatment of conditions that
would lead to bronchiectasis later in life. These include measles, whooping cough,
tuberculosis and early recognition and treatment of bronchial obstruction. It is important
to effectively and adequately treat these conditions in children as they might lead to
bronchiectasis subsequently.

Page 22 of 26

Respiratory disorders for DPHC & CPHC

LUNG ABSCESS
Definition
Large localized collection of pus or a cavity lined by chronic inflammatory tissue.
Aetiology
Most commonly by Staphylococcus aureus and K. pneumoniae in previously
health lungs
Inadequately treated pneumonia
Aspiration of gastrointestinal contents
Bronchial obstruction (tumor, foreign body)
Bacterial infection of a pulmonary infarct or a collapsed lobe
Septic emboli (septicemia, right heart emboli, IV drug use
Subphrenic or hepatic abscesses
Clinical features
Swinging fever
Cough productive of large amount of sputum, sometimes fetid and blood-stained
Pleuritic chest pain
Sudden onset of copious amount of foul sputum, if abscess ruptures into a
bronchus
Profuse systemic upset
Digital clubbing may develop quickly (within 10-14 days)
Anemia
Chest examination: signs of consolidation movement of chest wall reduced on
the affected side, dull percussion note, high-pitched bronchial breath sounds, and
fine crepitations initially and later coarse crepitations
Pleural rub
Rapid deterioration in general health with marked weight loss can occur if not
adequately treated
Complications
Investigations
Complete blood count: anemia and neutrophilia
Blood culture
Chest x-ray: walled opacity, often with fluid level
Sputum examination: microscopy, culture and cytology
Management
Antibiotics as indicated by sensitivity test or with aqueous penicillin G1.5-2.0
million units is satisfactory. Therapy can be switched to oral penicillin once a
clinical response is observed and should be continued until the cavity close.
Healing may take 6-12 months

Page 23 of 26

Respiratory disorders for DPHC & CPHC

If an anaerobic bacterial infection is suspected (e.g. from fetor of sputum) oral

metronidazole 400 mg 8 hourly should be added
Physiotherapy and postural drainage is of great value, especially when large
abscess cavity is formed
Abscesses that fail to resolve despite optimal medical therapy require surgical
intervention

RESPIRATORY FAILURE
When the lung function is inadequate for the metabolic requirement of an individual
resulting in hypoxia, it is labeled as respiratory failure. It could be hypoxic or
hypercapnic respiratory failure.
Arterial blood gas criteria for respiratory failure are arbitrarily taken as a PaO2 of less
than 60 mm Hg or a PaCO2 of more than 50 mm Hg.
Aetiology
Severe acute asthma
Emphysema
Pulmonary oedema
Pulmonary embolism
Pneumonia
COPD
Cardiac failure
Trauma
Pneumothorax
Narcotic drugs/CNS depression
Clinical features
Hypoxemic features
Dyspnoea
Cyanosis
Restlessness
Confusion
Anxiety
Delirium
Tachypnoea
Hypertension
Cardiac arrhythmias
Hypercapnic features
Dyspnoea and headache are the cardinal symptoms of hypercapnia
Peripheral and conjunctival hyperemia
Hypertension
Tachycardia
Page 24 of 26

Respiratory disorders for DPHC & CPHC

Tachypnoea
Impaired consciousness
Papilloedema
Asterixis

Investigations
Full blood count
Blood urea and serum creatinine
Arterial blood gases
Chest x-ray
Sputum and blood cultures (if febrile)
Management
Treatment of the patient with respiratory failure is directed towards the underlying
diseases with general and respiratory supportive care.
General and supportive care
Maintenance of adequate nutrition: overfeeding, especially with carbohydrate rich
formula/food should be avoided, because it can increase CO2 production and may
potentially worsen or induce hypercapnia in patients with limited ventilatory
reserve.
Psychologic and emotional support for the patient and the family
Skin care to avoid decubitus ulcers
Avoidance of nosocomial infections and stress gastric ulcers
Respiratory support
Oxygen via face mask to maintain PaO2 more than 60 mm Hg
Assisted/mechanical ventilation when indicated

BRONCHIAL CARCINOMA
Lung cancer is the leading cause of cancer deaths in both men and women. Ninety
percent of cases of lung cancer in men and seventy nine percent in women are directly
attributable to cigarette smoking.
Aetiology
Cigarette smoking is the most important factor
Exposure to environmental cigarette smoke (passive smoking)
Exposure to radon gas and asbestos
Familial predisposition is also recognized
Associated with certain diseases like pulmonary fibrosis, COPD and sarcoidosis
Clinical features
When the tumor arises from a large bronchus, symptoms arise early, but those arising in a
peripheral bronchus can attain very large size without producing symptoms.
May involve the pleura either directly or through lymphatics

Page 25 of 26

Respiratory disorders for DPHC & CPHC

May extend into the chest wall, invading intercostals nerves or brachial plexus, resulting
in severe pain
May spread into the mediastinum and invade or compress other structures in the
mediastinum.
Anorexia
Weight loss or asthenia
Cough or change in a chronic cough
Haemoptysis
Dyspnoea
Chest pain
Change in voice
Pleural effusion
Clubbing
Hypertrophic pulmonary osteoarthropathy (causing wrist pain)
Lymphadenopathy (supraclavicular or axillary)
Signs and symptoms depending on the site of metastasis

Page 26 of 26