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RRReeessspppiiirrraaatttooorrryyy DDDiiisssooorrrdddeeerrrsss ...................................................................................................... 1 fffooorrr DDDPPPHHHCCC &&& CCCPPPHHHCCC ........................................................................................................... 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

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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.


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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. Ventilation-perfusion 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


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• 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


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• 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)


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• 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 µg/spray twice daily in each nostril), mometasone furoate (200 µg once daily per nostril) or fluticasone propionate (200 µg once daily per nostril). The latter two have higher topical


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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


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• 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


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• 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.


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• Duration of antibiotic treatment is the same as for outpatients with community-acquired 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: β adrenoceptor antagonists, aspirin and other NSAIDs


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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


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• 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 β2 agonist (deriphyllin retard) • Mast cell stabilizers (ketotifen)

Management of chronic persisting asthma (step-up concept) • Occasional inhaled β2 agonists • Low dose inhaled steroids or other anti-inflammatory agents • High dose inhaled steroids or low dose inhaled steroids plus β2 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


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• 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 β2 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 β2 agonists • Aminophylline infusion, 500µg/kg/min • Continue nebulized β2 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


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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.


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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


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• 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


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• 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 β2 agonists or ipratropium • Moderate: regular short acting β2 agonists and/or ipratropium. Corticosteroid trial

may be considered • Severe: combination therapy with regular short acting β2 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


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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 • α1-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


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• 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.


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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


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• 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


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• 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


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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

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