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Clinical Assessment6
https://t.me/med1917
Long-term antibiotics for prophylaxis in COPD/bronchiectasis (usually
•
azithromycin). Previous prescriptions for this condition.
•
Immunosuppressive medications: e.g. oral corticosteroid use.
•
Bone protection if on regular corticosteroids e.g. calcium/vitamin D combi-
•
nation +/− oral bisphosphonate. Anticoagulant/antiplatelet drugs: may influence safety of procedures or
•
biopsies.
MICRO-facts
Medications that can cause/worsen respiratory symptoms:
ACE inhibitor: causes cough due to lack of degradation of
bradykinin. Amiodarone, methotrexate, nitrofurantoin: can cause pulmonary fibrosis. β-blockers: may worsen bronchoconstriction due to blockade of β2-adrenoceptors in the lungs. Non-steroidal anti-inflammatory drugs: may cause bronchospasm in asthmatics due to an increase in leukotriene production.
4. ALLERGIES
Ask about drug allergies before prescribing any drug.
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Relevant if anaphylaxis is suspected.
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Allergic/atopic disease is associated with asthma.
•
5. FAMILY HISTORY
Genetic diseases: cystic fibrosis, α1-antitrypsin deficiency.
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Atopic diseases: eczema, hay fever, asthma.
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Venous thromboembolism (VTE): may suggest a familial thrombophilia.
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Malignancy: although 50% of people born after 1960 will be diagnosed
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with some form of cancer in their lifetime (https://cancerresearchuk.org), this lacks specificity.
History of TB in the family.
•
6. SOCIAL HISTORY
Smoking history: see MICRO-Facts (below).
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Inhaled drugs.
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Housing: overcrowding is a risk factor for TB and infection.
•
Pets:
•
Respiratory Medicine
• Cats, dogs, rodents: may worsen atopic disease.
• Birds: associated with hypersensitivity pneumonitis and psittacosis
pneumonia.
1.2 Examination
https://t.me/med1917
MICRO-facts
Calculating “pack-years”
Pack-years=(number of cigarettes smoked per day) × (number of years smoked)/20.
7. OCCUPATION
Asbestos exposure: in shipyards, building, plumbing and family members
•
washing asbestos-covered work clothes (see Chapter 17: Occupational lung disease). Dust exposure: silicon, coal dust, flour.
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Occupational asthma (see Chapter 17: Occupational lung disease for high-
•
risk occupations).
8. TRAVEL HISTORY
Any travel to TB endemic regions? How long ago?
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Any other travel: may increase risk of atypical infection.
•
1.2 EXAMINATION
1. GENERAL INSPECTION
7
Around the bed area: inhalers, oxygen, nebuliser, sputum pot, CPAP or
•
NIV machine. Of the patient: colour, comfort, nutritional status and respiratory rate.
•
Signs of respiratory distress:
•
• Pursed-lip breathing.
• Use of accessory muscles.
• High respiratory rate (>20 breaths/min).
• Cyanosis (central or peripheral).
• Difficulty completing sentences.
2. HANDS
Clubbing: loss of angle between nail and nail bed, increased nail bed fluctu-
•
ance (feels spongy), increased curvature of nail and increased soft tissue bulk over terminal phalanx (Figure 1.1).
Respiratory Medicine
Clinical Assessment8
https://t.me/med1917
Figure 1.1 Apatient with clubbing of fingernails.
MICRO-facts
Respiratory causes of clubbing – “BE CALM”:
Bronchiectasis Empyema Cystic fibrosis Abscess Lung fibrosis Malignancy.
Tar staining: yellow/brown staining seen in smokers.
•
Muscle wasting:
•
• Generalised wasting/cachexia associated with emphysema or
malignancy.
• Focal wasting of intrinsic muscles between thumb and first finger due
to compression of the medial cord of the brachial plexus (T1 root) by apical lung cancer.
Tremor: fine tremor from β-agonist use.
•
Asterixis: flapping tremor of CO2 retention when wrist extended at 90 degrees.
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Purpura and muscle wasting in limbs: long-term or frequent corticosteroid use.
•
3. FACE
Central cyanosis (Figure 1.2).
•
Horner’s syndrome: miosis, ptosis and anhidrosis associated with Pancoast’s
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(apical) tumour. Facial swelling: from superior vena cava obstruction.
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Moon-like facies: Cushing’s syndrome precipitated by long-term or frequent
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Respiratory Medicine
corticosteroid use. Poor dentition: risk factor for lung abscess.
•
1.2 Examination
https://t.me/med1917
Figure 1.2 Apatient with central cyanosis, showing classic bluish discolouration of lips.
4. NECK
Inspect for raised jugular venous pressure (JVP): seen in right heart
•
failure (pulsatile) and superior vena cava obstruction (non-pulsatile).
Palpate the cervical lymph nodes.
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Palpate for tracheal deviation: the trachea will deviate towards a collapsed
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lung and away from a tension pneumothorax or massive effusion.
9
5. PRECORDIUM
Palpate the apex beat: deviation occurs in tension pneumothorax.
•
Auscultate.
•
6. CHEST
Inspection:
•
• Scars
• Symmetry
• Shape:
– Pectus carinatum (pigeon chest):
◯
Protrusion of the sternum and adjacent costal cartilages.
◯
Accompanied by rib indrawing.
◯
Historically associated with rickets.
◯
May be seen in severe childhood asthma.
– Pectus excavatum (funnel chest):
◯
A congenital abnormality causing localised depression of the lower end of the sternum.
Muscle wasting
•
Palpation:
•
• Assess chest expansion: Is it restricted? Does the chest expand
symmetrically?
Respiratory Medicine
Clinical Assessment10
https://t.me/med1917
•
•
Respiratory Medicine
• Check for tactile vocal fremitus: palpate as the patient says
“ninety-nine”.
– Transmission is increased in consolidation and decreased with effu-
sion or pneumothorax.
Percussion:
• Resonant: normal.
• Hyperresonant: pneumothorax if unilateral; emphysema if bilateral.
• Dull: consolidation, collapse and fibrosis.
• Stony dull: effusion, empyema.
Auscultation:
• Listen for air entry throughout the lung fields. Is it reduced?
• Are breath sounds:
– Vesicular? normal “rustling” breath sounds. – Bronchial? high-pitched “hollow” or “blowing” breath sounds. Similar
sound quality to listening over the trachea during normal breathing.
◯
e most common cause is consolidation e.g. pneumonia.
• Any added breath sounds?
– Wheeze: musical sound caused by airway narrowing. – Usually expiratory.
◯
Inspiratory when narrowing is severe.
◯
Associated with asthma and COPD.
– Stridor: harsh, rasping inspiratory sound caused by upper airways
obstruction.
– Crepitations (crackles): interrupted non-musical sounds mostly
occurring during inspiration similar to opening of hook-and-loop closures.
◯
Airways collapse on expiration and abruptly open during inspira­tion, causing a cracking noise.
◯
Typically, fibrosis causes fine end-inspiratory crackles.
◯
Bronchiectasis causes coarse biphasic crackles.
◯
Coarse crackles (ruttles) are caused by secretions within the larger airways.
◯
Crackles may also occur in pulmonary oedema.
– Pleural rub: creaking sound caused by the movement of inflamed
parietal or visceral pleural over each other.
◯
Described as the sound heard when a foot presses into snow.
• Assess for any change in the character of the sounds after cough-
ing: a change suggests the cause is bronchial secretions.
• Assess vocal resonance: ask the patient to say “ninety-nine” while you
auscultate.
– Sounds are transmitted more easily across consolidation (louder)
and less easily across pneumothorax, collapse or effusion (quieter).
1.3 Investigations in Respiratory Medicine
https://t.me/med1917
7. COMPLETING THE EXAMINATION
Examine the legs:
•
• For deep vein thrombosis if pulmonary embolism is suspected.
• For pedal oedema if cor pulmonale (see MICRO-Print) is suspected.
Examine the sputum pot.
•
Check oxygen saturation and temperature chart.
•
Take blood pressure.
•
MICRO-print Cor Pulmonale
“Cor pulmonale” is a term used to describe impaired right ventricular function caused by increased vascular resistance in the pulmonary circulation.
It is caused by chronic lung disease, e.g. COPD.
1.3 INVESTIGATIONS IN RESPIRATORY
MEDICINE
11
1. CHEST X-RAY (CXR)
One of the most commonly requested imaging investigations.
•
is is produced by the projection of X-rays through the patient onto a radio-
•
graphic plate. Differential absorption of X-rays by tissues of different densities results in five
•
main “shades” on a black-and-white scale (Table 1.3).
Table 1.3 Appearances on CXR.
STRUCTURE SHADE
Bone/calcified structures White Soft tissue Grey Fat Dark grey Gas Black Man-made structures/artifact Bright white
Respiratory Medicine
Clinical Assessment12
https://t.me/med1917
Figure 1.3 The anatomy of the lung, showing the lobe of the lung and fissures.
Structures that are identifiable in the lungs include:
•
• Blood vessels
• Interlobular fissures
• Walls of larger bronchioles.
e lung hila should be visible bilaterally.
•
Lung lobes are identifiable (see Figure 1.3).
•
NB: CXR appearances are covered with each condition throughout the
•
book.
2. ULTRASOUND
Ultrasound waves are produced by passing electrical current through a piezo-
•
Respiratory Medicine
electric crystal and emitted via a probe.
1.3 Investigations in Respiratory Medicine
https://t.me/med1917
e same probe detects the waves as they are reflected back by the tissues.
•
e relative echogenicity of tissues are represented by shades of grey.
•
In respiratory medicine, the principle uses of ultrasound are:
•
• To assess the pleural space e.g. for effusions and pleural thickening.
• For radiologically guided interventions e.g. chest drain insertion, pleu-
ral aspirations and pleural biopsies.
3. COMPUTED TOMOGRAPHY (CT)
CT uses a rotating X-ray tube and a row of detectors to measure X-ray
•
attenuations by different tissues inside the body. e data is reconstructed to produce a tomographic (cross-sectional) stack of
•
2D images that can be reformatted in different planes, e.g. sagittal, coronal, axial. Attenuation by tissue is represented by a greyscale.
•
• Denser material appears brighter.
Volume CT with contrast: also used in diagnosis of bronchial carcinoma,
•
pulmonary metastases and for assessment of pneumonia complications. CT pulmonary angiography (CTPA): used to identify pulmonary
•
embolism. High-resolution CT scans (HRCT): used to detect parenchymal lung
•
change, e.g. bronchiectasis and pulmonary fibrosis. High-resolution doesn’t mean “better”, and the lack of contrast limits their utility to these conditions. Interpretation of chest CT is usually performed by specialists.
•
13
4. ABG
PaO2: <8 kPa – hypoxaemia
•
• Always analyse PaO
• PaO
PaCO2 >6.5 kPa – hypercapnia
•
• PaCO
should be roughly 10kPa lower than inspired FiO2 with normal
2
lung function.
– e.g. if FiO2 is 40%, PaO2 should be ~30 kPa.
2
• High PaCO
tory failure.
• CO
is an acidic gas and so any respiratory condition causing raised
2
levels will cause a respiratory acidosis.
– If acute, the pH will be low, but if chronic there will be renal
compensation with a normal pH and a raised bicarbonate and base excess.
Acid-base status (Table 1.4)
•
with reference to the inspired FiO2.
2
is a measure of ventilation.
in combination with low PaO2 indicates type II respira-
2
Respiratory Medicine
Respiratory Medicine
https://t.me/med1917
Table 1.4 Identifying acid-base disturbances.
COMPLAINT PH CO Respiratory
↓ ↑ ↑
2
acidosis • Life-threatening asthma phase and may be chronically raised
Respiratory
↑ ↓ ↓
alkalosis pulmonary embolism
Metabolic
↓ ↓ ↓
acidosis Increased loss of bicarbonate to a fall in pCO
Metabolic
↑ ↑ ↑
alkalosis Loss of K+ e.g. diuretic use, plateau.
HCO
−
3
Acute respiratory failure: Elevation of HCO
COMMON CAUSES COMMENTS
−
occurs in late
3
• COPD exacerbation in COPD with established respira-
• Pneumonia tory failure.
• Inadequate ventilation:
• Chest wall abnormality such as severe scoliosis
• Obesity hypoventilation syndrome
• Neuromuscular disease
• Central depression of respiration (e.g. opiates)
Hyperventilation e.g. in anxiety or
Increased production of organic acids Compensatory hyperventilation leads
which will (at least
2
partially) offset the acidosis.
+
Loss of H
e.g. vomiting Rise in pCO2 is gradual and will
hyperaldosteronism
Clinical Assessment14
1.3 Investigations in Respiratory Medicine 15
https://t.me/med1917
5. PULMONARY FUNCTION TESTS
Peak expiratory flow rate (PEFR):
•
• is is a simple bedside test that is performed by inhaling to total lung
capacity then rapidly exhaling into the peak flow meter.
• PEFR is measured in litres per minute (L/min).
• It is most useful in the diagnosis and monitoring of asthma.
• Typically, PEFR will be reduced in asthmatics, exhibit diurnal variabil-
ity and improve in response to bronchodilator treatment.
• Occupational asthma can be associated with an improvement in PEFR
measurements when away from the workplace (weekends and holidays).
Spirometry:
•
• Lung volumes are measured by inhaling to total lung capacity and then
fully exhaling into the spirometer (Table 1.5). e key values are:
– Forced expiratory volume in 1 second (FEV1): the volume of air
that is exhaled in the first second of expiration. – Forced vital capacity (FVC): the total volume of air expired. – Ratio of FEV1/FVC.
Table 1.5 Spirometry findings in respiratory disease.
PATTERN OF RESPIRATORY FEV DISEASE FEV
Obstructive
Restrictive
FVC FVC COMMON CAUSES
1
↓ ↑/↔
↓ ↓↓
/
1
<0.7 • Asthma
• COPD
>0.8 Interstitial lung disease such as
idiopathic pulmonary fibrosis and hypersensitivity pneumonitis
Extra-thoracic lung restriction such
as obesity, kyphoscoliosis and neuromuscular diseases
Respiratory Medicine
Flow-volume loop:
•
• A plot of inspiratory and expiratory flow (y-axis) against lung volumes
(x-axis).
• On expiration in normal individuals: initially there is a rapid rise in
flow to the peak flow, due to:
– Greater elastic traction of alveolar septa on airway at the beginning
of expiration. – Greater expiratory muscle strength at the beginning of expiration. – Lower airway resistance initially.
• A near linear fall in flow rate occurs with continued expiration.