Examination notes 
Relevant radiology
Explanation of signs
​Lung function tests
​

1. Interstitial lung disease
2. COPD
3. Bronchiectasis
4. Thoracotomy scars
5. Kypho-scoliosis
6. SVC obstruction
7. Pleural Effusion
8. Collapse/ Consolidation
9. Carcinoma of the lung

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Interstitial Lung Disease

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• Usually a very straight forward diagnosis, the marks are in determining aetiology (idiopathic interstitial vs connective tissue associated), complications (pulmonary hypertension, complications of drug therapy eg steroids) and functional status
• Most commonly it is idiopathic pulmonary fibrosis (suspect if the individual is a male > 60) or ILD associated with a connective tissue disease (classically diffuse scleroderma)
• Clues to function at the bedside include presence of oxygen therapy (may require it longterm) and breathlessness at rest (MRC breathlessness scale)
• General findings
  • clues to aetiology of connective tissue disease eg malar flush, discoid rash, CREST features
  • Productive vs non-productive cough
  • Ankylosing spondylitis --> loss of lumbar lordosis and cervical lordosis, increase in thoracic kyphosis
• Peripheral hand signs
  • clubbing (present only in 50%) - AKA acropachy, hippocratic fingers. Other causes of clubbing exist as well
  • RA - rheumatoid nodules, synovitis, tendon rupture, ulnar deviation at wrist, swan-neck deformity etc
  • SLE - jacoud's arthropathy, discoid rash, vasculitic haemorrhages
  • dermatomyositis - gottron's papules, heliotrope rash
  • polymositis - mechanics hands (anti-synthetase syndrome)
  • Radiation therapy - radiation marks on skin, erythema
  • Sarcoidosis - erythema nodosum, lupus pernio, lymphadenopathy
• Generalised lymphadenopathy may be seen in sarcoidosis
• Eyes --> scleromalacia in vasculitis
• Nose --> polyps in Churg-Strauss, collapsed nasal septum in Wegner's
• Mouth --> central cyanosis, gingival hyperplasia if cyclosporin has been used
• Trachea --> usually central.
• FEV --> reduced in totality
• Thorax --> mediastinoscopy scar, LN biopsy scars, thoracoscopy scars, lung biopsy scars
• Chest expansion --> if predominant apical fibrosis (HP, fibrosing alveolitis secondary to ank spond, ABPA, sarcoidosis) reduced chest expansion locally, otherwise globally reduced. Normal >5cm
• Percussion --> dull over bases with reduced vocal fremitus
• Auscultation --> decreased air-entry, fine, end-inspiratory crackles at bases (if basal predominant), apical crackles if apical fibrosis predominant. Inspiratory squawks may be present with involvement of small airways (bronchiolitis) or in hypersensitivity pneumonitis
• Always examine for signs of pulmonary hypertension (RV heave, palpable P2, loud P2, signs of TR (systolic murmur LSE, greater with inspiration + v waves), signs of PR (graham steel murmur), pulsatile liver, ascites, oedema

Presentation
"Mr XR is a 64 yo male who presents with the key physical examination findings consistent with severe (functional comment) interstitial lung disease (diagnosis) and concomitant atrial fibrillation (diagnosis, complication). He also has features consistent with pulmonary hypertension (complication). In detail, Mr XR was breathless at rest. The fingers are clubbed. There was no evidence of hypertrophic pulmonary osteoarthropathy. There was no stigmata of connective tissue diseases. His respiratory rate was elevated at 30 breaths per minute resting, with a pulse rate of 128, which was irregularly irregular. He had a reduced forced expiratory time. There was no evidence of thoracic outlet syndrome. He did not have lymphadenopathy over the lymph node groups that I examined. His trachea was midline. General inspection of his chest was unremarkable - there was no evidence of scoliosis or significant kyphosis. Chest expansion was reduced bilaterally. There was decreased vocal fremitus bi-basally. Auscultation of the chest revealed decreased air-entry bilaterally, especially at the bases and extending up to the mid zones. There were fine end-inspiratory crackles at both bases. There were no audible squawks or wheeze. In addition, the JVP was elevated with absent 'a' waves but prominent 'v' waves. There was a pulsatile liver. A palpable second heart sound was heard over the pulmonic region with a left para-sternal heave.

Please interpret this patients CXR findings

• CXR may show findings of bilateral basal reticulonodular infiltrates (IPF/UIP), bilateral hilar adenopathy (sarcoid, TB), calcified nodules (TB), apical predominance (berryliosis, radiation, hp, sarcoid, abpa etc), calcified pleural plaques

What would you expect the lung function tests to show in a patient with IPF

• Have to be able to interpret spirometry and static volume tests
• Can have concomitant obstructive (FEV1/FVC <0.7) and restrictive (TLC <80%) patterns, especially if there is overlapping pathology
• Typically spirometric ratio is non-obstructive, but there is reduced FEV1 and FVC, suggesting a restrictive deficit
• Lung volumes are reduced
• DLCO is reduced, mainly due to decreases in V(a), but in more advanced disease KCo is also reduced. In good-pastures, DLCO may be elevated (lung haemorrhage)

What are the typical HRCT findings

• Basal predominance. Note is apical predominance suggests another pathology
• Reticular markings
• sub-pleural honey-combing. Note if there is ground-glass changes consider NSIP
• Traction bronchiectesis

What are the conditions known to cause predominant apical distribution fibrosis?

• mnemonic --> BREAST CLAPS
  • Berylliosis
  • Radiation pneumonitis
  • Extrinsic allergic alveolitis
  • ABPA
  • Sarcoidosis
  • Tuberculosis
  • Silicosis
  • Coal workers pneumoconiosis
  • Langerhans cell histiocytocis
  • Ankylosing spondylitis
  • Psoriasis
  • Note --> all inhaled agents apart from aesbestos causes APICAL distribution fibrosis

What are the conditions known to cause predominant basal distribution fibrosis?

• Use mnemonic RACIS
• ​rheumatoid disease (except Ank Spond and psoriasis)
• Asbestosis
• connective tissue disease (wegners, churg-strauss)
• IPF
• systemic administered drugs (MTX, bleomycin, bisulphan, amiodarone, nitrofurantoin)

What are the key components in the management of this patient who has been diagnosed with idiopathic pulmonary fibrosis?

• Always mention the three pillars (1) Modify Disease (2) Retard progression (3) Manage complications & support function. Under each sub-heading thing non-medical, pharmacological, surgical management
  • Modify disease --> currently there are no disease effect modifiers
  • Retard progression --> non-medical [exercise program, multi-disciplinary team specialising in ILD with dedicated ILD care nurse, smoking cessation, medication review with pharmacist to decrease fibrotic drugs], pharmacological [evidence for pirfenidone, nintedanib in reducing loss of FVC], surgical [lung tx if pt would qualify, always for pt who is young]
  • Manage complications --> non-medical [pulmonary rehabilitation, general rehabilitation programs, occupational therapy, physiotherapy, social worker for DSP etc, palliative care for relief of terminal dyspnoea], pharmacological [oxygen prescription, screen for pulmonary hypertension, treat chest infection]​

What are the HRCT findings you would observe in idiopathic pulmonary fibrosis?

• Peripheral (subpleural)
• Basal predominance with less changes at the apex
• Reticular changes (suggestive of fibrosis/thickening of the septal lines)
• Honeycombing – only at the edge, abutting the pleura -> pathognomonic feature of IPF
• Traction of bronchiectasis – due to airways being pulled apart, at middle of airways

What are some radiological findings that would argue against a diagnosis of idiopathic pulmonary fibrosis?

• Upper or mid lung: think sarcoidosis or hypersensitivity pneumonitis
• Peribronchovascular: think sarcoidosis
• Extensive group glass change: think NSIP
• Micronodules: think HP, MAC

You hear inspiratory squeaks on clinical examination. What interstitial lung disease does this signify?

• Squawks are heard from the middle to the end of inspiration in patients with hypersensitivity pneumonitis
• They are not pathognomonic of this condition, they may also occur in bronchiectasis and pneumonia
• It is hypothesised that the production of squawks occur via the oscillation of peripheral airways in deflated lung zones where the walls remain in apposition long enough to oscillate under the action of inspiratory flow - N Engl J Med 2014; 370:744-751

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Chronic Obstructive Pulmonary Disease

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General Inspection

• Presence of sputum cup with purulent sputum
• Presence of oxygen cylinder
• Increased work of breathing
• Central and peripheral cyanosis
• Ruddy complexion because of secondary polycythaemia
• cachectic appearance
• Tracheal tug
• Barrel chest with enlarged anterior posterior diameter
• Inhalers by bedside

FEV

• Prolonged expiratory time

Hands

• Clubbing only if in association with another disease
• Fine tremor if present from use of short acting beta agonists
• nicotine staining
• Peripheral cyanosis
• Asterixis secondary to CO2 retention
• Evidence of HPOA if COPD complicated by bronchogenic carcinoma
• Brusing, proximal myopathy

Face

• Polycythaemic facies
• Cushingoid facies
• Central cyanosis
• Oral candidiasis
• Tracheal tug

Chest

• Increased anterior-posterior diameter
• Bilaterally reduced breath sounds
• +/- early inspiratory crackles
• +/- expiratory wheeze
• Hoovers sign - placing the hands on the anterior chest with the thumbs coming together at the xiphisternum. Subsequent expansion paradoxically brings the thumbs closer together rather than further apart due to paradoxical movement of the rib cage inwards
• Hyper-resonant percussion note
• Signs of cor pulmonale (RV heave, loud P2, TR +/- PR murmur, pulsatile liver, systolic 'v' waves)

Peripherally

• Oedema

What is your differential diagnosis of a patient with a wheeze?

1. Asthma
2. Bronchiectesis
3. Bronchiolitis obliterans
4. ABPA
5. Localised - then fixed bronchial obstruction by tumour, foreign body, mucus plug

What is the aetio-pathogenesis of the expiratory wheeze?

• It has been hypothesised that wheezes are formed between the second and seventh generation of the airway tree as a result of airflow through a narrowed lumen causing oscillation of the gas and the airway walls. The walls have had to be narrowed almost to the point of apposition
• In severe asthma, a silent chest secondary to severe airflow limitation does not produce a wheeze because there isn't enough flow to generate the necessary sound energy
•  On audiometry, one would see sinusoidal oscillations with sound energy in the range of 100 to 1000 Hz N Engl J Med 2014; 370:744-751

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What investigations would you ask for?

1. Formal Spirometry
   1. Reduced spirometric ratio <0.70
   2. Decreased FEV1 to grade severity
   3. Bronchodilator reversibility (12% and 200ml post bronchodilator)
   4. Static lung volumes - Typically gas trapping with increase in TLC and RV
   5. In COPD have decreased KCO, whereas in asthma this tends to be normal
      1. V(alveolar) may be decreased compared to TLC due to poor gas admixture
2. CXR
   1. hyper-inflation - narrowed mediastinum, increased number of ribs, widened rib spaces, flattened hemidiaphragm
   2. Rule out mass, pneumonia, effusion
   3. Presence of bullae
   4. Pneumothorax
3. Arterial blood gases
   1. Type 1 respiratory failure
   2. Type 2 respiratory failure
4. Routine blood tests
   1. FBC looking for polycythaemia, leukocytocis with neutrophilia, reactive thrombocytocis
   2. UEC - may have hypokalaemia associated with SABA useage
   3. LFT - hepatic involvement is alpha-1 antitrypsin deficiency occurs
   4. CRP
5. ECG
   1. look for signs of right ventricular strain - strain pattern on V1 - V2, incomplete RBBB, right axis deviation, p pulmonale
   2. multifocal atrial tachycardia, which is characterised by HR >100 and at least 3 different P wave morphologies with varying PR intervals
6. Sputum culture
   1. Looking for common organisms such as pseudomonas spp, haemophilus spp
7. Alpha-1-antitrypsin levels
   1. Especially in a patient who has never smoked
8. HRCT
   1. Bullae
   2. Pattern of emphysema

How would you grade the severity of COPD according to Australian COPD-X guidelines?

• Mild: FEV1 60-80% pred
• Moderate: 40-59% pred
• Severe: <40% pred

How would you manage a patient with emphysema?

• In all patients smoking cessation is important
• Pulmonary rehabilitation programs increase quality of life scores, reduces dyspnoea and reduces hospital admissions
• Reduce anxiety, depression and fatigue
• Then break it down into the COPD-X stages
  • Confirm the diagnosis based on appropriate risk factors and spirometry
  • Optimise function:
    • Mild disease: SAMA as required
    • Moderate disease: SAMA as required and background long acting bronchodilators (LAMA or LABA), combination therapy may be the best
    • Severe disease frequent exacerbator phenotype: As moderate disease but with addition of inhaled corticosteroids
    • Severe COPD with respiratory failure use oxygen therapy if
      • pO2 < 55mmHg
      • pO2 < 60mmHg with pulmonary hypertension/RHF
      • Mortality benefit only with ≥ 16 hours/day
      • Portable oxygen not shown to have mortality benefit
  • Prevent Deterioration:
    • smoking cessation for all
    • Vaccination: influenza vaccine reduces number and severity of exacerbations, pneumoccocal vaccine reduces invasive disease
    • Long term antibiotics in frequent exacerbator phenotype: 250mg daily azithromycin - Significantly increased time to first exacerbation
  • Manage Exacerbations:​
    • Mainstays of therapy are bronchodilators and corticosteroids
      • No evidence nebuliser more efficacious than MDI and spacer (and may increase side effects)
    • Corticosteroids: Improve symptoms, FEV1 and PaO2 in moderate-severe exacerbations, 30 - 50mg daily, no advantage IV, 5 days likely adequate
    • Maintain SpO2 88 - 92%, because risk of worsening hypercapnia: alter V/Q mismatching, Haldane effect, decreased hypoxic drive
    • NIV for acute hypercapnic respiratory failure, decreased treatment failure, intubation, mortality, length of stay

How do vaccinations help in the management of COPD?

• Influenza vaccine reduces the rate and severity of influenza symptoms, including respiratory ones. A meta-analysis of 11 trials, including six performed exclusively in patients with COPD, found that, in patients with COPD, influenza vaccine significantly reduced the total number of exacerbations per patient compared with those who received placebo
• A meta-analysis of seven trials that assessed the effects of a 23 valent pneumococcal vaccine in patients with COPD found no significant effect on morbidity or mortality​

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Bronchiectasis

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General inspection

• Breathless at rest
• pectus excavatum - kartegener's syndrome
• oxygen mask
• sputum cup with copious amounts of purulent sputum
• dysphonic cough secondary to corticosteroid use
• Productive cough
• Prolonged forced expiratory time
• Cachectic appearance (especially in cystic fibrosis)

Hands

• ​Clubbing
• Peripheral cyanosis

Eyes & Mouth & Face

• Oral candidiasis
• Nasal polyps
• Signs of chronic sinusitis
• May have reduced cricoid-notch distance

Chest

• Expansion: May be increased if associated with hyperinflation
• Traction bronchiectesis may occur in fibrotic lungs with decreased air entry
• Percussion note is variable, may be dull over an area of collapsed/ consolidation
• Breath sounds: coarse late inspiratory crepitations (classically) which alter with coughing
• Signs of pulmonary hypertension

How would you investigate this patient:

• Saturations and temperature
• bedside spirometry
• Formal lung function tests including spirometry, lung volumes and diffusion coefficient
  • Difficult as can be obstructive, restrictive or mixed picture depending on the underlying pathology
  • Mainly obstructive findings however as the small peripheral airways are narrowed with transmural inflammation
• CXR
  • reticular markings
  • evidence of focal consolidation
  • Collapse secondary to mucus plugging
  • Peribronchial thickening --> tram tracking, ring shadows
• Blood tests
  • FBC (looking for neutrophilia, polycythaemia, reactive thrombocytocis)
  • UEC (secondary amyloidosis)
  • hypoalbuminaemia which is a poor prognostic sign
  • Aspergillus serology in case there is a component of ABPA
• Microbiology
  • looking for chromic colonising organisms such as S. aureus and P. aerugenosa

What are the causes of bronchiectesis

• There is an exhaustive list, however the most common is post infectious after recurrent childhood infections such as pertussis, measles, tuberculosis
• Secondary to bronchial obstruction due to broncholith, endobronchial tumour, lymph nodes
• Secondary to fibrosis
• Secondary to defect in the muco-cilliary barrier: cystic fibrosis, primary cilia dyskinesia, kartagener's syndrome
• Secondary to impaied immune response: hypogammaglobulinaemia
• ABPA: Hypersensitivity reaction to aspergillus with subsequent migration of formed immunoglobulins and immune complexes into central airways mediating type 3 hypersensitivity damage
• Congenital: bronchopulmonary sequestration

Describe the pathophysiology of bronchiectasis

• There is abnormal bronchial dilatation, destruction of the muscular and elastic components of the bronchial walls
• Internal luminal diameters of the airways exceeding the diameter of adjacent arteries
• Inflammatory process appeared to commence in the small airways
• Bronchi contain many lymphoid follicles and nodes
  • Subepithelial follicles cause partial bronchial obstruction, intraluminal follicles thicken wall
  • Follicles associated with loss of elastic tissue weakens the wall -> distortion of bronchial tree

What are some complications of bronchiectasis

1. Brain abscess
2. Amyloidosis
3. Disseminated infection
4. Hypoxic respiratory failure
5. lung abscess
6. Empyema
7. Pleurisy
8. Cor-pulmonale

How would you manage these patients?

• Use a similar paradigm to COPD-X
• Control symtpoms
  • pulmonary rehabilitation
  • Chest physiotherapy via specialised physiotherapists involved in postural drainage with percussion and vibration, flutter devices
  • mucosal clearance with nebulized saline and mucolytics
  • In CF pulmozyme which is recombinant DNAse
  • Maintain good hydration
• Optimise lung function
  • Smoking cessation
  • If obstructive picture consider bronchodilators
  • May require trial of corticosteroids if airway reactivity suspected
  • In CF, if G551D mutation may be suitable for ivakaftor, a Cl channel potentiator
  • Clinical trials undergoing for combined lumicaftor and ivakaftor for delta F508 mutation

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Thoracotomy scars

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General inspection

• Breathlessness
• State of cachexia
• Gross assymetry in chest expansion if present

Hands, arms

• Look for aetiology eg clubbing, nicotine staining, HPOA, T1 lesion
• Proximal myopathy in ectopic secretion of ACTH, immunosuppression

Face and neck

• Anaemia/ polythaemia facies
• Horner's syndrome in apical lung tumours
• tracheal deviation towards the lobectomy or pneumonectomy
• Palpable cervical lymph nodes

Chest

• This is where the money is
• In lobectomy (where a lobe of the lung has been excised)
  • Thoracotomy scar transverses the rib space, and it may appear very posterior
  • Trachea may or may not be displaced towards the affected side (probably not if the lower lobes are taken out)
  • Ribs are indrawn near the region of lobectomy
  • Decreased chest expansion locally at the region of the lobectomy
  • Decreased breath sounds at the region locally, bronchial breathing near the area of the trachea
  • Vocal resonance is decreased in the affected side
  • Apex beat may be displaced towards the affected side associated with mediastinal shift
  • Listen to the other unaffected side - there may be signs of hyper-expansion here and also signs of pathology (eg expiratory wheeze in COPD, coarse late inspiratory crepitations that alter with coughing in bronchiectasis)
• In pneumonectomy (where the whole lung has been excised)
  • Thoracotomy scar will be present
  • The chest wall will be flattened on the affected side
  • The trachea will be grossly deviated to the affected side
  • There will be mediastinal shift towards the affected side
  • There will be reduced chest expansion on all zones of the affected side
  • There will be absent breath sounds on all sides, but there may be bronchial breathing over the trachea
  • Note that the percussion note may be stony dull as the post pneumonectomy space fills with fluid

What are the pulmonary consequences of pneumonectomy?

• Postpneumonectomy lung volumes fall less than 50% because of over-expansion of the remaining lung. Despite this overexpansion, there is no pathological evidence of emphysema in the remaining lung.
• FEV1 and FVC decrease by less than 50%, as do DLCO - which typically corrects for lung volume
• Lung compliance decreases and airway resistance increases

How would you proceed to assess a patient's pre-operative pulmonary status in order to determine whether they would qualify for a pneumonectomy?

• If FEV1 > 2L or >80% AND DLCO >80% predicted then they should tolerate pneumonectomy well
• If FEV1<2L or <80%  OR DLCO <80% then an estimation of post-operative FEV1 or post-operative DLCO should be made, this is based on advanced imaging techniques or anatomical estimations based on the number of segments that are going to be resected
• If the post-operative predicted FEV1 or DLCO is <30% then the patient will not be suitable, however if greater than 60% then they are generally considered suitable
• If between 30 - 60%, a further exercise test may be performed, such as cardiopulmonary exercise testing. 

What pattern of lung function testing would be expected in a patient who had a left sided pneumonectomy secondary to a solitary pulmonary nodule however also had a background of heavy nicotine dependence

• A mixed pattern, with obstructive spirometry suggested by a spirometric ratio (FEV1/FVC < 0.7) and restrictive lung function tests with TLC <80%
• The DLCO will be reduced, and this may or may not 'correct' when accessible lung volume is taken into account, as DLCO = KCO x V(a)
• If there is severe emphysema, V(a) may be << TLC due to insufficient gas mixing secondary to obstructive lung disease

Name some common indications for a lobectomy

• Bronchiectasis with uncontrolled recurrent haemoptysis
• appropriate stage non-small cell lung cancer
• solitary pulmonary nodule of unknown cause
• Cystic fibrosis
• Tuberculosis
• Lung abscess

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Kypho-scoliosis and restrictive lung disease

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General inspection

• Significant postural deformity with prominent thoracic kyphoscoliosis
• Protuberant abdomen and reducible hernia secondary to ascites
• dorsal hump due to angulated ribs
• Positive adam's test where patient is asked to bend forward and asymmetry is noted
• Breathless at rest

Hands

• CO2 metabolic flap secondary to type 2 respiratory failure

Chest

• ​Significantly reduced chest expansion
• Signs of right heart failure as a result of nocturnal hypoventilation (particularly during REM sleep) that occurs in these patients

What are the causes of kypho-scoliosis that you are aware of?

• The majority of causes are idiopathic (80%), others can be associated with different disease states
• Neuromuscular diseases include post-polio syndrome, muscular dystrophy, cerebral palsy
• Vertebral diseases include osteoporosis, osteomalacia, potts disease
• connective tissue disease includes ehlers-danlos syndrome and marfan's syndrome

What would you see on polysomnography and pulmonary function testing in these patients?

• Nocturnal hypoventilation, with prolonged desaturation and rising CO2 especially during REM sleep
• Pulmonary function tests typically show a restrictive lung function pattern, however with preserved residual volume such that the TLC/RV ratio is increased
• Maximum inspiratory and expiratory pressure testing will be decreased due to mechanical disadvantage secondary to rib cage distortion

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Superior Vena Cava Obstruction Syndrome

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General examination

• Plethoric facies
• Upper limb oedema
• Distended neck veins
• Conjunctival suffusion
• Obvious neck mass

Hands

• Clubbing will suggest malignancy
• nicotine staining will suggest smoking
• Wasting of small muscles of hand C8 - T1 in pancoast syndrome

Upper limbs, face, eyes, neck

• oedematous limbs, plethoric and cyanosed
• venous angiomata may be prominent on face especially under tongue
• Fixed engorgement of neck veins
  • loss of double flicker of JVP
• Look for recent CVC insertion - thrombosis of catheter could be a mechanical cause
• Look for radiotherapy marks
• cervical, axillary lymphadenopathy
• Proceed to examination of thyroid if goitre
• Positive pemberton's sign

Chest

• Looking for aetiology eg signs of carcinoma of lung

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Image courtesy of N Engl J Med 2014; 371:1142

What are the causes of SVC obstruction

• Majority of causes are malignant
  • non–small-cell lung cancer (approximately 50% of patients), small-cell lung cancer (approximately 25% of patients), lymphoma, and metastatic lesions (each approximately 10% of patients)
• 35% causes are non-malignant
  • complication of cvc, thrombophilic states eg myeloproliferative disorders, mediastinal goitre, syphillis

What investigations would you order

• On first instance CXR - look for obvious mass
• Bloods assessing tumour burden, may see evidence of tumour lysis syndrome if large tumour with high mitotic burden (High K, high PO4, low Ca, high uric acid, LDH and renal failure
• Biopsy of mass,  Pleural effusion is common (affecting about two thirds of patients with the superior vena cava syndrome); thoracentesis and cytologic analysis should be strongly considered because they are simple to perform and expedient, although they yield a diagnosis in only about 50% of such patients - N Engl J Med 2007; 356:1862-1869
• CT with contrast, venogram if intervention 

How would you manage a patient with SVC obstruction

• General supportive measures
  • elevate the patient's head to decrease the hydrostatic pressure
• ​Specific treatment
  • ​Treat underlying cause - radiotherapy, chemotherapy or a combination
  • Stent can be placed before a tissue diagnosis is available, it is a useful procedure for patients with severe symptoms such as respiratory distress that require urgent intervention.

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