Respiratory Flashcards
What lung function tests can be done at home, at a GP surgery or in a specialist lab?
Home: peak flow (asthma) and oximetry GP: spirometry and oximetry Specialist lab: spirometry, transfer factor, lung volumes, bronchial provocation testing (asthma), respiratory muscle function, exercise testing
Define spirometry
Forced expiratory manoeuvre from total lung capacity until it’s empty followed by a full inspiration
What are the pitfalls to spirometry?
- Need an appropriately trained technician
- Effort and technique dependent: need good patient understanding and needs to have ability to complete it
- Patient frailty
- Pain/Patient too unwell e.g. if patient has a chest wall injury
Draw normal tidal breathing and label the different measurements that can be taken
What is the volume of normal tidal breathing?
Normal Tidal Breathing: 500ml
- Vital Capacity (VC): relaxed manouevre, the difference between total lung capacity and residual volume (the volume that cannot be blown out)
- Forced Vital Capacity (FVC): forced manouevre, patient breathes out as hard as possible
What graphs can be determined using spirometry?
Time/Volume Plot
- X-axis = time; Y-axis = volume
Flow/Volume Loop
- X-axis = volume; Y-axis = flow
Draw a time/volume graph and describe what it shows
- Most of the lung is emptied in the first second and then tails off as flow tails off until FVC
- FEV1 = Forced Expiratory Volume in 1 second i.e. the volume expelled from the lungs in one second
Can measure
- PEFR = Peak Expiratory Flow Rate
- FEV1
- FVC
- FEV1/FVC ratio: normal is >70% i.e. >70% of the VC should be expelled from the lungs in the first second. If <70%: airflow obstruction
Draw and describe the shape of a flow/volume loop
2 parts to the graph
- Negative: inspiration and positive: expiration
Flow is rapid to begin then gradually tails off in a linear fashion
- Rapid flow: effort dependent
- Tailing off: effort independent
Tailing off
- Due to airway resistance, the pressure inside the airway gradually decreases toward the mouth
- When you breathe out hard, there is extrinsic compression of the aiway forming a choke point (where pressure outside airway > pressure inside) therefore causing dynamic airway collapse and air will not be able to pass that point of collapse
What physiological process causes a gradual decline in flow in a linear fashion on a flow/volume loop?
- Due to airway resistance, pressure inside the airway decreases toward the mouth
- There is extrinsic compression of the airway when a person takes a hard breathe out
- This forms a choke point as the pressure outside the airway > pressure inside the airway, causing dynamic airway collapse
- Air cannot be forced past this point of collapse
How does COPD alter the flow/volume loop?
- With COPD, there’s a loss of support holding the airway open therefore there is more airway obstruction and the dyanmic airway collapse will occur at lower extrinsic pressures
- Loop: maintain the rapid expulsion (effort dependent) but there’s much quicker tailing off
i. e. church and steeple pattern
What are the normal reference ranges for FEV1?
FEV1 of 85% predicted may be considered normal
FEV1 of 100% predicted may represent significant decline if values were supra-normal at the beginning
- I.e. need to compare FEV1 values to previously recorded values
- Correlated for age, gender, race, height
Define obstructive lung disease and the general sub-groups
Definition - FEV1:FVC ratio <70%
- This can be determined using a time/volume plot
- FEV1 (<80% predicted) and FVC are both reduced, but FVC is reduced to a lesser extent
Generally - asthma or COPD
(Emphysema and CF are also obstructive lung diseases)
How do you determine the severity of COPD (using spirometry)?
- Severity stratified by %predicted FEV1
- Mild airflow obstruction: >80%
- Moderate: 50-80%
- Severe: 30-50%
- Very severe: <30%
How do you determine obstructive lung disease and how do you differentiate between asthma and COPD using spirometry?
- Reduced % predicted FEV1
- Reduced FVC, but to a lesser extent
- FEV1:FVC ratio <0.7 defines obstructive lung disease
- Flow/Volume loop: church and steeple pattern is also suggestive of obstructive lung disease
To differentiate COPD and asthma: salbutamol reversibility testing
- 400mg salbutamol (nebulished/inhaled)
- Spirometry before and 15mins after salbutamol
- 15% increase in FEV1 and 400ml reversibility in FEV1 - suggestive of asthma
What investigations can suggest asthma over COPD, other than reversibility salbutamol testing?
PEFR testing
- Look for diurnal variation (i.e. changes throughout the day)
- Response to inhaled corticosteroid with peak flow
Bronchial Provocation
- Tests sensitivity of airways with inhaled mist followed by spirometry
- Positive result = reduced breathing ability and suggests asthma
Spirometry before and after trial of inhaled/oral corticosteroid
Allergy testing
Give three examples of causes of a restrictive pattern on spirometry
- Interstitial lung disease
- Chest wall abnormality
- Previous pneumonectomy
- Neuromuscular disease e.g. MND, Guillain-Barre syndrome
- Obesity
- Poor effort/technique
How do you identify a restrictive pattern on spirometry?
Time/Volume loop
- FEV1 reduced <80% predicted
- FVC reduced to <80% predicted
- However, FEV1:FVC remains >70%
How do you interpret spirometry to determine if obstructive or restrictive patterns?
- Look at FEV1:FVC ratio
- If <70%: obstructive - If obstructed, look at %predicted FEV1 (COPD severity) and any reversibility (COPD v asthma)
- If FEV1:FVC is >70%, look at % predicted FVC
- If low, it suggests restrictive abnormality
NB can get a mixed picture e.g. COPD and obesity
What does transfer factor (TF) measure, how is it measured and what affects it?
TF: Measures the diffusion of respiratory gases at the lungs
How
- Single breath of a small concentration of carbon monoxide
- CO has a very high affinity to Hb
- Measure the conc. of CO in expired gas to derive uptake in the lung
Affected by
- Alveolar surface area
- Pulmonary capillary blood volume
- Hb concentration
- Ventilation and perfusion mismatch
What conditions cause a reduction in Transfer Factor (TF)?
- Emphysema (loss of alveolar surface area)
- Interstitial lung disease (ventilation-perfusion mismatch)
- Pulmonary vascular disease
- Anaemia (lower Hb concentrations for oxygen uptake)
How are lung volumes measured?
What affects lung volumes and how?
- Residual volume (RV) cannot be measured
2 methods of measuring total lung capacity:
- Helium dilution: inspire known quantitiy of inert gas
- Body plethysmography: respiratory manouevres in a sealed box and measuring air pressure changes
Restrictive lung disease: reduced lung volumes
Obstructive lung disease: RV increased in obstructive lung disease
What is oximetry, what does it encorporate what are the pitfalls?
- Oximetry: non-invasive measurement of Hb saturation by oxygen
- Depends on oxyhaemoglobin and deoxyhaemoglobin absorbing infrared differently
- Result depends on oxygenation and adequate perfusion (shock/cardiac failure could cause poor tissue perfusion and affect oximetry)
Pitfall
- Doesn’t measure CO2 therefore cannot measure ventilation: this can cause false reassurance with patients on high-flow oxygen with normal saturations (e.g. acute asthma, COPD)
What does the oxygen dissociation cuvre tell us and how does this affect COPD management?
There’s a plateau toward 100% Hb saturation
- If you increase dissolved blood O2 beyond this, there’s no increase in Hb saturations
Steep part of the dissociation curve
- At lower O2 pressures, small increases/decreases of inspired O2 cause much larger inc/decreases in O2 saturations
Affect on COPD management
- Can just give low-flow oxygen because a small inc. in inspired O2 greatly increases saturations
Define hypoxaemia and describe it’s aetiology
Definition: an abnormally low concentration of oxygen in the blood
Aetiology:
Ventilation-Perfusion Mismatch e.g. COPD, pneumonia
- Perfusion areas of lung that aren’t well ventilated
Hypoventilation e.g. NMD, drugs
- Causes T2 respiratory failure as there is failure to clear CO2 as well not taking up O2
Shunt e.g. congenital heart disease
- Blood is bybassing the ventilated lung
Low inspired oxygen e.g. altitude, flight
What is ventilation-perfusion mismatch and give two examples that cause V/Q mismatch?
Ventilation (V): the volume of gas inhaled and exhaled in a given time
Perfusion (Q): the volume of blood reaching the pulmonary capillaries in a given time
V/Q mismatch occurs to a degree in normal lungs:
- Apex: ventilation exceeds perfusion
- Base: perfusion exceeds ventilation (better perfusion in the bases due to gravity)
Examples of V/Q mismatch
- Pneumonic consolidation: areas of lung are perfused but not well ventilated. Blood from the well ventilated and poorly ventilated areas of lung mix causing hypoxaemia. Doesn’t fully correct with oxygen management.
- Shunt: extreme form of V/Q mismatch where the blood bypasses the lungs entirely, therefore there is no perfusion of lungs. No gas transfer at alveoli. Does not correct with oxygen adminisatration
How does reduced ventilation affect oxygen and CO2 levels?
The initial effect of reduced ventilation: T1 resp failure
i. e. reduced pO2 and normal/low CO2
- Oxygen levels are primarily affected because CO2 is more soluble and will still diffuse across the membrane
- All T1 resp failure can develop into T2 resp failure with low pO2 and pCO2
How do pneumonia, asthma and COPD cause reduced ventilation?
Pneumonia: alveoli are filled with exudate, impairing the delivery of air to the alveoli and lengthening the diffusion pathway for respiratory gases
Asthma: smooth muscle contraction, increasing resistance to airflow to the alveoli
COPD: structural airway damage caused by inflammatory changes lead to impaired gas exchange, which can worsen in an acute exacerbation
How is arterial pCO2 measured?
How is arterial pO2 measured?
pCO2 - arterial blood gas (ABG)
pO2 - oximetry
How do alveolar and arterial pO2 values differ?
What is the normal difference between these values?
What would an abnormal difference indicate?
- Alveolar pO2 will be higher than arterial
- The difference between alveolar and arterial oxygen partial pressures should be < 2-4kPa
- More than this suggests V/Q mismatch
Describe the systematic approach to blood gas analysis
- Always start with pO2
- Normal = 13kPa
- Respiratory failure is defined as a pO2 <8kPa and will need additional oxygen - Look at pCO2: T1 v T2 resp failure
- If pCO2 >6: T2 respiratory failure
- <6: T1 respiratory failure - Consider acid-base balance
- High H+ (>44) = acidotic
- If high H and T2 respiratory failure: acute respiratory acidosis
- Acute resp acidosis / decompensated T2 resp failure: elevated CO2, normal bicarb, acidotic
- If normal H and T2 resp failure: body has had time to compensate (days-weeks) by kidneys
- Compensated resp acidosis: elevated CO2, elevated bicard, not acidotic
- Acute on chronic resp acidosis: elevated CO2, elevated bicard, acidotic
Define COPD and list 3 aetiologies
Chornic Obstructive Pulmonary Disease
= characterised by progressive airflow obstruction, not fully reversible and do not change markedly over several months
Aetiology
- Smoking
- Environmental pollution
- Burning biomass fuel
- Occupational dust
- Alpha 1 anti-trypsin deficiency (genetic cause): alpha-1-antitrypsin is a serine proteinase inhibitor i.e. anti-protease
What are the effects of cigarette smoking on the lungs?
- Reduced cilia motility: cilia are damaged/destroyed by smoking therefore don’t clear secretions as effectively and so there’s an increased risk of infection
- Mucus hypertrophy and hypertrophy of Goblet cells (produce mucus)
- Airway inflammation: damaged lung proteases released from inflammatory cells and aren’t very responsive to inflammatory treatment
- Increased protease activity and anti-proteases are inhibited (smoking activates proteases which digest lung tissue and not enough anti-protease activity)
- Oxidative stress: increased free radicals e.g. hydrogen peroxide
- Squamous metaplasia: high risk of developing lung cancer
- Smoking increases permeability of airways and therefore carcinogens from smoke are absorbed into the body, increasing the risk of other cancers
What is a-1-antirypsin deficiency and when would you screen for a-1-antitrypsin deficiency?
A-1-antitrypsin deficiency: genetic cause of COPD
- this enzyme is a serine proteinase inhibitor i.e. protease inhibitor
- Therefore the body cannot combat against destructive protease activity
When to Screen
- Will develop emphysema much earlier on: if there is a young person with severe COPD or emphysema, screen for alpha-1-antitrypsin
What would COPD look like in someone with a-1-antitrypsin deficiency who developed COPD?
COPD in a-1-antitrypsin
- Pan-acinar emphysema
- Bullae around the edges of the lungs
- Characterised by swelling and tissue damage in the alveoli
Define the clinical syndromes of COPD
i.e. causing the pathogenesis
Chronic Bronchitis
- A chronic cough with sputum production on most days for at least 3 months in at least 2 years
- Narrowing of airways due to inflammation
- Other causes of a chronic cough need excluded
- A type of small airways disease
Emphysema
- Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
- Causes loss of elasticity and alveolar attachments leading to airway collapse on expiration
What is the pathogenesis of chronic bronchitis in COPD?
- Caused by inflammation of the airways >4mm in diameter
- Smoking induces inflammatory infiltrate around the airways
- Inflammatory infiltrate: principally neutrophilic with CD8 lymphocytes and macrophages
- Neutrophilic infiltrates aren’t very responsive to steroids
- Free oxygen radicals are released from neutrophils that destroy the support around the airways therefore loss of interstitial support
- Airways become distorted as inflammation leads to scarring and thickening
- Goblet cell hyperplasia therefore increased mucus production
- Airways become clogged leading to further inflammation
What happens as a result of small airway disease?
- Small airways = bronchioles
- Narrowing of bronchioles due to inflammation, mucus plugging and fibrosis
- Narrowed airways → insufficient breathing → air gets trapped in the peripheral lung
This leads to dynamic hyperinflation
- When you exercise, the respiratory cycle time shortens, less time to breath out so lungs don’t empty properly causing hyperinflated lungs causing less comfortable breathing
What are the cell types involved in inflammation in COPD?
- Neutrophils
- CD8 lymphocytes
- Macrophages
What are the inflammatory mediators seen in COPD?
- TNF, IL-8 and other chemokines
- Neutrophil elastase, cathepsin G (from activated neutrophils): these breakdown airway supports
- Elastase and MMP (from macrophages)
- ROS
What are the different types of emphysema seen in COPD?
Centri-Acinar
- Damage around respiratory bronchioles
- Damage to one segment of lung supplied by one respiratory bronchiole
- Seen more in upper lobes (with inhaled damage)
Pan-Acinar
- The whole acinus is destroyed
- Uniform enlargement from the level of the terminal bronchiole distally
- Get large bullae
- Associated with a-1-antitrypsin deficiency
- Loss of surface area and papillary bed for gas exchange: leads to hypoxaemia
What is the mechanism of airway obstruction in COPD?
- Loss of elasticity and alveolar attachments due to emphysema causes airway collapse on expiration
- This causes air trapping and hyperinflation, leads to increased work of breathing and breathlessness
- Goblet cell metaplasia with mucus plugging of the lumen
- Thickening and inflammaiton of the bronchiolar wall: smooth muscle hypertrophy and peri-bronchial fibrosis
How do you diagnose COPD and what investigations would be carried out
Consider diagnosis of COPD for those >35yrs, and smokers or ex-smokers with any of
- exertional breathlessness; chronic cough; regular sputum production; freq. winter bronchitis; wheeze
Spirometry
- obstructive pattern i.e. FEV1 <80%, reduced FVC and FEV1/FVC ration <70%
- church and steeple pattern on flow/volume loop
- can use FEV1 to determine severity of COPD
CXR
- Hyperinflated lungs: defined as 6 anterior or 9 posterior ribs above the diaphragm
- Dark lungs: loss blood vessels
- Flattened heart
- Flattened hemidiaphragms
- Ribs become flattened and more horizontal
How do you determine the treatment for a COPD patient?
What are the different treatment options?
Need risk assessment
- Look at exacerbations in last year and severity of airway limitation
- Look at symptoms and breathlessness
- Less exacerbations: treat symptoms
- More exacerbations: treat exacerbations
Treatment options
Inhaled bronchodilators: short acting (salbutamol (SABA)) and long acting (salmeterol (LABA) and tiotropium (LAMA))
Inhaled corticosteroids: beclomethasone, nudesonide (combination inhaler)
Mucolytics: carbocysteine (thins mucus and used symptomatically)
What is the class, indication, action and potential side effects of salbutamol?
Class: beta-adrenergic bronchodilator
Indications: COPD and asthma
Action:
- Short-acting beta-2 adrenoceptor agonist (SABA)
- Induces bronchodilating by relaxing bronchial smooth muscle
- Reduces airway inflammation: Inhibits pro-inflammatory cytokine release from mast cells and TNF-a from monocytes
- Increases mucus clearance from airways by stimulating cilia activity
Side effects:
- Tremour
- Tachycardia
- Sleep disturbances
- Headache
What is the class, indication, action and potential side effects of salmeterol?
Class: beta-adrenergic bronchodilators
Indication: asthma and COPD
Action:
- Long-acting beta-2 adrenoceptor agonist (LABA)
- Induces bronchodilation by relaxing smooth muscle
- Reduces airway inflammation: inhibits pro-inflammatory cytokine release from mast cells and TNF-a release from monocytes
- Increases mucus clearance by stimulating cilia activity
Side Effects:
- Tremour; tachycardia; sleep disturbances; headache
What is the class, indication, action and side effects of tiotropium?
Class: anti-muscarinic bronchodilator
Indication: asthma, COPD, rhinitis
Action:
- Long-acting M3 muscarinic receptor antagonist by producing bronchodilatory effects
- Reduces mucus secretion
- May increase bronchial mucus clearance by stimulating cilia activity
Side Effects:
- Dry mouth
- Constipation
- Cough
What is the class, indication, action and potential side effects of Beclamethasone?
Class: inhaled corticosteroid
Indication: COPD and asthma
Action:
- Anti-inflammatory effect on the airways
- Decrease the formation of pro-inflammatory cytokines
- Up-regulates beta-2-adrenoreceptors in the airways
Side effects:
- Osteoporosis
- Renal suppression
- Oral candidiasis
What is the basis for COPD personalised treatment?
Endotype ie. what’s driving the COPD?
- Persistent systemic inflammation
- Eosinophilic or T-helper cell: more steroid responsive
- Persistent pathogenic bacterial colonisation: may need long-term antibiotics
- a-1-antitrypsin deficiency
Phenotype i.e. how clinically bad is the disease
- Frequent exacerbations
- Persistent breathlessness
- Chronic bronchitis
What is the significance of blue bloaters and pink puffers?
Blue bloaters: Chronic bronchitis
- Low respiratory drive
- Type 2 respiratory failure: low pO2, high pCO2
- Chronic cough with sputum production
- Cyanosis (hypoxaemia) and warm peripheries
- Peripheral oedema
- Crackles, wheeze
- Obese
- Fluid retention: bounding pulse, flapping tremor, peripheral oedema, elevated JVP
- Confusion, drowsiness
Pink Puffer: Emphysema
- High respiratory drive
- Type 1 resp failure: low pO2 and pCO2
- Desaturates on exercise
- Dyspnoea and tachypnoea
- Use accessory muscle to stabilise breathing
- Decreased breath sounds
- Hyperinflation (barrel chest)
- Cachexia (wasting of the body due to severe chronic illness)
Compare and contrast the cause, inflammation and reversibility airflow limitation in asthma and COPD
Cause
Asthma: sensitising agent
COPD: noxious agent
Inflammation
Asthma: eosinophils, CD4, T lymphocytes, steroid responsive
COPD: neutrophils, CD8, T lymphocytes, macrophages, less steroid responsive
Reversibility and airflow limitation
Asthma: completely reversible
COPD: irreversible
Compare the clinical features of asthma and COPD
Smoker/Ex-smoker
COPD: nearly all. Asthma: possibly
Symptoms <35yrs
COPD: rare. Asthma: often
Chronic productive cough
COPD: common. Asthma: rare
Breathlessness
COPD: persistent and progressive. Asthma: variable
Night time waking with breathlessness and/or wheeze
COPD: uncommon. Asthma: common
Significant diurnal variability of symptoms
COPD: uncommon. Asthma: common
Define pneumothorax, comparing to normal, and list the causes
Definition: air within the pleural cavity (the potential, fluid-filled space between the parietal and visceral pulmonary pleura)
- Normally, there is negative intrapleural pressure formed by two opposing, balanced forces: outward with the chest wall and natural elastic recoil of the lung inward
- Any breach of the pleural space leads to collapse of the elastic lung
Causes:
- Traumatic: stabbing, fractured rib
- Iatrogenic: CT guided lung biopsy, pleural aspiration (if tip of needle touches lining of the lung, it may introduce air into pleural space)
- Spontaneous: primary (no underlying disease, patient tends to be younger) and secondary (underlying lung disease e.g. COPD, CF, emphysema)
What is a tension pneumothorax and describe the pathophysiology?
- Formation of a ‘one-way valve’ leading to increased intrapleural pressure
- Valve allows air to leak into the pleual space which then can’t escape
- Eventually the pressure builds up within the chest wall which compresses the heart and lung
- The pressure can impair venous return to the heart and prevent proper filling of the heart, reducing cardiac output
- Venous return impaired then cardiac output and BP falls
- Will result in cardiac arrest of there is no intervention
- Tracheal deviation away from t. pneumothorax
What is the treatment for a tension pneumothorax?
Immediate: insert venflox 2nd intercostal space mid-clavicular line to relieve pressure
What are the risk factors for a spontaneous pneumothoax?
- Male
- Smoking
- Tall
- Underlying lung disease (secondary)
What is the pathophysiology of a primary pneumothorax?
- Development of subpleural blebs (bubble packaging underneath the pleural surface)/ bullae at the lung apex
- If one of these blebs/bullae pop, air will leak into the pleural space
- Possible additional diffuse, microscopic emphysema (air trapping) below the surface of the visceral pleura
- Spontaneous rupture leads to a tear in the visercal pleura
- Air flows from airways into pleural space
- Pressure gradiant: -ve in pleural space, +ve in airways
Elastic lung then collapses
How many lobes do the right and left lungs have?
What are the fissures of the right and left lungs and what do they separate?
What are the layers of the pleura surrounding the lungs?
Right lung
- 3 lobes: superior, middle and inferior
- 2 fissures: horizontal (between superior and middle lobes) and oblique (between superior and inferior lobes)
Left lung
- 2 lobes: superior and inferior lobes
- 1 fissure: oblique fissure
Pleural layers
- Outer: parietal layer (lines inside of the ribcage and diaphragm)
Inner: visceral layer (lines the lungs)
What is the pathophysiology of a secondary pneumothorax?
There is an underlying lung condition
- Inherent weakness and destroyed lung tissue (e.g. emphysema)
- Increased airway pressure (e.g. asthma, ventilated patient) which could lead to rupture of air spaces in the lung
- Increased lung elasticity (e.g. pulmonary fibrosis)
- Patient is more symptomatic (poor underlying lung function)
- Management is more complex and prognosis is worse (chest drain often required)
More likely to require intervention
What are the signs and symptoms of a pneumothorax?
What would be some differential diagnoses for some of these signs and symptoms?
Symptoms
- Pleuritic chest pain: sudden and intensive stabbing pain in the chest when inhaling and exhaling
- Breathlessness (can be minimal if primary)
- Respiratory distress syndrome (esp if secondary): a type of respiratory failure due to widespread inflammation in the lung. Develop confusion/drowsiness, severe SOB, feeling faint and rapid, shallow breathing
Signs
- Reduced air entry to affected side
- Hyper-resonant to percussion
- Reduced vocal resonance
- Tracheal deviation in tension pneumothorax (+/- circulatory collapse): late sign
Differential diagnosis:
- Musculoskeletal pain, pneumonia, pleurisy (would head a pleural rub that isn’t heard with a pneumothorax)
What is the basis for management for a pneumothorax?
Determined by symptoms more than size
- A small pneumothorax could be very symptomatic in a severe COPD patient
- Complete lung collapse can be very well tolerated in a healthy patient
Size (2cm rim of air at axilla equates to 50% volume:
- <2cm: small - >2cm: large
What is the mainstay management for a pneumothorax
Management options:
Observation if small/asymptomatic
- Serial CXRs: repeat in 2 weeks
Aspiration
- 2nd intercostal space midclavicular line to aspirate air with a syringe
Intercostal chest drain with underwater seal
NB a tension pneumothorax always requires a chest drain
What are the management options for a pneumothorax if a chest drain doesn’t work?
- Video Assisted Thoracic Surgery (VATS): considered if pneumothorax isn’t resolved with a drain within 5 days
- Blebs can be stapled
- Talc pleurodesis: talc sprayed on the lining of the lung, causing an inflammatory reaction causing the lung to stick to the chest wall (very effective)
- Pleural abrasion/stripping: strip out the pleura and it will stick
- Surgical pleurodesis if a secondary pneumothorax occurs: high chance of recurrance
What professions need further advice following a pneumothorax, and what is that advice?
Flying: after a spontaneous pneumothorax has resolved on CXR, wait 7+ days before flying
- After a spontaneous pneumothorax has resolved on CXR, a patient should not scuba dive again
Define a pleural effusion and types
Definition: An abnormal buildup of fluid in the pleural space i.e. >15mls
Types: transudate or exudate
Describe the presentation, history and examination for a pleural effusion
Common presentations: SOB, weight loss (red flag), cough, chest pain
Could also present with: haemoptysis, legarthy, fever
History
- Onset: fall, change in medication? (Warfarin/Anticoagulants with a fall could cause a pleural effusion)
- PMH: previous malignancy, TB
- Smoking history
- Occupational history: asbestos exposure
Examination
- Systemic: clubbing, ascites, lymphadenopathy, other cardiac signs (commonest cause of pleural effusion is HF)
How do you classify effusions as transudate or exudate?
Light’s criteria
- Fluid protein : serum protein ratio >0.5
- Fluid LDH : Serum LDH ratio >0.6
Fluid LDH >2/3 maximum normal serum value
Any one of these = exudate
- Always send paired samples (borderline/subtle results)
Compare transudate and exudate general pathology
T: occurs due to increased hydrostatic pressure or low plasma oncotic pressure ie. inc. pressure pushing fluid into the pleural space
E: occurs due to inflammation and increased capillary permeability ie. underlying pathology altering/damaging the tissue and disrupting normal drainage of pleural fluid
T: usually bilateral
E: usually unilateral
List 3 causes of a transudate and exudate pleural effusion
Transudate:
- Heart failure, cirrhosis, renal failure
Exudate:
- Malignancy, infection, empysema (collection of pus), haemothorax (collection of blood, due to trauma)
Commonest cause of a pleural effusion: Heart failure
Outline a basic approach for investigating pleural effusions
Imaging
- CXR: >500ml to detect fluid
- If unilateral and not responsive to gravity: think empyema (infective)*
- CT: helps determine underlying pathology e..g. malignancy, heart
- US: allows visuals for interventions
Bloods
- To detect signs of infection
Sampling
- Local anaesthetic thoracoscopy
- Direct visuals of the pleural surface and can take biopsies of abnormal areas
- Indicated in undiagnosed cytology negative pleural effusions
- Diagnosis determined in 90%
- Well tolerated
- Only if necessary; want fewest number of interventions
- Never drain an undiagnosed effusion
What is one thing you should never do with a pleural effusion?
What are the main points about intervention?
- Never drain an undiagnosed pleural effusion
- Even if a patient is breathless with a large effusion, don’t treat until a diagnosis/cause has been identified as it’s safer to do more samples
- If very large, can drain some off but not dry
Note
- Minimal number of interventions
- Asymptomatic - hold off on drain
What is the treatment for a pleural effusion?
Guided by history, examinations and investigations
- Dependent on cause
- Take patient wellness into account: esp in the case of malignancy, how hard do you push for a diagnosis?
- Drainage often required
- If asymptomatic: hold off on drain
- Don’t drain until diagnosis is confirmed
What is a malignant pleural effusion?
What is the diagnosis?
- The build-up of fluid and cancer cells that collect in the pleural space (between the chest wall and the lung)
Primary pleural malignancy = mesothelioma
- Linked to asbestos, poor prognosis, supportive treatment
Metastatic Spread
- Most common malignant pleural effusion is secondary to lung cancer
- Breast and ovarian can also spread here as well
Diagnosis
- Aspiration to determine present cells
- Want as much information as possible before drying effusion to determine what chemo/drug to use
- Genetic testing of tissue
What is the treatment and prognosis for a malignant pleural effusion?
Treatment: symptom driven and patient centred
- Chest drain +/- talc pleurodesis (no space for effusion to reoccur): 80% effective, longer stay in hospital but don’t go home with a drain
- Indwelling pleural catherter: day patient but goes home with catheter, used if the lung doesn’t re-expand to reach the chest wall
- Patient choice unless talc failed/lung trapping
Prognosis: poor
What pleural infection is closely associated with causing pleural effusions?
What type of effusions can result and how would they be treated?
- Pneumonia (50% have an associated effusion)
- Parapneumonic effusion: accumulation of exudative pleural fluid associated with ipsilateral lung infection, mainly pnuemonia ie. any pleural effusion secondary to pneumonia (simple, complicated or empyema)
- Simple effusion: minimal SOB, treat the infection
- Complex parapneumonic effusion: signs an effusion is becoming an empyema: pH <7.2, LDH >1000, glucose <2.2, loculated on ultrasound
- Empyema: presence of pus or bacteria from culture, test pH and glucose if empyema is suspected