Download Pulmonary Oedema

WHEEZE
Definition - A wheeze is a continuous, coarse, whistling sound produced in the respiratory airways during
breathing.
Differential Diagnosis

Asthma
Bronchiolitis
COPD
Foreign Body
Drugs - beta-blockers can cause wheeze, and shouldn't be given to asthma sufferers!
Pulmonary oedema secondary to LVF
Anaphylaxis
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ASTHMA
What is asthma?
Asthma is a chronic lung condition in which there is chronic inflammation of the airways, and
hypersensitivity of the airways. Symptoms include wheeze, cough, chest tightness and SOB (dyspnoea). It is
often worse at night.
-
The immune response is CD4 mediated, and the lungs will show an eosinophil infiltrate
It is characterised by airflow obstruction which is varied over time, and reversible. Technically, asthma
exists where the obstruction is reversible by >15%, and COPD exists where it is reversible by <15%.
Airflow limitation – this is usually reversible, either spontaneously, or with treatment
Airway hyperresponsiveness – this occurs to a wide range of stimuli
Inflammation of the bronchi – with infiltration by eosinophils, T cells and mast cells. there is
associated plasma exudation, oedema, smooth muscle hypertrophy, mucous plugging and epithelial
damage.
The disease often ‘flares up’ with viral infections – which often cause a loud wheeze.
Aetiology
Intrinsic – this often starts in middle age, and is sometimes called late onset asthma. You cannot
find the trigger.
Extrinsic – this usually occurs in atopic individuals who have positive skin prick test results. This
type of asthma is present in 90% of childhood cases, and 50% of adults with chronic asthma. It is often
accompanied by eczema.
o Non-atopic individuals can develop asthma in later life via sensitisation to e.g. occupational
agents, aspirin, or as a result of taking β-blockers for hypertension or angina.
o Extrinsic asthma is basically a type I hypersensitivity reaction to something in the air
Atopy
This is a term used to describe people who often have allergies / asthma / hayfever, and where:
The trait runs in families (i.e. genetic component)
The individuals often have skin reactions to common allergens
The individuals have IgE antibody to many common allergens
The development of atopy – they hygiene hypothesis – this is a theory that states that growing
up in a ‘clean’ environment in the early years of life can cause atopy.
Airway hyperresponsiveness
You can test for this by asking the patient to inhale gradually increasing amounts of methacholine or
histamine. This is known as a bronchial provocation test. This will induce transient airflow limitation in
20% of the population – and these are the patients that exhibit airway hyperresponsiveness.
Pathology
The clinical symptoms and pathology are the similar for all types of asthma, they types below are all
intrinsic; the differences between types are:
Non-atopic asthma
o Does not appear to be immunologically mediated – i.e. there is not T cell involvement
o Is associated with recurrent respiratory tract infection (viral)
o Skin tests are negative
o Bronchoconstriction due to airway hyperresponsiveness, not as much due to inflammation and
leukocyte infiltration.
Aspirin induced asthma
Occupational asthma
Basic pathological principle
Exposure to the antigen will make CD4 T cells differentiate into T helper cells (Th2 type, as
opposed to Th1), and they will begin to secrete IL-4 and IL-5.
o IL-4 will cause B cells to become plasma cells and being secreting IgE.
o IL-5 will act on eosinophils and mast cells, making them reactive to the new antigen. Other factors
are also released that are chemotaxic for eosinophils.
This IgE will bind to mast cells in the mucosa. This initial exposure will not cause an allergic
reaction. The IgE sits there on the mast cell surface, waiting to come into contact with the antigen
again, perhaps for years
Upon re-exposure to the antigen, the mast cells will be activated, and will degranulate. This will
release inflammatory mediators.
there are increased numbers of mast cells in both the airway secretion, and the epithelial lining
of lung in asthmatics – thus increased response to any antigens.
o This causes the initial asthma attack. This is mainly the result of histamine and prostaglandin (as
well as leukotrienes; particularly LTC4) release by mast cells. This usually occurs within minutes of initial
exposure to the antigen.
Histamine – causes smooth muscle contraction, increased bronchial secretions, and increased
vascular permeability
o The late phase reaction occurs several hours after the initial reaction. It is caused by
the accumulation of eosinophils (and some neutrophils – but these are much more numerous in COPD)
at the site.
Exacerbating factors
Cold Air and exercise
Atmospheric pollution - Large amounts of dust, cigarette smoke, car fumes, and other allergens can
trigger asthma in some individuals. Large industrial incidents can trigger these on a large scale
population.
Ozone has also been a trigger in the past
Diet
Clinical features
Wheezing attacks
Periodic shortness of breath
Symptoms often worse during the night
Cough is frequent – and often misdiagnosed as bronchitis
Nocturnal cough alone can be a presenting feature
Some patients can have chronic symptoms
Attacks precipitated by a very wide range of triggers
Investigations
Respiratory function tests –
 PEF – the peak expiratory flow. Patients should take two readings per day, to show the variability of
the disease.
Spirometry – you can show the presence of asthma by demonstrating 15% improvement in FEV1 or
PEF following the inhalation of a bronchodilator
Exercise tests – these are often used to diagnose asthma in children. The child should run on a
treadmill for a max of 6 minutes – enough to increase the heart rate to at least 160bpm. Then test the
peak flow before and after. Test every 15 minutes after, again looking for 15% difference.
Trial of corticosteroids – this can be very useful in children at first presentation. You can trial
them on e.g. 20mg (30mg for up to 2 weeks in adults) prednisolone just for several days. This initial
dose is a one-off.
o make sure you measure lung function immediately before and after the course of steroids
o >15% improvement in FEV1 demonstrates the presence of asthma
o If the steroids are given for 2 weeks or less, you can stop the drug without tailing off the dose
Blood and sputum tests – you can test these for high number of esosinophils; and this may help
form your diagnosis, but is not diagnostic on its own
CXR – this will be normal, unless they are having a particularly bad exacerbation, in which
case, overinflation may be present. The use of CXR is good at excluding the possibility of a
pneumothorax.
Management
Stepwise management of asthma
1
2
3
Step
Occasional symptoms – less
frequent that daily
PEFR
100%
predicted
Symptoms more than 3x a
week (used to be symptoms
more than daily)
Severe symptoms
≤80%
predicted
50-80%
predicted
Treatment
PRN bronchodilators – ‘2 puffs as
required’ – which will deliver a dose of
around 200μg
Low dose inhaled corticosteroid(start at
200-400μg up to 800μg), or sodium
cromoglicate
Add long-acting β2 agonist, e.g. sertide
and symbicort are combinations of long
acting agonists and corticosteroids
4
Severe
symptoms
controlled by high
corticosteroids
not
dose
50-80%
predicted
5
Severe symptoms deteriorating
6
Severe
deteriorating
prednisolone
<50%
predicted
<30%
predicted
symptoms,
despite
Higher dose inhaledcorticosteroid – up to
2000μg. Consider leukotriene receptor
antagonist (e.g. monteleukast), or
theophyline
Add prednisolone 40mg daily
Hospital admission
Xanthines
Theophyline and aminophyline (which is metabolised to theophyline) have a role in asthma
treatment. They may be added to the use of β2 agonists in an acute attack. Aminophyline can be
given IV, and is metabolised to theophyline.
The role of leaukotriene receptor antagonists
These block the crucial LTC4 receptor, which contributes to much of the inflammatory response. These
drugs should be considered in anyone who is not well controlled on a middle dose of corticosteroids.
Treating the emergency admission
Features of acute severe asthma:
Inability to complete a sentence in one breath
RR>25
Tachycardia >110 bpm
PEF <50% predicted (or <50% patient’s own best)
Features of life-threatening attack:
Silent chest
Feeble respiratory effort
Cyanosis
Exhaustion
Bradycardia
Hypotenson
Exhaustion/confusion/coma
PEF <30% predicted normal or best – this is approximately 150L/min in adults
Pulsus paradoxus – on inspiration, the diastolic pressure decreases by 10mmHg. This is present in
about 45% of cases – but you have other things to worry about.
Tension pneumothorax is a possible complication
1)
a.
b.
c.
Hospital management – ideally you should start treatment before doing investigations!
(Do an ABG – it may be life-threatening if:
i. CO2 > 5kPa (high)
ii. O2 <8kPa (low)
iii. Low pH)
Start on 100% O2 (non-rebreathing mask) with the patient sat upright in bed
Give 5mg salbutamol with 0.5mg ipratropium bromide via nebulizer on 100% O2
d. Give hydrocortisone 100mg IV or 50mg prednisolone orally. Give both if very unwell
e. Do CXR to exclude pneumothorax
2) If life-threatening signs are present:
a.
Inform ITU and seniors
b. Give magnesium sulphate 1.2-2g IV over 20 minutes
c.
Change the nebulized salbutamol every 15 minutes, or give 10mg continuously per hour. Only
give more ipratropium every 4-6 hours
3) Repeat PEF every 15-30 minutes to assess the situation. If improving then gradually reduces O2
and nebs. If not, try and find senior, keep giving nebs, and consider aminophyline.
a.
Check pulse oximetry – aiming for sats >92%
b. Check blood gasses every 2 hours, and definitely within 2 hours of admission
c.
Record PEF’s and β-agonists when given / carried out
d. A maximum of 60mg/day of prednisolone can be given (orally)
e. You can give 200mg hydrocortisone every 4 hours for a max of 24 hours
f.
Give oral prednisolone for 5 days after they are starting to recover
g.
Ventilation is an option – you would have to call an anaesthetist
h. Patients have to have >75% predicted PEF for discharge
COPD
COPD is an umbrella term for several diseases characterised by airflow obstruction, most
commonly chronic bronchitis and emphysema, but also including bronchial asthma and brochiectasis.
Chronic bronchitis
is defined as cough and sputum production on most days for at least 3 months during the last two years.
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Pathology
Hypersecretion of mucus due to marked hypertrophy of mucus-secreting glands and hyperplasia of
goblet cells
Initially small airways are affected and this initial inflammation is reversible, whereas in later stages
larger airways become affected and the process is no longer reversible
Epithelial layer becomes ulcerated and squamous epithelium may be replaced by columnar cells,
resulting in increased gas diffusion distance
COPD is distinguished from restrictive pulmonary disease, a group of disorders characterised by decreased
lung capacity due to either chest wall or skeletal abnormalities, where FEV1 and FVC are both decreased
proportionately, resulting in a normal FEV1:FVC.
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Obstructive lung disease
COPD
Asthma
Bronchiectasis
CF
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Obstructive pattern lung disease:
Reduced FVC (<80% of normal)
Reduced FEV1:FVC ratio (<70%)
Reduced peak flow
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Epidemiology
Prevalence is approximately 1.5 million and mortality is 23,000/year in the UK
By 2020 it is likely to be the 3rd highest cause of death worldwide
Smoking accounts for 90-98% of all cases
Number of cases has stabilised in men, but is rising among women
Most commonly seen in ex-smokers > 35 years of age
COPD is unlikely to develop with a smoking history less than 10 pack years
Low socioeconomic status and low birth weight are predisposing factors
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Causes
Smoking
Coal mining
Genetic, i.e. α1 –antitrypsin deficiency causes emphysema
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Signs and symptoms
Tachypnoea
Use of accessory muscles of respiration
Hyperinflation caused by gas trapping
Reduced cricosternal distance , <3cm
Reduced chest expansion
Resonant chest sounds
Quiet breath sounds over areas of emphysematous bullae
Wheeze
Cyanosis
Cor pulmonale
Prolonged expiration
Pursed lip breathing
Dyspnoea
Cough, productive or non-productive
Regular exacerbations
Weight loss – a sign of very poor prognosis
Investigations
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Lung function - FVC<80% predicted; FEV1/FVC<0.7; increased residual volume
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CXR - possibly hyperinflation, but often normal; flat hemidiaphragms; large central pulmonary
arteries, decreased peripheral vascular markings; bullae; cylindrical heart
ECG– right atrial and ventricular hypertrophy suggestive of cor pulmonale, leading to large p waves on
ECG →p pulmonale
ABG – in advanced disease decreased Pa O2, increased PaCO2
Tests for α1-antitrypsin – haematocrit >45; normocytic normochromic anaemia; HB and PCV may be
raised →secondary polycythaemia
Gas transfer – reduced
Spirometry– varies from ≥80% in mild disease to <30% in very severe disease
Complications
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Respiratory failure
Cor pulmonale
Treatment of acute exacerbation
Give controlled O2 therapy beginning at 24%, increasing to 28% if after 20 minutes ABGs demonstrate a
steady or decreased PaCO2.
If PaCO2 has risen > 1.5kPa give doxapram or assisted ventilation.
Give nebulised salbutamol and ipratropium, and if measures are unsuccessful consider non-invasive
ventilation.
Also give a 5-7 day course of prednisolone 40mg.
Treat the cause, which is usually a chest infection most commonly caused by Streptococcus
pneumonia orHaemophilus influenza, i.e. give antibiotics if 2 or more of the Anthonisen criteria are met.
Management of long-term disease
Smoking cessation
Long-term oxygen therapy – give 2L via nasal prongs for at least 15 hours per day
o Known as LTOT – long term oxygen therapy
Nebulizer - salbutamol, ipratropium
Surgery, i.e. bullectomy in those who have large emphysematous bullae, or lung transplant in those
with end-stage emphysema.
Exercise training
Diet - to promote weight gain if weight loss experienced
Bronchiolitis
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This is the most common serious respiratory infection during infancy. It comes in winter epidemics,during
which time, 2-3% of all infants are admitted to hospital each year. The primary cause is RSV – respiratory
syncytial virus – which accounts for 80% of cases.
In more temperate climates, the epidemics come in the ‘wet’ season
Prognosis is good, but it does carry a mortality (~1%)
RSV
Highly Infectious
A single-stranded RNA virus
In adults, and older children, RSV only causes coryzal, and sometimes, flu-like symptoms.
Almost all children will have been infected at some stage by the age of 2
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Often, infants catch the virus from older siblings, who bring it home from school, or they catch it directly
themselves in environments with lots of children present.
Spread trough viral shedding, via coughing and sneezing. It can also live on surfaces and clothes outside
the body for up to 5 hours.
Other causes include parainfluenza, virus, influenza virus and adenoviruses
Pathology
Typically infection spread from the upper respiratory tract, into the medium and small bronchi, resulting in
epithelial necrosis. This results in oedema and epithelial shedding, which can cause obstruction, particularly
on expiration.
Clinical Presentation
o
o
o
o
Typically aged <18 months
Annual incidence is about 11% of those <12months
Usually occurs between Nov and April, with peak in Jan and Feb
Coryzal symptoms come first 2-3 days, followed by:
Dry cough
Increasing breathlessness (often RR >50), may include:
o Cough may continue for 1-2 weeks
Wheezing may/may not be present
Fever
Difficulty feeding – due to dyspnoea – is the main reason for admission
Symptoms often worse at night
Apnoea
Symptoms tend to be worse the younger the child. Children >” are rarely seriously ill, whilst those <^
months are at the greatest risk.
o
o
o
o
o
o
Signs and Symptoms that suggests severe disease:
Sharp, dry cough
Cyanosis
Pallor
Tachycardia
tachpnoea
Chest hyperinflation
 Liver displaced downwards
Prominent sternum
o Subcostal recession
o Intercostal Recession
o Prolonged expiration
o End-respiratory crackles on auscultation
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Investigations
RSV - can be easily tested for with nasopharyngeal mucous secretions.
X-ray – usually shows hyperinflation
Blood gases – low O2, raised CO2.
Management
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o
o
o
o
o
o
There is no specific treatment. The management is essentially supportive, and in many cases, will not
require hospitalisation.
Signs that suggest severe disease: lethargy, cyanosis, co-existing illness (e.g. immunodefiency, congenital
heart defects)
Oxygen
Delivered by nasal specs, head box, or in the smallest infants, tent. The amount of O2 is determined by pulse
oximetry and blood gas results.
Steroids and antibiotics should not be given! (no evidence) – although they often are used
Bronchodilators via nebuliser are often used, but are not of proven benefit.
Mist is not of proven benefit and should not be administered
Fluids – can be given IV or by NG tube.
Mechanical ventilation – is needed in about 2% of cases.
Prognosis
Most cases recover within 2 weeks
Bronchiolitis obliterans is a rare complication. This is a form of non-reversible lung damage, in which the
bronchioles become plugged by granulation tissue. There will be:
Very low FEV1 (<21% of normal)
Dry cough
SOB
Wheeze
There is very little treatment. Some cases may improve with a lung transplant.
There are many causes, not just RSV infection in childhood, often including occupational lung disease.
Prevention
There is an injection, containing monoclonal antibody; palivizumab. This is sometimes given to high risk
(usually pre-term) babies. It reduces the severity of the infection and the risk of serious consequences. Its
use is limited due to the cost, and the need for several injections.
Pulmonary Oedema
Pulmonary oedema occurs when fluid leaks from the pulmonary capillary network into the lung interstitium
and alveoli. It forms when there is:
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Imbalance of Starling forces (increased pulmonary capillary pressure, decreased plasma oncotic
pressure, increased negative interstitial pressure)

Damage to the alveolar-capillary barrier
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Lymphatic obstruction
Aetiology
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Raised pulmonary capillary pressure:
o
Heart:
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Ischaemic heart disease - acute coronary syndromes, mechanical complications of
acute myocardial infarction (MI) such as ventricular septal rupture, right ventricular
infarction
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Valvular - acute aortic or mitral regurgitation, severe aortic stenosis, endocarditis

Severe hypertension
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Acute arrhythmia
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o
Acute myocarditis
Left atrial myxoma
Cardiac tamponade
Aortic dissection
Cardiomyopathy, e.g. postpartum cardiomyopathy
Drugs: myocardial depression, e.g. alcohol; fluid retention, e.g. NSAIDs
Renal:
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Acute renal failure, chronic renal failure
Renal artery stenosis
o
Iatrogenic fluid overload
o
Cerebrovascular insult
o
High output heart failure, e.g. septicaemia, thyrotoxic crisis, anaemia, shunts
Increased pulmonary capillary permeability:
o
Acute respiratory distress syndrome (ARDS)
o
High altitude
o
Inhaled or aspirated toxic substances
o
Radiation
o
Liver failure
o
Fat embolism or amniotic fluid embolism
Lymphatic obstruction, e.g. mediastinal carcinomatosis, silicosis
Acute or chronic upper airway obstruction
Clinical Presentation
Symptoms:
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Patient is usually severely breathless, sweaty, nauseated and anxious.
Initially they may have a dry or productive cough (sometimes with pink, frothy sputum).
Patients may also develop paroxysmal nocturnal dyspnoea or orthopnoea.
Signs:
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Patient is in respiratory distress, pale, sweaty, tachypnoeic and tachycardic.
They may be cyanosed, have evidence of congested neck veins and a raised JVP.
Bibasal/widespread rales or fine crackles are usually heard listening to the chest.
Oxygen saturation is usually <90% on room air.
Assess for a gallop rhythm (3rd heart sound) and murmurs suggestive of valve stenosis or
regurgitation.
Hypotension - the triad of hypotension (SBP <90 mmHg), oliguria, and low cardiac output is known
as cardiogenic shock
In hypertensive heart failure, a high blood pressure, tachycardia, vasoconstriction present with
signs of pulmonary oedema without extensive systemic congestion.
Where pulmonary oedema occurs in association with right heart failure, hepatomegaly and
peripheral oedema are usual.
Investigations
1.
Blood tests:
o
U&Es, creatinine, sodium, potassium, glucose, cardiac enzymes, liver function tests,
clotting tests (INR)
o
Arterial blood gases and pH
o
Brain natriuretic peptides (BNPs) - thought to be helpful in distinguishing acute pulmonary
oedema from other causes of dyspnoea, but no consensus regarding reference values in
2.
3.
4.
5.
6.
acute heart failure. Raised BNP levels are also found in acute coronary syndromes (ACSs),
pulmonary embolism and acute severe dyspnoea not due to heart failure.
ECG: look for evidence of arrhythmia, myocardial infarction or other cardiac disease, e.g.
leftventricular hypertrophy.
Chest X-ray: to exclude other causes of breathlessness and confirm pulmonary oedema.
Echocardiogram: ESC guidelines suggest that all patients with AHF should be evaluated with
echocardiogram as soon as possible, as it frequently determines treatment strategy.
Non invasive monitoring: body temperature, respiratory and heart rate, urine output, pulse
oximetry and ECG telemetry, daily weights.
A urinary catheter enables accurate measurement of urinary output which helps rapidly to assess
diuretic response and fluid balance.
The Killip classification further subdivides prognosis:
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Class I (no signs of left ventricular dysfunction): hospital mortality 6%
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Class II (S3 gallop with mild/moderate pulmonary congestion): hospital mortality 30%
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Class III (severe pulmonary oedema): hospital mortality 40%
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Class IV (cardiogenic shock): hospital mortality 80-90%
Management
Initial treatment

Give oxygen (if available) by face mask: 100% if no pre-existing lung disease (but even in patients
with COPD, give high oxygen flow initially but monitor with blood gases to ensure hypercapnia is
avoided). Aim for oxygen saturations ≥95% (>90% in those with COPD).

Insert an IV cannula and give:
o
Analgesia and sedation where the patient is in pain or distressed. Diamorphine 2.5-5 mg IV
slowly (or morphine 5-10 mg IV slowly) relieves anxiety, pain and distress, as well as both
producing transient venodilation and reducing myocardial oxygen demand. An anti-emetic
may be required.
o
Nitrates are first-line vasodilators where SBP >90 mmHg and there is no serious obstructive
valvular disease. Give sublingual or buccal nitrate, e.g. GTN spray 2 puffs sublingual, or 1-3
mg buccal isosorbide dinitrate.
o
Furosemide 20-40 mg IV (slowly) produces transient venodilation and subsequent diuresis.
This may need to be repeated based on response of clinical symptoms - diuretic
effectiveness is greatly reduced in presence of hypotension and where patients are chronic
oral diuretic users.
Allergic alveolitis/Occupational lung disease/ Inhalation lung injury
In extrinsic allergic alveolitis, there is diffuse, granulomatous inflammation of the lung parenchyma and
airways in people who have been sensitised by repeated inhalation of organic antigens in dust.
Pathogenesis
The pathogenesis is thought to involve both cell-mediated and immune complex-mediated hypersensitivity
reactions. There may also be a genetic predisposition.
It can be associated with many occupations and hobbies. Examples are:


Farmer's lung - one of the most common forms. Due to exposure to mouldy hay. Major antigen
isSaccharopolyspora rectivirgula.
Bird-fancier's lung - one of most common forms. Due to exposure to avian proteins, e.g. pigeons,
parakeets.
Epidemiology

The annual incidence of interstitial lung diseases has been estimated as 30:100,000 with
hypersensitivity pneumonitis accounting for less than 2% of these cases.
Risk factors


Pre-existing lung disease
Specific occupations (including farmers, cattle workers, ventilation system workers, vets, people
working with grain and flour, those whose job involves working with chemicals)
Clinical Presentation
Acute form

Symptoms usually start 4-6 hours after exposure to the sensitising antigen and resolve quickly,
usually within days.

There is a flu-like illness with fever, chest tightness, dry cough and dyspnoea. Associated symptoms
include malaise, chills, headache, generalised aches and pains, anorexia and tiredness.

Symptoms are directly related to level of exposure and low-level acute exposure may produce mild
symptoms that last for just a few hours.

Signs include fever, tachypnoea and bibasal fine inspiratory crackles. Wheeze is rare.

In very severe cases, patients may develop life-threatening respiratory failure with cyanosis,
respiratory distress at rest and high fever.
Chronic form

In the chronic form there are often no systemic symptoms except weight loss and gradual
diminution of exercise tolerance due to dyspnoea.

If the source of the antigen is removed, there may only be partial improvement of symptoms.

Cyanosis and clubbing may develop.

Tachypnoea, obvious respiratory distress and inspiratory crackles over the lower lung fields may be
present.

Eventually there may be chronic hypoxaemia and pulmonary hypertension with right heart failure.
Differential diagnosis
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Infection (bacterial, fungal, viral including tuberculosis)
Connective tissue disorders causing interstitial lung disease
Pulmonary fibrosis (including idiopathic)
Asthma
Sarcoidosis
Histoplasmosis
Drug-induced interstitial lung disease
Investigations

Blood tests: inflammatory markers may be raised but are non-specific. There may be serum
antibodies detectable in some patients. Antigen-specific IgG antibodies' analysis and antibody titre
level may also be helpful.
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Chest X-ray: in the acute form this may be normal in some or show diffuse micronodular interstitial
shadowing. In the subacute form, there may be micronodular or reticular opacities in the mid/upper
lung fields. In the chronic form, there may be features of fibrosis with loss of lung volume.
CT scanning: high resolution CT is a good way to evaluate the stage of disease and usually shows
typical changes.
Lung function testing: this can help to determine the degree of respiratory
impairment.Spirometry shows a restrictive defect in acute and subacute forms but there may be a
mixed restrictive/obstructive picture in the chronic form. Oxygen saturation may be reduced with
further desaturation on exercise. There may also be reduced capacity of the lungs to diffuse carbon
monoxide
Bronchoalveolar lavage: analysis of the lymphocyte count and CD4/CD8 cell ratio in
bronchoalveolar lavage fluid may aid diagnosis. There is usually a lymphocytosis and the CD4/CD8
ratio is reduced to less than 1.
Transbronchial or open lung biopsy: this may show characteristic histopathological features.
Possible diagnostic criteria

Exposure to a known offending antigen

Positive precipitating antibodies to the offending antigen

Recurrent episodes of symptoms

Inspiratory crackles on physical examination

Symptoms occurring 4-8 hours after exposure

Weight loss
Management
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Supplemental oxygen should be given to treat hypoxaemia.
Corticosteroids may be indicated for the treatment of severe acute and subacute forms and for
chronic forms that are severe or progressive. However, steroids don't seem to alter the long term
outcome. Exposure to the offending antigen still needs to be avoided as well.
In advanced chronic disease, pulmonary fibrosis can still progress and death can occur despite
aggressive corticosteroid therapy.
Treatment in chronic or residual disease is supportive.