Respiratory Flashcards
What is acute bronchitis?
Acute bronchitis is a type of chest infection which is usually self-limiting in nature. It is a result of inflammation of the trachea and major bronchi
What is acute bronchitis is associated with?
oedematous large airways and the production of sputum
What is the timeline of acute bronchitis?
The disease course usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time
What is the leading cause of acute bronchitis?
viral infection is the leading cause. Around 80% of episodes occur in autumn or winter.
What is the typical presentation of acute bronchitis?
cough: may or may not be productive
sore throat
rhinorrhoea
wheeze
The majority of patients with have a normal chest examination, however, some patients may present with:
Low-grade fever
Wheeze
How do you differentiate acute bronchitis from pneumonia?
History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
What investigations do you do for acute bronchitis?
acute bronchitis is typically a clinical diagnosis
however, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated
What is the treatment for acute bronchitis?
analgesia
good fluid intake
consider antibiotic therapy if patients:
are systemically very unwell
have pre-existing co-morbidities
have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
the BNF currently recommends doxycycline first-line
doxycycline cannot be used in children or pregnant women
alternatives include amoxicillin
Define allergy disorder and its MOA
Allergy is a broad topic, with allergic disorders resulting from a variety of mechanisms. Many immediate reactions involve type 1 hypersensitivity, where an allergen is recognised by IgE antibodies, triggering cytokines to be released from mast cells (with histamine an important component of this).
What other conditions are allergies associated with?
allergic rhinitis, eczema, asthma and food allergies
Name some common allergens:
Dust mites
Foods (especially nuts, shellfish, eggs, milk and certain fruits)
Grass and tree pollens
Animal dander
Medications (e.g. penicillins, aspirin, ibuprofen)
Insect bites and stings
Name some common signs and symptoms of allergies
Itchy skin or eyes
Rashes (classically urticarial in IgE mediated hypersensitivity)
Gastrointestinal upset (diarrhoea, abdominal pain or nausea and vomiting)
Swelling of the eyes, lips, mouth or throat
Rhinorrhoea
Sneezing
Shortness of breath or wheeze
Deterioration in asthma or eczema symptoms
Conjunctivitis
What are the investigations for allergens?
First line investigations are either skin prick testing or blood testing for specific IgE levels to different food allergens
Skin prick testing involves injecting allergens (as well as positive and negative controls) into the skin then assessing these after 15 minutes to detect to which allergens a person is sensitised
Serum specific IgE testing is possible for a wide range of allergens but can take several weeks to be resulted
Some patients may be “sensitised” to specific allergens i.e. they have positive test results but no symptoms of allergy when exposed to that allergen
Because of this, testing should be targeted based on the clinical history as otherwise false positive results are common
In cases of confirmed food allergy, follow-up testing may be done to see if patients have developed tolerance to that allergen
If results of initial tests are unclear, the gold standard diagnostic test for food allergy is an oral food challenge where small quantities of the suspected allergen are administered under medical supervision and uptitrated to see if symptoms are provoked
What is the management for allergy disorder?
First line investigations are either skin prick testing or blood testing for specific IgE levels to different food allergens
Skin prick testing involves injecting allergens (as well as positive and negative controls) into the skin then assessing these after 15 minutes to detect to which allergens a person is sensitised
Serum specific IgE testing is possible for a wide range of allergens but can take several weeks to be resulted
Some patients may be “sensitised” to specific allergens i.e. they have positive test results but no symptoms of allergy when exposed to that allergen
Because of this, testing should be targeted based on the clinical history as otherwise false positive results are common
In cases of confirmed food allergy, follow-up testing may be done to see if patients have developed tolerance to that allergen
If results of initial tests are unclear, the gold standard diagnostic test for food allergy is an oral food challenge where small quantities of the suspected allergen are administered under medical supervision and uptitrated to see if symptoms are provoked
What are the complications of allergy disorder?
Malnutrition and failure to thrive in children can occur due to restrictive diets
Anaphylaxis is a life-threatening medical emergency and can lead to circulatory collapse and death if not treated promptly
Reduced quality of life can result from stress and anxiety surrounding avoiding allergens e.g. in social situations or when travelling.
What is the prognosis of allergy disorder?
Some allergies are more likely to persist than others, with many children growing out of milk, egg, soy or wheat allergies.
Others such as peanut allergy are sometimes outgrown (usually before the age of 10) but may persist into adulthood.
In what ways can asbestos lung disease present?
There are several ways asbestos exposure can manifest in the lungs, including pleural plaques, diffuse pleural thickening, pleural effusions, lung cancer and mesothelioma
What is the most common way asbestos lung presents?
Pleural plaques - these are benign and do not undergo malignant change. They, therefore don’t require any follow-up. They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
Which conditions is pleural thickening in asbestos lung disease similar to?
empyema or haemothorax
What is asbestosis?
Asbestosis is one manifestation of asbestos lung disease and is a chronic restrictive interstitial fibrotic lung disease that typically manifests 10-20 years following exposure to asbestos fibres (often through occupational risks).
What are the signs and symptoms of asbestosis?
Symptoms:
Progressive dyspnoea manifesting over months-years
Dry cough
Weight loss
Fatigue
Signs:
Bilateral fine end-expiratory crepitations, predominantly basal
Finger clubbing
Cyanosis
What are the investigations for asbestosis?
Pulmonary function tests: the expected finding is a restrictive pattern (reduced FVC and TLC with a normal FEV1/FVC ratio) with decreased diffusion capacity.
Chest x-ray: bilateral shadowing, predominantly at the bases. Other manifestations of asbestosis exposure may be seen for example pleural plaques.
Asbestosis typically causes lower lobe fibrosis.
High resolution CT: may show honeycombing, traction bronchiectasis and parenchymal bands especially in the lower zones (all signs of fibrosis).
What are the treatments for asbestosis?
Smoking cessation: essential to reduce lung cancer risk and progression of asbestosis.
Pulmonary rehabilitation: Helps to improve lung function and quality of life.
Oxygen therapy: consider if significant hypoxaemia.
Vaccination against influenza and pneumococcal disease.
Name the malignant disease of the pleura crocidolite (blue) asbestos causes?
Mesothelioma
What are the possible features of mesothelioma?
progressive shortness-of-breath
chest pain
pleural effusion
What is the treatment for mesothelioma?
Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy. Unfortunately, the prognosis is very poor, with a median survival from diagnosis of 8-14 months.
What is the most common cancer caused by asbestos?
lung cancer is actually the most common form of cancer associated with asbestos exposure.
What is the relationship between smoking and lung cancer with asbestos exposure?
has a synergistic effect with cigarette smoke in terms of the increased risk. Therefore, smoking cessation is very important as the risk of lung cancer in smokers who have a history of asbestos exposure is very high.
What is asthma and what three things does it involve?
Asthma is a common disease of the airways, involving reversible bronchoconstriction, hyperreactivity and chronic inflammation
What symptoms is asthma characterised by?
intermittent ““asthma attacks”” with wheeze, cough, shortness of breath and chest tightness.
The above symptoms should be episodic and usually show diurnal variation (worse at night or in the early morning).
What two other conditions is asthma linked to?
allergic rhinitis, and eczema
Name some triggers for asthma?
Cold air and exercise
Pollution and cigarette smoke
Allergens such as animal dander, dust mites and pollen
Irritants such as perfumes, paints or air fresheners
Medications such as NSAIDs or beta-blockers
MOA of asthma:
These trigger a type 1 hypersensitivity reaction which is mediated by IgE. T Helper 2 cells produce IL4, IL5 and IL13 cytokines which activate the humoral immune system, leading to the proliferation of eosinophils, mast cells and dendritic cells. These cells then produce more inflammatory mediators such as leukotrienes and histamine.
This inflammation contributes to airway hyperresponsiveness leading to bronchospasm, as well as mucus hypersecretion that also obstructs airways. Over time in severe asthma, airway remodelling mediated by fibroblasts causes chronic obstruction and thickening of smooth muscle.
What are the risk factors for asthma?
Family history of asthma or atopy
Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis)
Exposure to smoke, including maternal smoking in pregnancy
Respiratory infections in infancy
Prematurity and low birth weight
Obesity
Social deprivation
Occupational exposures (e.g. flour dust, isocyanates from paint)
Signs of asthma during an exacerbation or attack?
Tachypnoea
Increased work of breathing
Hyperinflated chest
Expiratory polyphonic wheeze throughout the lung fields
Decreased air entry (if severe)
What are the common investigations for asthma?
FeNO (fractional exhaled nitric oxide) testing: offer to all adults to confirm eosinophilic airway inflammation, considered positive if >40 parts per billion.
Spirometry: offer to all > 5 years old to confirm airway obstruction (i.e. FEV1/FVC<70%), may be normal if patient is not symptomatic at the time of testing.
Bronchodilator reversibility: if spirometry confirms obstruction, a bronchodilator (e.g. salbutamol inhaler) is given and spirometry repeated to assess response to treatment. An improvement in FEV1 of 12% or more or 200ml is a positive result.
When might investigations for asthma have a false negative?
may be falsely negative in patients treated with inhaled corticosteroids
If there is diagnostic uncertainty following the initial asthma investigations what can then be offered?
If there is diagnostic uncertainty following the above tests, patients may be asked to monitor their peak flow twice a day over 2-4 weeks and keep a diary of the readings. This is then used to assess peak flow variability (the difference between the highest and lowest readings as a percentage of the average PEF). Variability >20% is a positive result
If there is still uncertainty, patients may be referred to specialist services for a direct bronchial challenge test, where histamine or metacholine is inhaled to trigger bronchoconstriction. Airway hyperresponsiveness is assessed by looking at the concentration of the triggering medication required to cause a 20% decrease in FEV1 - 8mg/ml or less is a positive result.
How often should a personalised asthma plan be reviewed?
Annually
What are some non-pharmacological management of asthma?
Teach good inhaler technique and review this regularly
Spacer devices can be used to optimise medication delivery
Regular peak flow monitoring
Smoking cessation
Advice on avoiding triggers where possible (e.g. allergens, certain medications)
Ensure vaccinations are up to date, including annual influenza vaccination
Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected
What are the first steps for pharmacological asthma management?
Prescribe all patients a short-acting beta-2 agonist (SABA) such as salbutamol to use as a reliever inhaler Patients using a SABA 3 times per week or more/with asthma symptoms 3 times per week or more/who wake at night once a week or more also need an inhaled corticosteroid (ICS) which is started at a low dose (200mg), such as beclomethasone.
If adequate control is not achieved in asthma with a SABA and ICS what is then offered?
a leukotriene receptor antagonist (LTRA) such as montelukast - this is a tablet taken every night.
If a SABA, ICS and LTRA is not working what do we then do in asthma management?
The next step would be adding a long-acting beta-2 agonist (LABA) such as salmeterol - the ICS should be continued but the LTRA may be stopped if it was not felt to have been of benefit.
If asthma is still not controlled with SABA + low dose ICS + LABA +/- LTRA what do we then do?
switched to a regimen of low dose ICS + maintenance and reliever therapy inhaler (MART) +/- LTRA
What is a MART?
MART is a combination inhaler with ICS and a fast-acting LABA (e.g. beclomethasone + formoterol which is also known as Fostair), which is used as both a reliever inhaler and as maintenance treatment.
If ICS + MART is not working then what?
The next step would be increasing the ICS dose from low to moderate, either continuing with a MART inhaler or going back to separate inhalers. At this stage consider referral to secondary care.
What can they prescribe at secondary care for asthma if still poorly controlled?
switching to a high dose ICS, oral steroid treatment or an additional medication (e.g. a muscarinic receptor antagonist or theophylline). This would usually be under a specialist clinic, and patients may also be able to access newer therapies such as biologics (e.g. omalizumab, which targets IgE)
Other than patients who are not responding to treatment for asthma, who should also be referred to secondary care?
Uncertainty regarding diagnosis
Suspected occupational asthma
Severe or life-threatening asthma requiring admission to hospital
Multiple exacerbations requiring oral steroid treatment per year
Clinical features of a moderate asthma attack?
PEFR > 50% of predicted or best
No features of severe/life-threatening asthma
Clinical features of a severe asthma attack?
PEFR 33-50% of predicted or best
Heart rate > 110
Respiratory rate > 25
Unable to complete sentences in one breath.
Accessory muscle use
Normal CO2
Clinical features of a life threatening asthma attack?
PEFR < 33% of predicted or best
Oxygen saturation < 92% or cyanosis
Altered conciousness/confusion
Exhaustion/poor respiratory effort
Cardiac arrhythmia
Hypotension
Silent chest
PaO2 < 8kPa
Normal PaCO2 - suggest that the patient has life-threatening asthma, as it would be initially low due to hyperventilation. As the patient tires, they become normocapnic then hypercapnic
What investigations does one do during an acute asthma attack and why?
Peak expiratory flow rate (PEFR) to help assess severity as per the classification above and monitor response to treatment.
Arterial blood gas if the patient is hypoxic to assess oxygenation and ventilation in patients - CO2 is expected to be low due to hyperventilation and if this is raised this indicates the asthma attack is near fatal.
Portable chest X-ray if a trigger such as pneumonia or a complication such as pneumothorax is suspected clinically.
What is the management for an acute asthma attack?
Recognise that this may be a medical emergency, assess using an ABCDE approach and escalate early to senior colleagues/critical care if not responding to treatment
Titrate oxygen to maintain saturations of 94-98%
Nebulised salbutamol driven by oxygen (if out of hospital, give up to 10 puffs of inhaled salbutamol and call an ambulance if not responding)
The BNF advises that patients should take 40-50mg prednisolone for ≥5days following an acute asthma episode. A Cochrane review of six trials indicated that a short course of corticosteroids could reduce the risk of relapse following an acute exacerbation of asthma. The first dose can be given in A&E
If the asthma attack is life threatening or severe and they are not responding to initial treatment what can one do then?
If the attack is severe or life-threatening or if response to salbutamol has been poor, add nebulised ipratropium bromide
Give prednisolone 40-50mg orally, or IV hydrocortisone if the patient is unable to swallow
Can consider IV magnesium sulphate and/or aminophylline if the patient is not responding to nebulisers
If the patient continues to deteriorate despite maximal therapy, they may require intubation and ventilation in an intensive care setting (for example in cases of severe hypoxia or exhaustion)
After an asthma attack how soon after discharge from hospital should patients be reviewed to assess their symptoms, inhaler technique and current management.
Within 2 days
What are patients at risk from using an ICS for asthma and what can patients do to reduce this?
oral thrush, which is associated with steroid inhaler use. The risk of oral thrush can be reduced with correct inhaler technique, using a spacer with the inhaler and rinsing and spitting after inhaler use. The problem may be persistent, in which case, alternative causes, such as immunosuppression from malignancy or diabetes, should be excluded, and the patient may require nystatin therapy
What pathological findings can be seen in histology for asthma?
Curschmann spirals
In order for a patient to be discharged from hospital after an acute asthma attack what is required?
A stable period of 24 hours on the regular asthma treatment regime
What is samter’s triad in regards to asthma and was clinical significance does it have?
asthma, nasal polyps and aspirin sensitivity (sometimes also known as Aspirin Exacerbated Respiratory Disease or AERD). It is very classical for patients with asthma to have worsening symptoms following aspirin, as well as beta blockers, and great care should be taken with these medications in this population
What are the spirometry results for a severe asthma exacerbation?
Typical spirometry results for obstructive respiratory disease are a low FEV1 and reduced FEV1/FVC (<70% predicted). FVC is preserved
What would you find on an arterial blood gas of someone during a severe asthma exacerbation?
respiratory alkalosis and hypoxemia
What is bronchiectasis?
Bronchiectasis is a chronic lung disease where inflammation and obstruction causes damage to the bronchial walls leading to their permanent dilation. This damage may affect the whole lung or only one lobe (for example in cases caused by airway obstruction).
What causes bronchiectasis?
40% of patients will have no identifiable cause for their bronchiectasis. The most common identified cause is a previous severe lower respiratory tract infection, for example pneumonia, TB or influenza.
Other causes of bronchiectasis include:
Immunodeficiency (HIV, common variable immunodeficiency)
Defective mucociliary clearance (cystic fibrosis, primary ciliary dyskinesia e.g. Kartagener syndrome)
Allergic Bronchopulmonary Aspergillosis (ABPA)
Autoimmune disease (rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease)
Airway obstruction (inhaled foreign bodies, bronchial carcinoma, severe obstructive lung disease e.g. COPD/asthma)
Chronic aspiration
Congenital defects of the large airways (Marfan’s, tracheobronchomegaly)
Name some symptoms and signs of bronchiectasis?
Symptoms include:
Productive cough lasting at least 8 weeks
Copious production of purulent sputum
Dyspnoea
Haemoptysis
Chest pain
Fatigue
Weight loss
On examination patients may have:
Coarse crackles on auscultation
Wheeze
Rhonchi (snoring sounds caused by secretions in the larger airways)
Finger clubbing
What investigations should all patients have for bronchiectasis and why?
Sputum culture: to look for colonising bacteria (specialist follow up is required for those carrying MRSA, pseudomonas or mycobacteria).
Spirometry: to look for comorbid COPD and asthma and assess severity of obstruction.
Blood tests: inflammatory markers (WCC, CRP) for infective exacerbations.
Chest X-ray: usually abnormal, with increased lung markings, tram-track opacities and ring shadows.
High-resolution CT chest: the diagnostic test for bronchiectasis, may also give an indication to the underlying cause and can be used to quantify severity. May show lack of tapering of airways, increased ratio of bronchi to adjacent pulmonary arteries, bronchial wall thickening and impacted mucus. - thickened bronchial walls in “tram-tracking” and “signet-ring” form
Dependent on clinical features name some further tests one may do for bronchiectasis to isolate the cause?
Rheumatoid factor, anti-CCP, ANA and ANCA
Serum immunoglobulins: if low suspect antibody deficiency, if IgE raised may indicate ABPA
HIV serology
Testing for cystic fibrosis: genetic testing or sweat chloride, all under 40s should be tested as well as older patients with features of CF
Bronchoscopy: should be done if bronchiectasis is focal to rule out an obstructing malignancy or foreign body
What is the conservative management for bronchiectasis?
Patient education on self-management including sputum clearance exercises
Smoking cessation support
Referral to pulmonary rehabilitation for patients with disabling breathlessness
Nutritional support for patients with a BMI < 20
Influenza and pneumococcal vaccination
Chest physiotherapy e.g postural drainage
What is the medical management for bronchiectasis?
Identify acute exacerbations - these usually present with worsening breathlessness, increased sputum production, fevers and malaise - and treat with antibiotics tailored to sputum cultures
Long-term antibiotic prophylaxis should be considered in patients with 3+ exacerbations per year or exacerbations causing significant morbidity - again this should be tailored to sputum cultures e.g. nebulised colomycin for carriers of Pseudomonas aeruginosa
Treat comorbidities e.g. ensure on appropriate inhalers for asthma or COPD
The initial management includes chest physiotherapy to facilitate the removal of secretions, inhaled bronchodilators to improve airflow, and antibiotics to treat bacterial infections. Other treatments such as mucolytics, macrolide antibiotics, and immunomodulators may also be used depending on the severity and underlying cause.
What is the surgical management for bronchiectasis?
Lung resection may be considered in certain patients with localised disease in order to reduce exacerbations or treat haemoptysis
Specialist services may also consider referral for lung transplantation in severe cases of bronchiectasis not responding to medical management
What is primary ciliary dyskinesia? (Kartagener’s syndrome)
PCD is an autosomal recessive disorder of dysfunctional cilia. Cilia are important as they determine the orientation/laterality of internal organs and line the inner walls of bronchi. Consequently, their dysfunction results in bronchiectasis and recurrent infections. Percussion usually changes at the RIGHT lung base due to movement of the liver during inspiration and expiration. This patient displays this phenomena at their LEFT lung base, suggesting situs invertus – a key features of PCD
What are the most common infectious agents for bronchiectasis?
Haemophilus influenzae, Pseudomonas aeruginosa, TB, Bordetella pertussis (otherwise known as whooping cough) and Allergic Bronchopulmonary Aspergillosis (ABPA)
What to do if a patient presents with a persistent cough with large volumes of green sputum, coarse inspiratory crepitations, fever, and respiratory rate greater than 25 bpm
This may indicate bronchiectasis with possible superimposed bacterial infection. This would require hospital admission for IV antibiotics treatment.
What is asthma-COPD overlap syndrome?
a clinical condition characterised by persistent airflow limitation with several features usually associated with both asthma and chronic obstructive pulmonary disease (COPD). Patients exhibit increased reversibility of airflow obstruction, eosinophilic bronchial and systemic inflammation, and increased response to inhaled corticosteroids.
What are the risk factors for asthma-COPD overlap syndrome?
Genetic factors, environmental exposures - airborne pollutants and and allergen exposure, smoking, poorly controlled asthma, recurrent respiratory infections, increased age and female gender
What is the stereotypical presentation of asthma-COPD overlap syndrome?
a patient with a history of smoking, presenting with persistent breathlessness that is progressive and worsened by exercise. The patient may also have a chronic cough with expectoration, recurrent wheezing episodes often triggered by respiratory infections or exposure to allergens, and frequent exacerbations requiring systemic corticosteroids or antibiotics.
What are the symptoms of asthma-COPD overlap syndrome?
Respiratory Symptoms
Dyspnoea: Patients commonly experience dyspnoea which is persistent, progressive and aggravated by exertion. It may be accompanied by orthopnoea in severe cases.
Cough: Chronic cough is another common symptom, often productive with clear or white sputum. This may worsen in the morning or during the night.
Wheezing and Chest Tightness
Patients can present with recurrent wheezing episodes which are often triggered by respiratory infections or exposure to allergens. These episodes are associated with chest tightness and may not fully respond to bronchodilators.
Exacerbations
Frequent exacerbations requiring treatment with systemic corticosteroids or antibiotics are common in ACOS patients. These exacerbations are generally more severe than those seen in asthma or COPD alone.
What may you find on a physical examination of asthma-COPD overlap syndrome?
might reveal prolonged expiration, wheezing on auscultation, hyperinflation of the chest and use of accessory muscles for respiration indicating respiratory distress.
In advanced stages, signs of cor pulmonale such as peripheral oedema and raised jugular venous pressure may be observed.
What pulmonary function tests would you do for asthma-COPD overlap syndrome and what would you expect to see?
These are essential for diagnosing ACOS as they provide objective evidence of airflow obstruction and reversibility, both hallmark features of this condition.
Spirometry: This is the first-line investigation. A post-bronchodilator FEV1/FVC ratio less than 0.7 confirms persistent airflow limitation, suggestive of COPD. Evidence of reversibility (an increase in FEV1 by ≥12% and ≥200ml following bronchodilator administration) may suggest asthma.
Bronchial Challenge Test: In cases where spirometry results are inconclusive, a bronchial challenge test with methacholine or histamine can be used to assess airway hyperresponsiveness, a characteristic feature of asthma.
What radiological examinations would you do for asthma-COPD overlap syndrome and what would you expect to see?
Chest X-ray: This is usually the first-line radiological investigation. It can help identify alternative diagnoses or complications like pneumonia or pneumothorax.
High-Resolution Computed Tomography (HRCT): This can be considered when there is suspicion of other co-existing conditions such as bronchiectasis or interstitial lung disease.
What would a blood test show in asthma-COPD overlap syndrome?
Full Blood Count (FBC): May show eosinophilia, often seen in asthma.
IgE: Elevated levels can support a diagnosis of asthma but should not be used in isolation to diagnose ACOS.
What would a sputum analysis show in asthma-COPD overlap syndrome?
Eosinophilic inflammation is more characteristic of asthma, while neutrophilic inflammation is more common in COPD. However, this test is not routinely performed due to its technical demands and limited availability.
What do you do to assess severity and risk factors for asthma-COPD overlap syndrome?
Evaluate the severity of symptoms using validated tools such as the Medical Research Council (MRC) dyspnoea scale or COPD Assessment Test (CAT).
Identify risk factors for exacerbations, including previous exacerbation history, high eosinophil count, poor lung function, smoking status and comorbidities.
What is the pharmacological management for asthma-COPD overlap syndrome?
Inhaled corticosteroids (ICS) combined with long-acting beta2-agonists (LABA) are the first-line therapy for most patients with ACOS.
Add-on therapies such as long-acting muscarinic antagonists (LAMA) may be considered in patients who remain symptomatic or have frequent exacerbations despite ICS/LABA treatment.
Consider short-acting bronchodilators for rescue therapy in all patients.
What lifestyle modifications do we do for asthma-COPD overlap syndrome?
Promote smoking cessation in smokers. Provide support through counselling or pharmacotherapy if appropriate.
Encourage regular physical activity and a balanced diet to maintain optimal body weight.
What are coronaviruses?
Coronaviruses are a family of single-strand positive sense RNA viruses, named for their crown-like appearance under electron microscopy. They can cause respiratory diseases in both animals and humans.
What three strains of coronaviruses have caused pandemics?
Three strains have caused pandemics: Severe Acute Respiratory Syndrome (SARS), Middle Eastern Respiratory Syndrome (MERS), and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2), also known as COVID-19.
What are risk factors for severe disease from coronaviruses?
Demographics: older age, male sex, ethnic minority populations
Immunocompromise: immunosuppression, HIV
Comorbidities including diabetes, respiratory, cardiovascular, renal, liver, neurological diseases
Signs and symptoms of coronaviruses?
Typically, symptoms appear within 5 days of infection. Symptoms include fevers, cough, anosmia, dyspnoea, fatigue, myalgia, headache and diarrhoea.
Complications can develop early or after several days. Symptoms of severe disease include worsening breathlessness, coughing up blood, cyanosis, cold/pale/mottled skin, collapse and altered mental status
What are the investigations for coronaviruses and specifically covid-19?
Diagnosis of Covid-19 can be with rapid lateral flow tests or a swab sent for RT-PCR.
For people with signs of severe disease or complications, consider the following:
Bloods: FBC (may show lymphopenia), U&E, LFT, glucose, clotting, CRP, ESR, LFH, iron studies, cardiac markers as indicated
ABG may show low PaO2, acidosis or raised PaCO2
Chest X-ray showing ground-glass opacity or consolidation
Blood & sputum cultures
What is the management for mild covid-19?
In a case of suspected or confirmed Covid-19, it is important to take precautions such as isolation & wearing appropriate PPE when interacting with positive cases.
For most cases of mild infection, patients can be managed conservatively at home with advice on self-care and measures to reduce transmission. If they are at high risk of complications, antiviral or antibody treatment may be indicated.
If a patient shows signs of severe covid-19 what is then the management?
If a patient has signs of severe disease or complications, admit to hospital. If they are acutely unwell, follow an A-E approach, get help early & consider initiating sepsis pathways. It is important to consider treatment escalation planning. Patients may require:
Oxygen therapy if hypoxic
Symptom management, for example analgesia or antipyretics
Antivirals such as remdesivir
Biologic treatments such as IL-6 inhibitors, or JAK inhibitors
Steroids such as dexamethasone, especially if there is an oxygen requirement
VTE prophylaxis
Treatment of secondary infections
Patients with critical illness may require ICU or HDU admission. They may need respiratory support (non-invasive ventilation, mechanical ventilation), prone positioning and specific treatments guided by specialists.
What are the complications of covid-19/coronaviruses?
Acute respiratory distress syndrome
Venous thromboembolism
Heart failure & other cardiac pathology
Acute kidney injury
Acute liver injury
Sepsis
Paediatric multisystem inflammatory syndrome in children
Neurological sequelae
Secondary bacterial infection
Long Covid
What is COPD?
Chronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive.
What are the risk factors for COPD?
Tobacco smoking and passive smoke exposure
Marijuana smoking
Occupational exposure to dusts and fumes
Household air pollution from wood or coal burning
Alpha-1 antitrypsin deficiency
Prognosis is variable, with the following factors associated with higher morbidity and mortality:
Poor exercise tolerance
Smoking
Low body mass index
Multi-morbidity and frailty
Exacerbations requiring admission to hospital or frequent exacerbations
Severe obstruction on spirometry (as measured by a lower FEV1)
Chronic hypoxia
Cor pulmonale
What are the two conditions that are part of COPD?
Chronic bronchitis and emphysema
What is chronic bronchitis?
As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs. Cilia are not able to remove the excess mucus and so it obstructs the small airways. Ongoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.
What is emphysema?
Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants.
Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.
This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.
How does the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity?
airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations.
What are the two measures used to quantify symptom severity in COPD?
CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale
What are the signs and symptoms of COPD?
Shortness of breath that worsens with exertion
Reduced exercise tolerance
Chronic productive cough
Recurrent lower respiratory tract infections
Wheeze
In more advanced cases, systemic symptoms such as weight loss and fatigue may be present
What may you see on an examination of COPD?
Wheeze or crackles on auscultation
Accessory muscle usage
Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)
Cyanosis
Hyperinflation of the chest
Cachexia
Raised JVP and peripheral oedema (indicating cor pulmonale has developed)
What is the diagnostic investigation for COPD and key to classification of COPD severity?
spirometry
Fev1/FVC ratio <0.7 confirms obstruction
also do a Sputum culture - during exacerbations to target antibiotic therapy
What other investigations would you do in COPD to see over conditions which may be caused by the COPD?
Bloods - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an echocardiogram if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history
ECG - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:
Right axis deviation
Prominent P waves in inferior leads
Inverted P waves in high lateral leads (I, aVL)
Low voltage QRS
Delayed R/S transition in leads V1-V6
P pulmonale
Right ventricular strain pattern
RBBB
Multifocal atrial tachycardia
Why and what would you see in a chest X-ray of someone with COPD?
used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.
What is the conservative management for COPD?
Patient education, ensure all patients have a personalised self-management plan
Smoking cessation support
Nutritional support and dietician referral if malnourished
Annual influenza and one-off pneumococcal vaccination
Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)
Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques
What is the initial medical management for COPD?
For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler
Bronchodilator therapy
What is the next step of medical management of COPD if they have features of asthma (diurnal variation, atopic dermatitis) or steroid responsiveness?
The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone, budesonide).
If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).
What is the next step of medical management of COPD if they don’t have steroid responsiveness or asthma?
add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium).
If patients require even further medical management for COPD what is then offered?
Patients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).
Other medical treatments that may be considered include:
Oral mucolytic therapy - for patients with a chronic cough productive of sputum.
Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.
Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.
Long-term oxygen therapy (LTOT)
NICE recommends offering a short course of PO corticosteroids and PO antibiotics as standby medication for patients who have had multiple exacerbations of COPD within one year
When should COPD patients be referred for long term oxygen therapy?
Oxygen saturations <92% in air or cyanosis
FEV1 <30% predicted (consider referring if <49%)
Polycythaemia
Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)
This assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation)
Patients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):
PaO2 below 7.3kPa
PaO2 7.3-8kPa with any of secondary polycythaemia (hematocrit would need to be >55% for polycythaemia to be diagnosed), nocturnal hypoxia, peripheral oedema or pulmonary hypertension (pulmonary artery pressure of >25mmHg)
Which COPD patients should not be offered long term oxygen therapy?
Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires.
When is surgery considered for COPD? And what type of surgery is recommended?
In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered.
Particularly in patients where there is predominant upper lobe emphysema and sufficient lung function reserve
Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung.
Name some complications of COPD:
Depression and anxiety, pneumothorax, cor pulmonale, polycythaemia, acute exacerbations
Explain acute exacerbations in COPD and their treatment:
These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic.
Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected.
Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).
Patients requiring hospital admission should also receive steroids and antibiotics if indicated.
They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required.
Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.
Explain why polycythaemia happens in COPD:
Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia).
This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis.
Explain why cor pulmonale happens in COPD?
Cor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.
The pathophysiology is as follows:
Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.
This increases vascular resistance in the lungs.
The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.
Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).
Peripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.
Explain why pneumothorax happens in COPD:
These occur when a bulla ruptures, releasing air into the pleural cavity.
Explain depression and anxiety in COPD:
Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews.
The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life.
Referral to psychological services for support may be appropriate, as well as holistic assessment and management.
What are the three oral antibiotics recommended by NICE for infective exacerbations of COPD?
IECOPD in the first instance are amoxicillin, doxycycline, or clarithromycin
60 year old patient with a history of COPD is admitted with increasing shortness of breath. On examination, he has a large body habitus and his skin is slightly blue in colour.
What would you expect his V/Q ratio to be?
The patient is of the ‘blue bloater’ phenotype of COPD where chronic bronchitis and hypoxaemia predominate. These patients are under-ventilated due to their chronic airway inflammation and a controlled reduction in respiratory rate; due to the increased energy required to get air through the narrowed airways, the body responds by increasing cardiac output instead. This leads to a low V/Q ratio, as ventilation is decreased compared to perfusion, which is maintained by the increased cardiac output
In COPD what would you expect the diffusing Capacity of the lungs for Carbon Monoxide
Reduction: The patient has a history of chronic obstructive pulmonary disease. The histology finding of destruction to the alveolar walls is indicative of emphysema. In this condition the DLCO is reduced due to the destruction of the alveolar wall, the surface available for diffusion is reduced
When someone is given oxygen for a severe COPD exacerbation what do we have to be careful of?
over-oxygenating him. achieving saturations of 96% he is losing his hypoxic drive and is hypoventilating. This is shown by his reduced work of breathing and looking calmer, which is in fact a decreasing level of consciousness due to CO2 narcosis.
oxygen saturation should be aimed for 88-92%
What controlled measure of oxygen delivery should we use in COPD patients when in hospital for exacerbation?
Venturi mask
What to do in severe respiratory distress due to COPD exacerbations when when optimal medical therapy is insufficient.
non-invasive ventilation with BiPAP is an effective intervention
What is the management of suspected pneumothorax in a patient with COPD and hypoxia
initially provide high flow oxygen via non-rebreathe mask aiming for saturations of 94-98%, prioritising the treatment of hypoxemia over hypercapnia.
hypoxia will cause death quicker than hypercapnia. If a patient is found to be a chronic retainer then you should aim for saturations of 88-92% by titrating the oxygen supply down
Explain the GOLD scale for COPD severity and what management is offered when?
COPD severity can be classified according to the GOLD criteria, which uses a combination of FEV1/FVC ratios and symptoms to categorise patients:
* GOLD A 0–1 exacerbations per year + fewer symptoms * GOLD B 0–1 exacerbations per year + more symptoms * GOLD C 2 or more exacerbations per year + fewer symptoms * GOLD D 2 or more exacerbations per year + more symptoms
All patients who are classified as GOLD B or higher should be offered pulmonary rehabilitation. This consists of a structured programme of exercise and education. There is consistent evidence that these programmes reduce dyspnoea, fatigue and manage the emotional aspect of the diagnosis, leading to an overall improvement in quality of life.
What is influenza?
Influenza or ‘flu’ is a single-stranded RNA virus infecting the respiratory tract.
How many pathogenic serotypes of influenza are there?
three - A, B, C
How is the influenza serotype decided?
determined by surface antigens haemagglutinin and neuraminidase, which are rearranged in host organisms such as birds and animals to produce different strains
Explain the different serotypes?
Influenza A – capable of causing pandemics and epidemics; no animal reservoir
Influenza B –capable of epidemics only, animal hosts include pigs and birds
Influenza C – only found in cattle
What are the risk factors for severe infection and complications from influenza?
Hyposplenism
Chronic diseases of the respiratory, cardiovascular, renal, liver, neurological systems
Diabetes mellitus
Immunosuppression
Morbid obesity
Pregnancy
What are the symptoms and signs of influenza and how long is the incubation period for?
The incubation period is typically 1–4 days and patients can remain infectious for 7–21 days.
Symptoms include:
Fever ≥ 37.8°C
Nonproductive cough
Myalgia
Headache
Malaise
Sore throat
Rhinitis
How does one diagnose influenza?
When prevalence is high, uncomplicated influenza can be diagnosed clinically. If patients have severe symptoms or complications, rapid testing (PCR) and laboratory testing can be used but should not delay treatment.
If a patient appears acutely unwell with influenza what should one consider?
manage with an A-E approach, seek help early and consider starting the sepsis six
What is the general principal management for influenza?
Largely supportive (analgesia, antipyretic, fluids, oxygen)
Antiviral treatment with neuraminidase inhibitors (eg. oseltamivir (Tamiflu®) or zanamivir if within 48 hours of symptom onset and at risk of complications. Oseltamivir may also be prescribed for previously healthy people presenting with influenza within 48 hours of treatment onset.
Infection control and respiratory isolation to prevent onward transmission
What are the complications of influenza?
Pulmonary – viral pneumonia, secondary bacterial pneumonia (particularly S. aureus) , worsening of chronic conditions (eg. COPD and asthma)
Cardiovascular – myocarditis, heart failure
Neurological – encephalopathy
Gastrointestinal – anorexia and vomiting are common
Explain the influenza vaccine:
Influenza vaccine is an inactivated vaccine tailored each year according to recent outbreaks. It provides partial protection against influenza and is recommended for certain patient groups (eg. those aged over 65, with chronic conditions, healthcare workers and nursing home residents).
What are interstitial lung diseases?
interstitial lung disease (ILD) encompasses a large group of diseases that cause inflammation and ultimately fibrosis of the interstitium of the lung.
What are the most common forms of interstitial lung disease?
idiopathic pulmonary fibrosis and hypersensitivity pneumonitis.
What is Idiopathic pulmonary fibrosis?
a progressive, fibrotic lung disease of unknown cause
It is the commonest form of ILD
What does imaging show for idiopathic pulmonary fibrosis?
usual interstitial pneumonitis
The diagnosis can be made on HRCT alone if the characteristic signs of peripheral basal honeycombing are present.
What is the classic patient with idiopathic pulmonary fibrosis?
Patients tend to be older (mean age of presentation is 74 years), male and it is more common in smokers.
What is hypersensitivity pneumonitis and what are the specific symptoms?
Inhalation of specific environmental agents can trigger a hypersensitivity reaction in the lungs.
This was previously known as “extrinsic allergic alveolitis”.
A one-off exposure to a trigger can cause acute onset flu-like symptoms such as fever, cough and shortness of breath
What is farmer’s lung?
a type of hypersensitivity pneumonitis caused by mould spores on hay or straw
Best investigation is Serum precipitins for Aspergillus and mould antigens
What is sarcoidosis and what are the specific symptoms?
Sarcoidosis is a rare multisystem disease characterised by the formation of noncaseating granulomas
Presentation depends on the organs affected
Constitutional symptoms include fatigue, weight loss, low-grade fever, arthralgia, lymphadenopathy and enlarged parotid glands
Pulmonary symptoms are the same as in other forms of ILD (dry cough, dyspnoea, reduced exercise tolerance)
What are the neurological manifestations of sarcoidosis?
Neurological manifestations include meningitis, peripheral neuropathies and Bell’s palsy
What are the ocular manifestations of sarcoidosis?
Ocular manifestations include uveitis and keratoconjunctivitis sicca
What are the cardiac manifestations of sarcoidosis?
include arrhythmias and restrictive cardiomyopathy
What are the abdominal manifestations of sarcoidosis?
hepatomegaly, splenomegaly and renal stones
What are the dermatological manifestations of sarcoidosis?
include erythema nodosum and lupus pernio
Name some other causes of interstitial lung disease?
Lung damage due to infarction, pneumonia or tuberculosis
Irritants such as coal dust or silica
Connective tissue disease such as rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis or Sjogren’s syndrome
Medications including Amiodarone, Nitrofurantoin and Bleomycin.
Radiation to the chest area (e.g. for breast cancer)
What is a common way to classify interstitial lung disease?
where in the lung is predominantly affected (apices or bases)
If an ILD affects the upper zones what could it be?
Hypersensitivity pneumonitis
Ankylosing spondylitis
Radiotherapy
Tuberculosis
If an ILD affects the lower zones what could it be?
Rheumatoid arthritis
Asbestosis
Idiopathic
Drugs
Sarcoidosis
What are the symptoms of interstitial lung disease?
Symptoms tend to have an insidious and progressive onset, and may include:
Dry cough
Shortness of breath
Reduced exercise tolerance
Fatigue
Anorexia
Weight loss
What are the signs of interstitial lung disease?
Signs on examination include:
Cyanosis
Clubbing
Cachexia
Fine end-inspiratory crackles
location depends on where in the lung is affected
do not clear on coughing
There may also be symptoms and signs of associated diseases e.g. arthropathy in connective tissue disease.
What bloods would you do for ILD and what would you expect to see?
FBC may show eosinophilia in hypersensitivity pneumonitis
U&Es, LFTs, bone profile to look for other manifestations of systemic disease (e.g. hypercalcaemia in sarcoidosis)
CRP may be raised in ILD due to inflammation
Autoimmune screen (rheumatoid factor, ANA, ANCA, ENA, Scl-70 antibodies) if connective tissue disease is suspected
Serum precipitins to specific allergens (e.g. in bird fanciers’ lung)
Serum angiotensin-converting enzyme if sarcoidosis suspected
What is the gold standard investigation for ILD?
High resolution CT
What typical findings would you see on a CT for ILD?
Typical findings include honeycombing, ground-glass changes and traction bronchiectasis (where areas of contracting fibrosis pull the bronchioles apart)
What would a chest x-ray show for ILD?
Chest X-ray usually shows reticular and nodular shadowing
The area of the lung affected can help to determine the cause of ILD
Bilateral hilar lymphadenopathy may be seen in sarcoidosis
What would a spirometer show for ILD?
shows a restrictive pattern (FEV1/FVC ratio > 0.7), decreased total lung capacity and TLCO
What is the management for idiopathic pulmonary fibrosis
Two antifibrotic drugs are currently licensed which slow the progression of fibrosis; these are pirfenidone (which reduces fibroblast proliferation) and nintedanib (a tyrosine kinase inhibitor) for FVC 50%-80% of predicted
Other important management considerations include early palliative care involvement, consideration of ambulatory and long-term oxygen therapy if hypoxic and pulmonary rehabilitation
Smoking cessation advice and support
Referral for lung transplantation assessment if no absolute contraindications (e.g. active substance abuse)
What is the management for hypersensitivity pneumonitis?
There is the potential for reversal if the causative agent can be identified and removed
If symptoms persist despite this, steroids should be trialled
If there is no response to steroids, other immunosuppressive therapies may be considered (e.g. cyclophosphamide, azathioprine)
In idiopathic pulmonary fibrosis what lung function tests would you expect to see?
Low vital capacity (VC), total lung capacity (TLC), and transfer capacity of the lung carbon monoxide (TLCO).
Name some drugs that can cause pulmonary fibrosis?
Amiodarone, rugs that can cause pulmonary fibrosis include nitrofurantoin, methotrexate, bleomycin, busulfan and sulfasalazine. This usually requires months to years of exposure.
What type of hypersensitivity reaction is hypersensitivity pneumonitis?
Type 3
Which connective tissue diseases are known causes of ILD
rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis or Sjogren’s syndrome
What is a lower respiratory tract infection?
A lower respiratory tract infection, also known as a chest infection, is an infection of the lower large airways and/or alveoli.
What are the three classifications of a lower respiratory tract infection?
Acute bronchitis: acute inflammation of the bronchial airways with no evidence of pneumonia
Pneumonia: infection of the lung tissue and alveoli compromising respiratory function
Bronchiolitis: is inflammation of the smaller airways (bronchioles), typically presenting in young children
What causes acute bronchitis?
usually due to viruses such as rhinovirus, influenza, parainfluenza and coronavirus amongst others. The less common bacterial cases are caused by similar pathogens to those causing pneumonia.
What causes community acquired pneumonia?
usually bacterial in aetiology. Streptococcus pneumoniae is the most common cause, in addition to Haemophilus influenzae, Staphylococcus aureus, group A streptococci, Moraxella catarrhalis and atypicals. Viruses such influenza, respiratory syncytial virus and coronavirus can also cause pneumonia.
What are the signs and symptoms of a lower respiratory tract infection?
Cough is usually the main presenting symptom. Patients may also experience:
Breathlessness
Wheeze
Pleuritic pain
Fever
Elderly people and children may have atypical presentations. People with pneumonia often appear more unwell than bronchitis alone.
What are the examination findings of bronchitis?
wheeze, rhonchi, mild systemic features
What are the examination findings of pneumonia?
appear more unwell, focal chest signs, consolidation, abnormal observations
What are the general investigations for lower respiratory tract infections?
FBC, U&E’s, CRP, LFT’s, ABG/VBG
Chest X-ray
if appears septic: lactate, urine output, blood cultures
sputum culture if moderate-severe
consider pneumococcal and legionella urinary antigen tests
Do an arterial blood gas if oxygen saturations below 92%
What is used to assess the severity of lower respiratory tract infections?
CURB-65 - used to stratify mortality risk
What does the CURB-65 test consist of?
Confusion (reduced AMTS)
Urea >7.0mmol/l
Respiratory rate ≥30 breaths/min
Blood pressure (systolic) <90mmHg =/<60 diastolic
65 years old or over
If a patient is acutely unwell with a lower respiratory tract infection what should one start?
sepsis six
Explain the different scores of CURB-65?
0-1: low risk
2: intermediate risk
3-5: high risk
(for CRB-65, take 1 point off these thresholds)
Use this, combined with clinical judgement, when deciding whether to admit.
Management of acute bronchitis?
Unless very unwell, this can usually be managed as an outpatient. Patients can be advised to try over-the-counter remedies, stop smoking if applicable and safetynetted for worsening or persistent symptoms. Antibiotics, typically doxycycline, can be considered if a person’s CRP is over 100mg/l or if the person is over 65 years and/or has comorbidities, or they appear unwell. A delayed antibiotic presription may be given if the CRP is over 20mg/l.
Name some complications of acute bronchitis?
Acute bronchitis is usually mild & self-limiting, although the cough may persist for up to 6 months. Acute bronchitis may be complicated by development of pneumonia.
Name some complications of pneumonia?
Pleural effusion, empyema or abscess formation
Acute respiratory distress syndrome
Sepsis, disseminated infection
What is pneumonia?
Pneumonia is an inflammatory condition of the lung parenchyma caused by infection. Alveoli become filled with inflammatory cells and microorganisms, leading to consolidation of the lung tissue. This impairs gas exchange and can lead to hypoxia.
What is the commonest cause of pneumonia?
Streptococcus pneumonia, followed by Haemophilus influenzae and Moraxella catarrhalis - these are typical pneumonias
Name the features of an atypical pneumonia?
Atypical pneumonias have a variety of atypical features, e.g. a more insidious onset, extra-pulmonary symptoms such as headache and varying appearances on chest imaging.
Name some strains that cause atypical pneumonia?
Mycoplasma pneumoniae, Legionella pneumophila and Chylmydophila psittaci
Define hospital acquired pneumonia?
defined as pneumonia that started 48 hours or longer after admission
Name some strains that cause hospital acquired pneumonia?
Gram negative organisms such as Pseudomonas aeruginosa, as well as Staphylococcus aureus are more common in these environments.
Name some specific features of Klebsiella pneumonia
Usually a cavitating pneumonia affecting the upper lobes presenting with red-currant sputum.
It is caused by a gram-negative anaerobic rod.
Increased risk in the immunocompromised, elderly and in alcohol excess.
Name some specific features of Staphylococcal pneumonia
A bilateral cavitating bronchopneumonia due to staphylococcal aureus, a gram-positive cocci found in clusters.
Commoner in intravenous drug users, elderly patients, or as a superadded bacterial infection in those with influenza.
Name some features of Mycoplasma pneumonia
Presents with flu-like symptoms of arthralgia, myalgia, dry cough and headache.
Primarily affects younger patients.
Associated with an autoimmune haemolytic anaemia caused by cold agglutinins - look for low haemoglobin and high reticulocyte count - Positive cold direct Coomb’s test
May lead to erythema multiforme (target-shaped rash), Stevens-Johnson syndrome, Guillain-Barre syndrome and meningoencephalitis.
Best investigation is serology
Name some features of Legionella pneumonia
Fever, myalgia and malaise followed by dyspnoea and a dry cough are typical presenting features.
Caused by a Gram-negative bacillus
Occurs in those exposed to contaminated water e.g. in humidifiers or cooling systems.
Typically causes hyponatraemia and deranged liver function tests.
Definitve investigation is a Urinary antigen enzyme immunoassay test
Name some features of Chlamydophila psittaci pneumonia
An intracellular bacteria acquired from contact with infected birds such as parrots.
Features include lethargy, arthralgia, headache, anorexia, dry cough and fever.
What are the different 30 day mortality percentages for CURB-65?
CURB-65 0 - 0.7%
CURB-65 1 - 3.2%
CURB-65 2 - 13%
CURB-65 3 - 17%
CURB-65 4 - 41.5%
CURB-65 5 - 57%
For the different CURB-65 scores what management and treatment plans should we do?
A CURB-65 score of 0-1 requires home treatment, 2 should consider hospital admission, 3-5 admit to hospital and consider ITU referral.
Symptoms of pneumonia?
Fever
Malaise
Rigors
Cough
Purulent sputum
Pleuritic chest pain
Haemoptysis
Signs of pneumonia?
Tachypnoea
Tachycardia
Hypotension
Cyanosis
Pyrexia
Dullness to percussion over the consolidated area
Increased vocal resonance/ tactile vocal fremitus over the consolidated area
Bronchial breathing over the consolidated area
Pleural rub may be heard due to inflammation of the adjacent pleura
Bedside tests for pneumonia?
Bedside:
Sputum for microscopy, culture and sensitivity
Consider arterial blood gas if hypoxaemic
Urinary legionella and pneumococcal antigens
ECG to look for complications e.g. atrial fibrillation
What are the blood tests for pneumonia?
Blood cultures if febrile
FBC and CRP for inflammatory markers
U&Es to look for an AKI
LFTs may be deranged e.g. in Legionella, baseline important when giving antibiotics
Mycoplasma serology if atypical pneumonia suspected
HIV testing should be offered to all patients with recurrent pneumonia (and all patients in a high prevalence area such as London)
What may you see in imaging for pneumonia?
Chest X-ray: may show lobar consolidation or bilateral consolidation in atypical infections, parapneumonic effusions may also be seen.
CT chest may be indicated in some cases (e.g. suspected underlying malignancy, suspicious findings on X-ray)
What is conservative management for pneumonia?
Oxygen if low saturations
IV fluids if dehydrated
Analgesia for myalgia or chest pain
Escalate for respiratory support (e.g. continuous positive airway pressure or intubation and ventilation) if patients are severely unwell - consider escalation status and patient wishes
What is medical management for pneumonia?
Amoxicillin ± a macrolide are first-line
Oral antibiotics for patients managed in the community (e.g. amoxicillin 500mg three times a day for 5 days)
IV antibiotics for those admitted with more severe pneumonia (e.g. co-amoxiclav and clarithromycin)
Different regimens are indicated for those with penicillin allergies and local guidelines should be consulted
Antibiotics should be tailored to antimicrobial sensitivities when these are resulted
Why should patients with pneumonia have a repeat x-ray after 6/8 weeks?
to screen for an underlying lung cancer (as this may be masked on initial imaging by infective changes).
What indicates progression to respiratory failure?
A worsening respiratory condition with increasing tachypnoea, decreasing oxygen saturations, and new-onset bronchial breath sounds
What are the symptoms of Pneumocystis pneumonia?
Symptoms include exertional dyspnoea, dry cough, and cachexia, as evidenced by bilateral infiltrates on chest X-ray.
Intravenous drug use and HIV infection are significant risk factors for developing it.
exertional desaturation = pneumocystis pneumonia
To investigate do a silver stain
What condition is streptococcus pneumoniae associated with?
herpes labialis (cold sores).
A history of COPD increases the risk of pneumonia caused by which organism?
Haemophilus Influenzae, a gram-negative coccobacillus
Name some key symptoms of pneumococcal pneumonia caused by Streptococcus pneumoniae.
A high fever, productive cough with rust-coloured sputum, and shortness of breath
one complication of pneumonia is emphysema - explain the symptoms and treatment
Empyema is the term given for the complication of pneumonia where a collection of pus forms within the pleural space. They tend to present as either failure to recover fully with antibiotics alone or with a characteristic “swinging fever” as seen in this question.
They need to be treated with surgical drainage
Which lobe has consolidation in it when there is a loss of the right cardiac border?
right middle lobe is the part of the lung between the horizontal fissure and oblique fissure
In post-influenza pneumonias with Gram-positive cocci seen on sputum culture what should we consider adding for suspected Staphylococcus aureus infection
Flucloxacillin
Patients being treated with clarithromycin should be careful of which drug interaction?
Patients with community-acquired pneumonia being treated with clarithromycin should temporarily discontinue statin therapy due to an increased risk of myopathy caused by drug interactions.
Which antibiotics are recommended by NICE as the first-line treatment for hospital-acquired pneumonia?
the recommended first-line treatment options for hospital-acquired pneumonia include meropenem or piperacillin/tazobactam. These antibiotics are effective against the most common pathogens that cause hospital-acquired pneumonia, including Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (MRSA). Piperacillin/tazobactam is usually used as the first-line treatment with meropenem reserved for patients with penicillin allergies.
define an upper respiratory tract infection?
An upper respiratory tract infection (URTI) is a usually viral infection that causes inflammation of the upper airways, referred to as a “cold”.
Name some other viruses that cause URTIs?
Coronaviruses
Adenoviruses
Enteroviruses
Respiratory syncytial virus
Metapneumovirus
Influenza viruses
What virus causes the most URTI?
rhinoviruses
Name some signs and symptoms of URTIs?
Coryza (which may manifest as rhinorrhoea, nasal congestion and loss of smell)
Sneezing
Cough
Sore throat (may be erythematous on examination)
Low-grade fever
Malaise
Headache
Hoarse voice
Conjunctival injection
What investigations does one do for URTI?
In patients admitted to hospital, nasal and/or throat swabs may be done for viral assays or polymerase chain reaction (PCR) tests for common viruses. This allows appropriate isolation of infectious patients and rules out differentials such as COVID-19 or influenza that have specific treatments indicated.
What is the management plan for URTI?
Adequate fluid intake
Rest
Vapour rubs (e.g. Vicks)
Inhaling steam or using nasal saline drops to help with nasal congestion
Lozenges or analgesic sprays for sore throat
Simple analgesia (paracetamol/ibuprofen) for fevers or pain
Intranasal congestants should be used in the short term only as these can cause rebound symptoms if used chronically
Prevent spread with good hand-hygeine, avoid sharing towels etc.
Safety net people to seek medical advice if symptoms continue to worsen or are not improving beyond 10 days
Complications of URTI?
Acute otitis media is common in young children and presents with worsening ear pain
Sinusitis may occur and is characterised by facial pain and tenderness with ongoing nasal congestion
Exacerbations of COPD or asthma may be triggered by URTIs
Pneumonia or other superadded bacterial infections may occur, especially in vulnerable patients such as smokers, those who are immunosuppressed or elderly or have comorbidities
Prognosis of URTI?
URTIs are in general mild and self-limiting conditions
They generally resolve over around a week in adults or up to 2 weeks in children
Symptoms typically peak over 2-3 days
Some symptoms (especially cough) may continue for several weeks
Define lung cancer?
Lung cancer refers to a primary malignancy arising from the lung parenchyma or the bronchi
How is lung cancer classified?
Cancers are classified as small cell (SCLC) or non-small cell (NSCLC), with 80% being non-small cell. The main histological subtypes of NSCLC are squamous cell cancers and adenocarcinomas.
What are the risk factors of lung cancer?
Tobacco smoking (e.g. cigarettes, pipes, cigars)
Passive smoke exposure
Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica)
Radon exposure
Family history of lung cancer
Radiation to the chest (e.g. in lymphoma treatment)
Air pollution
Immunosuppression (e.g. HIV, medications)
Increasing age
Where do small cell lung cancers come from?
neuroendocrine cells of the lung
Where do adenocarcinoma (NSCLC) come from?
alveolar type 2 epithelial cells
Where do squamous cell carcinomas (NSCLC) come from?
basal epithelial cells
Where do large cell carcinomas (NSCLC) come from?
Come from a variety of epithelial cells
Name some rarer subtypes of NSCLC?
sarcomatoid or salivary gland-type lung cancers
Explain the different stages of lung cancer?
This can then be used to classify lung cancers into stage 1 to 4, where stage 1 is localised and small (under 4cm), stages 2 and 3 are locally advanced and stage 4 is metastatic.
Symptoms of lung cancer?
Persistent cough
Haemoptysis
Dyspnoea especially on exertion
Chest pain
Weight loss
Recurrent chest infections, or infections resistant to treatment
Anorexia
Signs of lung cancer?
Cachexia
Finger clubbing
Lymphadenopathy (supraclavicular or persistent cervical)
If there is lung collapse due to an obstructing tumour - absent breath sounds, trachea deviated towards side of collapse
If there is a malignant pleural effusion - stony dull on percussion, decreased breath sounds over affected area
Name some paraneoplastic presentations of lung cancer
Cushing syndrome, Syndrome of inappropriate ADH secretion, Lambert-Eaton myasthenia syndrome, humeral hypercalcaemia of malignancy
hypertrophic pulmonary osteoarthropathy
Explain the paraneoplastic presentation of Cushing syndrome in lung cancer
usually SCLC producing ectopic ACTH, presents with dorsal cervical fat pads, truncal obesity, hypertension, striae and proximal muscle weakness
Explain the paraneoplastic presentation of syndrome of inappropriate ADH secretion in lung cancer
usually SCLC, present with symptoms of hyponatraemia e.g. fatigue, nausea, weakness, confusion or seizures
Explain the paraneoplastic presentation of Lambert-eaton myasthenia syndrome in lung cancer
usually SCLC, due to autoantibodies to presynaptic calcium channels at the neuromuscular junction develop proximal muscle weakness that improves with repeated movement, as well as autonomic effects such as dry mouth, lightheadedness, constipation, urinary symptoms and erectile dysfunction
Ptosis and double vision can also occur in LEMS. LEMS is caused by voltage-gated calcium channel antibodies
Explain the paraneoplastic presentation of humeral hypercalcaemia of malignancy in lung cancer
usually squamous cell carcinomas (SCC) that release parathyroid hormone-related protein (PTHrP) that mimics PTH and causes hypercalcaemia, leading to symptoms of bone pain, constipation, anorexia, abdominal pain, excessive thirst and confusion
Explain the paraneoplastic presentation of hypertrophic pulmonary osteoarthropathy in lung cancer
usually adenocarcinomas or squamous cell carcinoma which cause a periosteal reaction of bones, resulting in clubbing and arthritis especially affecting wrists and ankles
Which patients should be referred on a 2 week wait pathway in primary care for lung cancer?
Aged 40+ with unexplained haemoptysis
Chest X-ray findings suspicious for lung cancer
When should urgent chest x-rays be done for suspected in lung cancer?
done for patients aged 40+ who have one of these symptoms and have ever smoked (or two symptoms if they are never smokers):
Cough
Fatigue
Shortness of breath
Chest pain
Weight loss
Anorexia
Also An urgent chest X-ray should be considered in patients aged 40+ with any of:
Persistent/recurrent chest infection
Finger clubbing
Supraclavicular or persistent cervical lymphadenopathy
Thrombocytosis
Chest signs consistent with lung cancer (e.g. reduced breath sounds, dullness to percussion)
What might you see on a chest x-ray of someone with lung cancer?
Lung mass (may be rounded or spiculated, squamous cell carcinomas may cavitate)
Consolidation (where there is infection downstream of the tumour obstructing an airway)
Bulky hilum (especially squamous cell carcinomas which often arise centrally)
Lobar collapse (due to bronchial obstruction, especially squamous cell carcinomas)
Pleural effusion
Can you name some other investigations that should be done for suspected lung cancer?
Sputum cytology - low sensitivity but may be of use in patients who decline or cannot have a biopsy
Diagnostic thoracocentesis - i.e. a pleural tap; if a pleural effusion is present this should be done and the fluid sent for cytology as well as cell count, microscopy, culture, glucose, LDG and protein (to determine whether it is a transudate or exudate)
Blood tests - including FBC for anaemia and thrombocytosis, U&Es for hyponatraemia and baseline renal function, LFTs for baseline liver function (may be deranged in liver metastases), bone profile for hypercalcaemia, CRP for superadded infection, clotting if interventions planned
CT chest with contrast - should be done after chest X-ray to better characterise any lesion seen and investigate for local spread
Biopsy - to confirm the diagnosis and subtype of cancer, may be done percutaneously for peripheral tumours or via bronchoscopy for central masses
Once a lung cancer is diagnosed, further investigations may include:
Spirometry - to assess lung function to determine if a patient is suitable for surgical intervention
CT chest abdomen and pelvis - to stage the cancer (determine if there are any metastases)
PET-CT scan - a more sensitive way to stage the cancer and look for local or distant spread
CT or MRI head - may be done as part of staging investigations if curative treatment is planned, or if there are symptoms suspicious of intracranial metastases
What is the conservative management for lung cancer?
Holistic support and an MDT approach (e.g. clinical nurse specialist involvement, palliative care input for troubling symptoms or end of life care, signpost to support e.g. Macmillan groups)
Smoking cessation
Discussions around advance care planning where appropriate
Explain when chemotherapy is used in lung cancer as medical management?
first line in most cases of small cell lung cancer and stage 3 or 4 non-small cell lung cancer - this is with palliative intent (i.e. not aiming to cure the disease but to prolong life and improve symptoms). It is also offered to some patients prior to (neoadjuvant) or after (adjuvant) curative surgery.
Explain when immunotherapy is used in lung cancer management?
used especially in advanced non-small cell lung cancer; this includes medications such as pembrolizumab or atezolizumab (again with palliative intent).
Explain targeted therapies in the treatment of lung cancer?
exist for patients with specific mutations, e.g. erlotinib for patients with advanced non-small cell lung cancers with EGFR-TK mutations.
Explain radiotherapy in the treatment of lung cancer?
may be curative (for example in early non-small cell lung cancer) or palliative - it is often combined with chemotherapy or other treatment modalities.
Explain supportive therapies in lung cancer?
Supportive therapies include analgesia, oxygen if hypoxic and opioid treatment for breathlessness.
Explain surgical management of lung cancer?
Lobectomy is the standard curative therapy for early stage lung cancers (which can be open or thoracoscopic in approach).
Some small tumours can be removed with a wedge resection.
More extensive surgery such as a pneumonectomy (removal of a lung) may be required depending on the size and location of the tumour, however patients need to have adequate FEV1 on pre-operative spirometry to be appropriate for surgery (over 2L for a pneumonectomy).
All patients undergoing surgery should also have mediastinal and hilar lymph nodes sampled (to look for metastases) or resected (removed) to reduce the chances of recurrence.
Name some common sites of metastatic spread for lung cancer?
Lymph nodes
Liver - this can cause significant pain due to stretching of the liver capsule
Brain - may cause nausea and vomiting, headaches, seizures, personality changes, sensory or motor symptoms, dysphasia or cerebellar symptoms, depending on where in the brain is affected
Bones - mostly osteolytic metastases, can cause bony pain and pathological fractures; there is a risk of metastatic spinal cord compression with vertebral metastases
Adrenal glands - may cause flank pain and adrenal insufficiency
The contralateral lung or elsewhere in the ipsilateral lung
The most common site is brain for metastases
Name the local complications of lung cancer?
horner’s syndrome - due to an apical (Pancoast) tumour, causes ipsilateral anhidrosis, miosis and partial ptosis - cervical sympathetic plexus
Superior vena cava obstruction (SCVO) - lung cancer is the commonest cause of SCVO, causing symptoms of breathlessness, dizziness, headache and swelling of the face, neck and arms. This is a medical emergency due to the risk of airway obstruction.
Malignant pleural effusion
Hoarse voice - secondary to invasion of left recurrent laryngeal nerve
Persistent lower respiratory tract infection due to obstructing tumour
Raised hemidiaphragm secondary to invasion of phrenic nerve
Brachial plexus injury secondary to tumour invasion from a Pancoast tumour
What are the three classic features of hypertrophic pulmonary osteoarthropathy?
periostitis (inflammation of the periosteum, the connective tissue layer surrounding bone), digital clubbing and painful arthropathy of large joints are present in the history
For small cell lung cancer what would you expect to see on a histology specimen?
The cells have dense neurosecretory granules
What is the most common type of cancer in non smokers and particularly prevalent in asian women?
adenocarcinoma
What are characteristic imaging findings of mesothelioma?
Mesothelioma classically manifests in the pleura, rather than the lung itself like most other forms of lung cancers. The pleura thickens and some areas become plaque like due to continued proliferation.
In cases of early-stage, resectable lung adenocarcinoma (non-small cell lung cancer) what is the advised management
surgical intervention, specifically lobectomy, is the primary definitive management for optimal outcomes.
Lobectomy (with hilar and mediastinal lymph node resection/sampling) is first-line treatment for those with stage I or II cancer who are medically fit for surgery. This surgery is done with curative intent. NSCLC
What is the first line for NSCLC with those staged I-III
Radiotherapy:
Is first-line for those with stage I-III disease who are not suitable for surgery.
This treatment is given with curative intent.
What is offered to those with NSCLC stage III or IV>
Chemotherapy
First line regimes use a combination of:
Third-generation chemotherapy agent: e.g. docetaxel, paclitaxel or gemcitabine
Platinum agent: e.g. carboplatin or cisplatin
When is combination therapy offered for NSCLC?
Adjuvant chemotherapy should be offered to patients who have undergone a complete resection
Adjuvant radiotherapy is offered to patients who have had a incomplete resection of their tumour
All patients with stage I-III disease who are not suitable for surgery should be considered for chemoradiotherapy
What is the treatment for limited stage SCLC? SCLC without distant metastasis (T1-4, N0-3, M0).
First line treatment involves:
4-6 cycles of Cisplatin-based combination chemotherapy
Concurrent or adjunct thoracic radiotherapy is only considered if there has been a good response to chemotherapy
What is the treatment for extensive stage SCLC? defined as SCLC with distant metastasis (T1-4, N0-3, M1)
First line treatment involves:
Platinum-based combination therapy where the patient is reassessed for a response after each cycle (up to a maximum of 6 cycles)
Concurrent or adjunct thoracic radiotherapy can be considered if there has been a good response to chemotherapy at both the primary and metastatic sites.
What is offered for relapse after initial treatment for lung cancer?
For all stages of SCLC second-line therapy can be considered in those who have relapsed. This includes:
Further chemotherapy (maximum 6 cycles)
Palliative radiotherapy to control local symptoms
What is the immediate treatment for a superior vena cava obstruction (raised JVP and inspiratory stridor)?
Immediate oral dexamethasone 8mg
What is the test for superior vena cava obstruction?
Confirmed by the positive Pemberton’s sign. This is when a patient raises both hands above their head causing facial plethora, venous congestion and respiratory distress. Sitting the patient upright and providing oxygen may provide symptomatic relief. Dexamethasone can be administered to reduce swelling and therefore the pressure on the SVC
What are occupational lung diseases?
Occupational lung disease encompasses a variety of respiratory disorders caused by inhalation of dust, chemicals, or proteins in the workplace
Name some occupational lung diseases?
Conditions such as pneumoconiosis, occupational asthma, and hypersensitivity pneumonitis are included under this umbrella term. Pneumoconiosis is induced by mineral dusts like silicosis from silica exposure and asbestosis from asbestos exposure. Occupational asthma, triggered by irritants like isocyanates or grain dust, is the most common work-related lung disease in developed countries.
Hypersensitivity pneumonitis results from an immune response to inhaled organic antigens or low molecular weight agents. Chronic obstructive pulmonary disease (COPD) can also be work-related, particularly in smokers exposed to fumes and dust. Mesothelioma and lung cancer are severe potential outcomes related to asbestos exposure
What are the 4 main work related agents?
dusts, gases and fumes, biological agents, and radiation
Can you explain dust exposure in greater detail?
Silica: Workers in mining, quarrying, construction and ceramic industries are at increased risk of developing silicosis due to inhalation of silica dust.
Coal: Coal workers’ pneumoconiosis (CWP) is associated with coal mining.
Asbestos: Asbestosis is predominantly seen in individuals involved in asbestos mining, shipbuilding, roofing and plumbing.
Can you explain gases and fumes exposure in greater detail?
Sulphur dioxide: It is commonly encountered in industries related to burning of fossil fuels such as power plants.
Nitrogen oxides: These are produced during high-temperature combustion processes like welding.
Ozone: Workers involved in photocopying or welding are at risk due to ozone exposure.
Can you explain biological agent exposure in greater detail?
Moulds and fungi: Occupations involving agriculture, forestry or gardening present a risk for hypersensitivity pneumonitis due to exposure to moulds or fungi.
Bacteria or animal proteins: Workers exposed to water aerosols (e.g., air conditioning systems), or those handling animals may develop extrinsic allergic alveolitis.
Can you explain radiation exposure in greater detail?
Lung cancer risk increases significantly with exposure to radon gas in uranium miners and millers. This risk is further amplified in smokers.
What is the aetiology of occupational lung disease?
Trigger an inflammatory response with inflammation and fibrosis leading to tissue remodelling
What is the severity and progression of lung disease based on?
dose-response relationship, duration of exposure, individual susceptibility, presence of pre-existing lung disease and smoking status
What are the two type of diseases based on inhalation of dust?
Pneumoconioses: These are caused by the inhalation of inorganic dusts. They include asbestosis (asbestos), silicosis (silica), coal worker’s pneumoconiosis (coal dust) and berylliosis (beryllium).
Organic Dust Diseases: Resulting from exposure to organic materials such as moulds, spores or proteins. Examples include farmer’s lung (mouldy hay), bird fancier’s lung (bird proteins) and malt worker’s lung (malt dust).
What are the two type of diseases based on toxic gases and fumes?
Inhalation fever syndromes: Caused by acute high-level exposures to certain agents like metal fume fever (metal oxides) and polymer fume fever (polytetrafluoroethylene).
Toxic pneumonitis: Occurs due to chronic low-level exposure causing inflammation of the lungs. Examples include chlorine gas, ammonia, sulfur dioxide.
What is the disease related to a hypersensitivity reaction (occupational lung disease)?
Hypersensitivity Pneumonitis: This is an allergic reaction to inhaled substances leading to inflammation in the alveoli. It includes extrinsic allergic alveolitis, which itself has several subtypes such as farmer’s lung or bird fancier’s lung.
What is the occupational lung disease related to lung cancer/ mesothelioma?
Lung cancer: Occupational exposure to certain substances like asbestos, radon, chromium, nickel and coal products can increase the risk of developing lung cancer.
Mesothelioma: A rare form of cancer that affects the pleura. It is strongly associated with asbestos exposure.
What is the disease due to occupational infections? Occupational lung disease
Tuberculosis: Particularly common in healthcare workers or those working in close contact with affected patients.
Anthrax: Associated with handling infected animal products.
Presenting features of occupational lung disease?
Cough: This is often the first symptom to develop. It may be dry or productive, depending on the nature of the disease.
Dyspnoea: Shortness of breath is another common symptom that may occur at rest or during physical exertion.
Chest tightness or pain: These symptoms may be present, especially in cases involving pleural disease.
Sputum production: In some cases, patients may produce sputum which can vary in colour and consistency based on the underlying condition.
What would be included in a detailed examination of occupational lung disease?
Pulmonary function tests (PFTs): These can show restrictive or obstructive patterns, reduced diffusion capacity and other abnormalities that point towards specific conditions such as pneumoconiosis or occupational asthma.
Radiographic findings: Chest X-rays or CT scans can show nodular infiltrates, fibrosis, pleural thickening or other changes consistent with occupational lung diseases.
Laboratory investigations: Certain blood tests may show raised inflammatory markers. Bronchoalveolar lavage (BAL) and biopsy might be required for definitive diagnosis in some cases.
Occupational history: A detailed occupational history is crucial to identify potential exposure to harmful substances. This includes the type of work, duration of exposure, use of protective equipment and any previous respiratory problems.
What is management for occupational lung disease?
early diagnosis, patient education, symptom management, reducing exposure, supportive care
What are the complications for occupational lung disease?
Pulmonary Fibrosis: This is a common complication that results from the deposition of excess fibrous connective tissue (fibrosis) in the lungs. It leads to stiffening or scarring of lung tissue which impairs oxygen uptake.
Chronic Obstructive Pulmonary Disease (COPD): Patients with occupational lung disease are at an increased risk for developing COPD, characterised by chronic bronchitis and emphysema. This results in progressive airflow limitation and reduced respiratory capacity.
Lung Cancer: Certain occupational exposures such as asbestos, silica dust, diesel exhaust, and certain gases can significantly increase the risk of developing lung cancer.
Pleural Disease: Asbestos exposure is also associated with pleural conditions including pleural effusion, diffuse pleural thickening, pleural plaques and malignant mesothelioma.
Hypoxemia: Chronic inflammatory changes can impair gas exchange leading to hypoxemia - a decrease in arterial blood oxygen levels. This may result in cor pulmonale if untreated.
Cor Pulmonale: Chronic hypoxemia can lead to right-sided heart failure or cor pulmonale due to increased resistance in the pulmonary circulation.
How does simple pneumoconiosis? what condition does it increase the risk of? and what condition may it lead to?
Asymptomatic, COPD, May lead to progressive massive fibrosis
How does progressive massive fibrosis present? Which lobes does it most commonly affect? What will be found on a chest X-ray and what pattern does it show on spirometry?
- Exertional SOB
- Cough +/- black sputum
upper lobe fibrosis, restrictive pattern
What is silicosis? Which condition is it a risk for? Which occupations is it most prevalent in? And what do we see on a chest X-Ray?
Fibrotic lung disease caused by inhalation of silica
TB
- Stonemason
- Pottery
- Ceramics
‘Egg shell’ calcification of hilar lymph nodes
What is a pneumothorax?
A pneumothorax refers to a collection of air in the pleural cavity (space between the visceral and parietal pleura) which may cause collapse of the underlying lung parenchyma.
How is a pneumothorax classified?
They may be spontaneous or traumatic (including iatrogenic causes).
Spontaneous pneumothoraces can be further divided into primary pneumothoraces (in patients without an underlying lung disease) and secondary (in patients with underlying lung diseases such as COPD or asthma).
Would Patients aged over 50 years old with a significant smoking history who present with a spontaneous pneumothorax having a primary or secondary pneumothorax?
Secondary
What is a tension pneumothorax?
A tension pneumothorax occurs when the defect in the pleura that has led to the pneumothorax creates a one-way valve effect whereby air can enter the pneumothorax but not leave it. - This causes the pneumothorax to progressively expand, putting pressure on the heart and great vessels and causing mediastinal shift - This is a medical emergency that rapidly leads to cardiac arrest if untreated
What are the signs and symptoms of a pneumothorax?
Sudden onset shortness of breath
Pleuritic chest pain
Dry cough
Tachypnoea and increased work of breathing
The following signs will be found on the affected side of the chest:
Unilateral reduced expansion
Unilateral hyper-resonance to percussion
Reduced or absent breath sounds
Reduced vocal resonance or tactile vocal fremitus
Patients with a tension pneumothorax may present additionally with what signs and symptoms?
Patients with a tension pneumothorax may also have:
Tracheal deviation to the contralateral side
Tachycardia
Hypotension
Distended neck veins
What do we do in patients who have a suspected tension pneumothorax?
Patients with a suspected tension pneumothorax should be diagnosed and treated with needle decompression based on the clinical picture, with no delay for investigations.
For other patients, an erect PA chest X-ray is diagnostic.
When are chest x-rays used in pneumothorax?
CT chest should be used in high-risk patients where it is not clear from the chest X-ray whether it is safe to place a chest drain.
What is the management for a tension pneumothorax?
If a tension pneumothorax is suspected, emergency management is to decompress this by inserting a large-bore cannula into the second intercostal space on the affected side, or fifth intercostal space if a traumatic cause is suspected, as per ATLS guidelines.
If this fails, open thoracostomy should be done immediately
After initial emergency decompression, a chest drain should be inserted
What is the management pathway for primary or secondary spontaneous pneumothoraces?
What does the pneumothorax pathway mean for conservative management?
Conservative management involves no intervention for the pneumothorax, and patients are monitored to ensure they do not deteriorate and any symptoms resolve
What are the ambulatory devices used in pneumothorax?
Ambulatory devices (e.g. pleural vents) are one-way valves which allow air to leave the pneumothorax but not re-enter it - They can be inserted in a simple procedure under local anaesthetic - Patients can then be followed up as outpatients
What do with do with patients with larger pneumothoraces (usually 2cm or larger on CXR - CT may be used if unclear) or those with high-risk features (significant hypoxia, bilateral pneumothoraces, underlying lung disease, 50 or older with a significant smoking history, haemopneumothorax)?
chest drain and admission for monitoring
What do we do in symptomatic patients without high-risk features but with pneumothoraces large enough for treatment (2cm or larger)
management depends on their priorities - Conservative management allows avoidance of any procedure - Both needle aspiration and ambulatory devices offer more rapid symptomatic relief (ambulatory device insertion may not be available in all hospitals)
What follow up do we do in the management of pneumothoraxes?
All patients should be reviewed in an outpatient clinic 2–4 weeks after presenting with a pneumothorax (with repeat chest imaging)
Patients should be advised on smoking cessation if relevant
Advise patients not to fly until 7 days after chest imaging has confirmed resolution of the pneumothorax
Advise patients they should not take part in underwater diving for life (except in rare cases where they have been treated with bilateral open surgical pleurectomy)
What is the management for patients with persistent pneumothorax following chest drain insertion for secondary pneumothorax, especially those with underlying COPD?
should be considered for early discussion with cardiothoracic surgery for possible video-assisted thoracic surgical repair.
How does a pneumothorax affect the V/Q ratio?
results in less ventilation and a lower V/Q ratio
What should you expect to see on a patent chest drain?
Fluid swinging
A patent chest drain allows fluid to move synchronously with respiratory pressure changes within the thorax.
What does a persistent bubble in the water seal chamber of a chest drain indicate?
an ongoing air leak
What is type 1 respiratory failure?
Type 1 respiratory failure (T1RF) is defined as hypoxaemia (PaO2<8kPa) with low or normal levels of carbon dioxide in the arterial blood.
What is type 2 respiratory failure?
Type 2 respiratory failure (T2RF) is defined as hypoxaemia (PaO2<8kPa) with hypercapnia (PaCO2>6.5kPa).
By what mechanisms do type 1 respiratory failure occurs?
V/Q mismatch
Diffusion Limitation
Shunting
Explain V/Q mismatch?
The commonest cause of T1RF
An imbalance in ventilation versus perfusion of the lungs leading to inefficient oxygenation
A low V/Q occurs when alveoli are not sufficiently ventilated e.g. in airways disease
A high V/Q occurs when there is limited blood flow in the lungs e.g in pulmonary embolism
Explain diffusion limitation?
Impaired gas exchange across the alveolar membrane
May be due to inflammation or fibrosis of the membrane e.g. in idiopathic pulmonary fibrosis
May be due to a decrease in the available surface area for diffusion e.g. emphysema
Carbon dioxide is more soluble than oxygen hence why hypoxaemia is commonly seen without hypercapnia
Explain shunting?
Refers to blood that passes through the lungs without undergoing gas exchange
May be a physiological response to V/Q mismatch as if there are alveoli with very poor ventilation the blood that goes to them will not be ventilated
Anatomical shunting may be seen e.g. in pulmonary arteriovenous malformations
Can also cause hypercapnia and T2RF if severe
By what mechanisms do type 2 respiratory failure occur?
Increase in dead space
Reduced minute ventilation
Explain why there can be an increase in dead space?
Dead space is ventilated but not perfused and so there is no gas exchange
There is always some anatomical dead space e.g. the airways
There may also be dead space in unperfused alveoli
This alveolar dead space increases if capillaries are destroyed e.g. in emphysema or interstitial lung disease
Explain why there can be reduced minute ventilation?
Minute ventilation is the total amount of air entering the lungs per minute
If it decreases, there is a decrease in alveolar ventilation
It is equal to respiratory rate x tidal volume
Conditions that reduce respiratory rate include respiratory depressants such as alcohol or opiate medications
Conditions that reduce tidal volume include neurological disorders such as motor neuron disease or chest wall deformities
Symptoms of respiratory failure?
Dyspnoea
Headache
Light-headedness
Confusion
Drowsiness
Agitation
Symptoms related to underlying cause e.g. productive cough and fever in pneumonia
Signs of respiratory failure?
Tachypnoea (although respiratory rate may be low in some cases of T2RF e.g. opiate overdose)
Cyanosis
Accessory muscle usage
Nasal flaring
Signs of central nervous system dysfunction e.g. reduced GCS, irritability
Signs related to underlying cause e.g. wheeze in a COPD exacerbation
Signs related to hypercapnia (i.e. T2RF only):
Flushed skin
Bounding peripheral pulses
Asterixis
Tachycardia or arrhythmia
Drowsiness
What is the diagnostic investigation for respiratory failure and differentiates between type 1 and type 2 and shows whether type 2 is acute or chronic?
Arterial Blood gas
Why does it show on arterial blood gas to show whether a respiratory failure is chronic or acute?
In chronic T2RF, a longstanding respiratory acidosis is compensated for by an increase in bicarbonate above the normal range of 22-26 mmol/L
pH may therefore be normal despite a high PaCO2
e.g. COPD, neuromuscular disorders
In acute T2RF, there is not time for renal compensation and bicarbonate retention
Bicarbonate is normal
pH is low (respiratory acidosis)
e.g. acute severe asthma, opiate overdose
What other investigations could we do for respiratory failure to see the undergoing cause?
Sputum sample in suspected pneumonia or an infectious exacerbation of COPD
Blood tests e.g. WCC and CRP if infection suspected
Chest X-ray to investigate for infection, pneumothorax etc.
CTPA if pulmonary embolism is suspected
How does one treat T2RF and what does one have to consider?
Supplementary oxygen is required to correct hypoxaemia
However caution is needed in patients at risk of or in T2RF as overoxygenation causes worsening hypercapnia
This is multifactorial, with one important mechanism being oxygen-induced vasoconstriction increasing V/Q mismatch and dead space, decreasing CO2 clearance
Because of this, patients known to be at risk of CO2 retention should have lower target oxygen saturations (usually 88-92%)
Oxygen can be delivered by a variety of devices
In an emergency, high-flow oxygen via a non-rebreather mask should be initiated
Oxygen should then be weaned to target saturations (usually 94-98% if the patient is not known to retain CO2)
Delivery may be via nasal cannulae or a face mask depending on flow rate
How is severe T2RF treated?
Severe T2RF may be treated with non-invasive ventilation (NIV)
This is often referred to as BIPAP (Bi-level Positive Airway Pressure)
This works by delivering higher pressures in inspiration and lower pressures in expiration to improve ventilation
Examples of when NIV may be used include COPD with respiratory acidosis or T2RF in the context of neuromuscular disease
Contraindications are the same as for CPAP
Intubation and ventilation is also an option for severely unwell patients not responding to other treatments
Consideration should be given to treatment escalation plans, involving the patient and their family as much as possible
For example, a patient with end-stage COPD or terminal cancer may not have the physiological reserve to survive an ITU admission and so in the event that they were not responding to medical treatment +/- CPAP/NIV, a decision may be made to palliate
How is T1RF treated?
Severe T1RF may be treated with continuous positive airway pressure (CPAP)
This works by splinting open the airways and alveoli by blowing air into the lungs at high flow rates via a face mask
This reduces respiratory effort as well as expanding collapsed areas of the lungs (which is called “recruitment”)
Examples of when CPAP may be used include pneumonia and pulmonary oedema
Contraindications include confusion, vomiting (due to aspiration risk) or untreated pneumothorax (as CPAP would worsen this by blowing more air into it)
What are the complications of respiratory failure?
A decline in lung function after recovery from the acute illness
Hypoxic ischaemic injury to other organs (e.g. the brain)
Cor pulmonale
Polycythaemia
Death
What are the complications associated with CPAP and NIV?
Mask leak
Pressure sores from tight-fitting masks
Hypotension
Aspiration (due to gastric inflation)
Pneumothorax
Epistaxis
What are the complications associated with invasive ventilation?
Dental injury during intubation
Barotrauma (pressure-induced trauma to the lungs)
Ventilator-associated pneumonia
Tracheomalacia
Complications of immobility (e.g. venous thromboembolism, pressure ulcers)
What is sarcoidosis?
Sarcoidosis is a multi-system disease that is characterised by the formation of non-caseating granulomas around the body. This leads to inflammation and scarring in the organs affected, most commonly the lungs and skin. Other organs affected include the nerves, the brain, the heart, the liver and the eyes.
What are the pulmonary manifestations of sarcoidosis?
Dry cough
Dyspnoea
Reduced exercise tolerance
Chest pain
Clubbing
Fine crackles on auscultation
What are the dermatological manifestations of sarcoidosis?
Erythema nodosum (inflammation of subcutaneous fat leading to tender nodules especially on the shins)
Lupus pernio (red/purple plaques and nodules on the face)
Hyper or hypopigmentation of the skin
What are the neurological manifestations of sarcoidosis?
Meningitis
Peripheral neuropathy
Facial nerve palsy (may be bilateral)
Headache
Seizures/encephalopathy
What are the ocular manifestations of sarcoidosis?
Uveitis
Keratoconjunctivitis sicca
Glaucoma
What are the cardiac manifestations of sarcoidosis?
Arrhythmias
Restrictive cardiomyopathy
Syncope
What are the abdominal manifestations of sarcoidosis?
Fatigue
Weight loss
Arthralgia
Low-grade fevers
Lymphadenopathy
Enlarged parotid glands
What is lofgren’s syndrome? and what are the symptoms?
a type of acute sarcoidosis
Fever
Polyarthralgia
Erythema nodosum
Bilateral hilar lymphadenopathy (seen on chest X-ray)
What is Heerfordt’s syndrome? and what are the symptoms? a rare subacute variant of sarcoidosis
Fever
Uveitis
Parotid swelling
Facial nerve palsy
What are the bedside examinations in sarcoidosis?
ECG looking for arrhythmias or changes related to hypercalcaemia (e.g. QT shortening)
Mantoux test looking for evidence of exposure to tuberculosis (an important differential)
Lung function testing - if pulmonary sarcoidosis suspected
Ophthalmological examination if ocular sarcoidosis suspected
What are the blood tests in sarcoidosis? And what are we looking for?
FBC may show lymphopenia, anaemia or raised white cells
LFTs for liver disease
Renal function for renal impairment (not common in sarcoidosis)
Bone profile for hypercalcaemia
ESR may be raised due to chronic inflammation
Serum ACE is elevated in around 60% and normalises if the disease resolves (with or without treatment)
What imaging studies do we do for sarcoidosis?
Chest x-ray to stage sarcoidosis
High resolution CT chest scan
PET scanning
Echocardiogram
What are the different stages for sarcoidosis shown on a chest x-ray?
Stage 1 - Bilateral hilar lymphadenopathy (BHL)
Stage 2 - BHL with peripheral infiltrates
Stage 3 - Peripheral infiltrates alone
Stage 4 - Pulmonary fibrosis
What other investigations may we do in sarcoidosis to confirm the diagnosis?
Biopsy is required to confirm the diagnosis in most cases (with a classic presentation of chronic pulmonary disease or a clear case of Lofgren’s syndrome being exceptions) - this is looking for the classic finding of noncaseating granulomas
Bronchoalveolar lavage may also be done in suspected pulmonary sarcoidosis, with classic findings of raised lymphocytes and an elevated CD4/CD8 ratio
What is the conservative treatment for sarcoidosis?
Patient education and support
Smoking cessation
No active treatment is needed in many cases of sarcoidosis
What is the medical treatment for sarcoidosis?
Steroids e.g. oral prednisolone with a higher dose at induction which is then reduced to a lower maintenance dose
Second line immunosuppressants (e.g. if steroids contraindicated or not effective) include methotrexate, mycophenolate or azathioprine
Third line treatment is usually with biologics (e.g. infliximab)
When should medical treatment be used for sarcoidosis?
Medical treatment should be started only if sarcoidosis symptoms are affecting quality of life or there is significant risk of morbidity or mortality from sarcoidosis
What is surgical treatment for sarcoidosis?
Rarely in severe cases of pulmonary sarcoidosis a lung transplant may be considered
In cases of pulmonary sarcoidosis complicated by aspergilloma, surgical management of haemoptysis is sometimes required
What are the complications for sarcoidosis?
Pulmonary fibrosis (stage IV pulmonary sarcoidosis
Cor pulmonale
Pulmonary hypertension
Aspergillomas can form in cavities left by granulomatous pulmonary disease
Arrhythmias and sudden death in cardiac sarcoidosis
Low mood and anxiety
Complications of long-term steroid use (e.g. osteoporosis, hyperglycaemia)
What is tuberculosis?
Tuberculosis (TB) refers to infection with the Mycobacterium tuberculosis bacterium. It usually affects the lungs, but can infect multiple other organ systems. Patients may have latent TB which means that they are infected but have no symptoms and are not contagious, or active TB.
TB transmission is usually via inhalation of infected droplets which are produced when someone with active TB coughs, sneezes or spits.
What are the risk factors for TB?
HIV increases the risk of TB by 16 times, and TB is the leading cause of death amongst people with HIV; all patients diagnosed with TB should be offered a HIV test
Other forms of immunosuppression increase the risk of infection and of reactivation of latent TB; patients on medications such as infliximab, azathioprine and ciclosporin are particularly at risk and should be screened for TB before starting these
Close contacts of infected patients - household members of someone with active TB have a 1 in 3 risk of infection, however other close contacts (including healthcare workers) are also at increased risk
Being from a high-risk country - countries with high rates of TB include India, Pakistan, Romania, Somalia and Eritrea
Homelessness - strongly related to other risk factors such as overcrowding, malnutrition, drug and alcohol abuse and recent stays in prison
Children have a greater risk of infection although this is usually latent
Elderly patients have an increased risk of TB reactivation due to immune senescence
What is the bacterium for TB?
Mycobacterium tuberculosis is a type of aerobic, slow growing bacteria.
They are described as acid fast bacilli, which means they are resistant to acid staining.
What is meant by primary TB?
If active disease develops immediately, this is called ‘primary TB’
What is meant by miliary TB?
In some cases this primary infection disseminates widely via the bloodstream - this is known as miliary TB due to the characteristic pattern on chest X-ray when re-infection of the lungs occurs via circulating bacteria
What is meant by ‘reactivation of TB’?
If latent disease later becomes active (e.g. if a patient becomes immunosuppressed), this is referred to as a ‘reactivation of TB’ which may be in the lungs or at distant sites
What are the systemic symptoms and signs of TB?
Night sweats
Fevers
Weight loss
Malaise
Lymphadenopathy
lymph nodes are typically enlarged and non-tender
may form sinus tracts if chronic
cervical and supraclavicular nodes are most commonly affected
What are the respiratory signs and symptoms of TB?
Chronic productive cough
Haemoptysis
Shortness of breath
Collapse or pleural effusion leading to dullness on percussion and reduced breath sounds over the affected area
What are the neurological signs and symptoms of TB?
Meningitis causing headaches and meningism
Focal neurological signs (classically cranial nerve lesions due to involvement of the basal meninges)
Decreased consciousness
What are the genitourinary signs and symptoms of TB?
Renal TB may present with haematuria and flank pain
Epididymo-orchitis may present with pain and swelling
Salpingitis (TB of the fallopian tube) may cause pain and vaginal bleeding
What are the musculoskeletal signs and symptoms of TB?
Pott’s syndrome (spinal TB) causes back pain, spinal deformities and neurological deficits
Arthritis causes joint pain and swelling
Osteomyelitis may lead to a painful ‘cold abscess’ with localised swelling and erythema, sometimes wiht a draining abscess
Psoas abscesses may present with a classic triad of fever, limp and back pain
What are the gastrointestinal signs and symptoms of TB?
Ileocaecal TB can cause bowel obstruction with abdominal pain and constipation
Ascites may result from perotineal TB
Intestinal TB may mimic IBD with abdominal pain and bloody diarrhoea
What are the pericardial signs and symptoms of TB?
Pericardial effusions may cause a raised JVP and pulsus parodoxus
Constrictive pericarditis also causes a raised JVP and may present with signs of right-sided heart failure such as peripheral oedema and hepatic congestion
What are the cutaneous signs and symptoms of TB?
Erythema nodosum (tender nodules, usually on the shins)
Lupus vulgaris refers to painful nodular skin lesions caused by TB, usually around the face
Miliary TB may spread to the skin causing a widespread rash
Scrolfuloderma is direct invasion of the skin from a TB-infected lymph node or bone, forming ulcerating and fistulating tracts from subcutaneous nodules usually around the neck area
What are the adrenal signs and symptoms of TB?
TB is the leading cause of adrenal insufficiency worldwide
Symptoms include fatigue, lightheadedness, nausea and abdominal pain
Signs include hypotension and skin hyperpigmentation
Who should be screened for latent TB?
Close contacts of known active TB cases
Patients about to start immunosuppressant treatment such as anti-TNFa agents (as this would put them at risk of reactivation)
Patients who are significantly immunocompromised (e.g. late-stage HIV, bone marrow or organ transplant recipients)
NHS employees working with patients
Patients arriving in the UK from a high risk area (some will have pre-screening before moving)
Patients in underserved groups in high-prevalence settings e.g. homeless people, prisoners and people attending substance misuse services may also be offered screening by local TB teams as part of outreach programmes and active case finding.
What screening investigations are done for latent TB?
The Mantoux test involves injecting tuberculin intradermally
The person then returns after 2-3 days to assess the local skin reaction
Induration of 5mm or more is considered a positive test
The Interferon-gamma release assay (IGRA) test is a blood test which detects the white blood cell response to TB antigens
It is quicker than the Mantoux test to perform
Fewer false positives are seen with the IGRA test (e.g. it is negative in patients who have had a BCG vaccine whereas this can make the Mantoux test inconclusive)
Patients with a positive screening test should be referred to TB services for further investigations and treatment.
What are the investigations for active TB?
Sputum samples for microscopy, culture and sensitivity testing (MCS)
At least three early morning samples should be sent
In patients who cannot produce sputum, broncheoalveolar lavage or sputum induction may be used
Samples are stained with Ziehl-Neelsen or Auramine staining before microscopy
Patients who are ‘smear positive’ have acid-fast bacilli seen on microscopy, which is a correlate of infectivity
If microscopy is negative, culture may still be positive but this takes several weeks to return due to the slow-growing nature of myocobacteria
Early morning urine sample MCS for suspected genitourinary TB
This is looking for genitourinary TB
Sterile pyuria (where white cells but not bacteria are seen in the urine) may indicate TB
ECG may show evidence of pericardial effusion (e.g. small complexes) or pericarditis (e.g. ST changes)
What blood tests do we do for active TB?
FBC, CRP, liver and renal function to look for evidence of infection and get a baseline before starting antibiotics
Mycobacterial blood MCS which may take several weeks to be resulted similarly to sputum cultures
HIV testing should be offered to all patients with suspected TB
What imaging tests do we do for TB?
Chest X-ray which may show:
Cavitation - most common symptom
Pleural effusion
Mediastinal or hilar lymphadenopathy
Parenchymal infiltrates, especially in the upper lobes
Miliary TB (tiny nodules throughout the lung fields)
Joint or spinal X-rays if suspected skeletal involvement
CT head for suspected CNS TB
Ultrasound of lymphadenopathy, the genitourinary system or the abdomen
Echocardiogram for suspected pericardial disease
The most common CXR finding in TB is a patchy pattern of opacification, sometimes described as “fibronodular”
What other tests do we do for TB?
Biopsies or needle aspiration of sites of suspected extrapulmonary TB (e.g. lymph node biopsy)
PCR eg. GeneXpert is a molecular test for TB which also looks for rifampicin resistance
This can be performed on multiple specimen types e.g. sputum or tissue
This gives rapid results and so is particularly useful if there is a high suspicion of TB
Further resistance testing may be done after a diagnosis of TB is made to determine appropriate antibiotic treatment
Lumbar puncture for suspected CNS TB - CSF should be sent for MCS and labelled as suspected TB
What vaccine do we give for the prevention of TB?
The BCG vaccine is a live attenuated vaccine that is given to protect against TB
It also protects against leprosy and can be used to treat some bladder cancers
It is not a routine part of the UK’s childhood vaccination schedule but is given to babies (or children up to 16) at higher risk of TB including those who:
are close contacts of a pulmonary TB case
live in an area with more than 40 cases of TB per 100,000 people per year (e.g. all of London)
have lived in a country with high TB rates for 3 months or more
have a parent/grandparent born in a country with high TB rates
It is 80% effective against severe forms of TB in childhood (e.g. meningitis) but is significantly less effective in respiratory disease
Because of this, it is only offered to adults with occupational exposures (e.g. healthcare workers, vets, prison guards)
It should not be given to:
people with a positive Mantoux test (which should be offered to adults prior to vaccination)
immunosuppressed people (because it is a live vaccine so could reactivate)
people who have previously had TB
What do we give to treat latent TB?
Options for patients with no evidence of active infection include:
Three months of isoniazid, pyridoxine and rifampicin
Six months of isoniazid and pyridoxine
What is the conservative treatment for TB?
Referral to the local multidisciplinary TB team for specialist management
Patient education including encouraging adherence, giving information and explaining how to seek help if they experience symptoms of relapsing disease
Contact tracing
TB is a notifiable disease and so should be reported promptly to the local health protection team
Infection control measures, for example advising patients with active pulmonary TB to wear a mask until they have completed 2 weeks of antibiotic treatment
Identification of patients who may need additional support to comply with treatment (e.g. those who are homeless), for example directly observed therapy (where a key-worker observes the patient taking every dose of antibiotics)
Identification of patients with multidrug and extensively drug-resistant TB
What is the medical treatment for active TB?
The standard regimen for active pulmonary TB, which is 2 months of isoniazid (with pyradoxine), rifampicin, ethambutol and pyrazinamide, followed by isoniazid (with pyradoxine) and rifampicin alone for a further 4 months
Longer courses of antibiotics in TB meningitis, pericardial and spinal TB
Steroids may be added in the initial weeks of antibiotic treatment for CNS and pericardial TB
Multidrug-resistant TB often requires 18-24 months of treatment with at least six drugs
These second-line antibiotics include amikacin, macrolides, quinolones and capreomycin
What is the surgical treatment for TB?
In selected cases of multidrug or extensively drug-resistant TB a lung resection may be considered
This is either unilateral or of both lung apices
Patients need adequate lung function to be eligible
Some types of extra-pulmonary TB may warrant surgical treatment e.g. drainage of renal abscesses
What are the complications of rifampicin?
Red/orange discolouration of bodily fluids
CYP450 induction (i.e. reduces effectiveness of other medications such as the combined oral contraceptive pill)
Hepatotoxicity
What are the complications for isoniazid?
Peripheral neuropathy (prevented by co-administration of pyridoxine to prevent vitamin B6 deficiency)
Hepatotoxicity
CYP450 inhibition
What are the complications for pyrazinamide?
Arthralgia
Hyperuricaemia (may cause gout)
Hepatotoxicity
What are the complications for Ethambutol?
Retrobulbar neuritis causing colour blindness and loss of visual acuity
Visual side effects are more common in chronic kidney disease so dose adjustment may be required
What are the complications of TB?
Bronchiectasis resulting from permanent airway damage from infection and inflammation
Antibiotic resistance especially in patients who have previously been treated for TB; around 10% of people diagnosed with TB in the UK have resistance to at least one of the four first line antibiotics with rifampicin resistance being commonest
Onwards transmission of TB especially if untreated or there is resistance to treatment
Psychosocial distress which may be exacerbated by stigma and social isolation
Aspergillomas may form in cavities that may persist after TB treatment
Pulmonary fibrosis may occur due to permanent lung damage from pulmonary TB
Death - TB kills around 5% of people diagnosed in the UK, with significantly higher mortality in countries where there is poor access to healthcare
mnemonic to remember complications of TB drugs:
Eye-thambutol (Optic neuritis)
- Isoniazid (Im-so-numb-azid) (peripheral neuropahty)
- Rifampicin (red-orange-pissin) red/orange secretions
Which treatment for rheumatoid arthritis should patients undergo TB evaluation due to its association with TB reactivation?
infliximab
What would it show on a lumbar puncture of tuberculosis meningitis?
lymphocyte predominance, low cerebrospinal fluid (CSF) glucose, high CSF protein and AFB smear positivity
What is the treatment for tuberculosis meningitis?
standard treatment with rifampicin, isoniazid, pyrazinamide and ethambutol for the initial 2 months. After this, patients are treated with rifampicin and isoniazid for a further 10 months (as opposed to 4 months for patients with active tuberculosis without central nervous system involvement).
