Respiratory Flashcards
Define acute respiratory distress syndrome.
Syndrome of acute and persistent lung inflammation with increased vascular permeability.
- Acute onset
- Bilateral infiltrates consistent with pulmonary oedema
- Hypoxaemia - PaO2 /FiO2 < 200mmHg regardless of the level of positive end-expiratory pressure (PEEP)
- No clinical evidence for increased left atrial pressure (pulmonary capillary wedge pressure PCWP <18mmHg)
- ARDS is the severe end of the spectrum of acute lung injury (ALI)
Explain the aetiology /risk factors of acute respiratory distress syndrome.
Severe insult to the lungs or other organs induces the release of inflammatory mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance.
Causes:
- Sepsis
- Aspiration
- Pneumonia
- Pancreatitis
- Trauma / Burns
- Transfusion - massive, transfusion-related lung injury
- Transplantation (bone marrow, lung)
- Drug overdose / reaction
- Alcohol misuse
- Smoke inhalation
- Drowning
- E-cigarette and vaping product use
Summarise the epidemiology of acute respiratory distress syndrome.
1 in 6000 per year in UK
Recognize the presenting symptoms of acute respiratory distress syndrome.
- Rapid deterioration of respiratory function
- Dyspnoea
- Respiratory distress
- Cough
- Symptoms of aetiology
Recognize the signs of acute respiratory distress syndrome on physical examination.
- Cyanosis
- Tachypnoea
- Tachycardia
- Widespread inspiratory crepitations
- Hypoxia refractory to oxygen treatment
- Bilateral signs
- May be asymptomatic in early stages
Identify appropriate investigations for acute respiratory distress syndrome and interpret the results.
- CXR
- Bloods
- Echocardiography
- Pulmonary artery catheterisation
- Bronchoscopy
CXR
- Bilateral alveolar and interstitial shadowing
Bloods
- FBC
- U&E
- LFT
- ESR / CRP
- Amylase
- Clotting
- ABG
- Blood culture
- Sputum culture
- Plasma BNP < 100pg/mL may distinguish between ARDS and heart failure (cannot exclude if critically ill)
Echocardiography
- Severe aortic or mitral valve dysfunction or low left ventricular ejection fraction favours haemodynamic oedema over ARDS
Pulmonary Artery Catheterisation
- PCWP <18mmHg
- High PCWP does not exclude ARDS as patients may have concomitant left ventricular dysfunction
Bronchoscopy
- If cannot determine from history
- Exclude differentials - e.g. diffuse alveolar haemorrhage
- To lavage fluid for microbiology - mycobacteria, Legionella pneumophila
- For cytology - eosinophils, viral inclusion bodies, cancer cells
Diffuse Alveolar Haemorrhage
- Frothy blood in airways
- Haemosiderin-laden macrophage from lavage fluid
Define arterial blood gas.
A collective term applied to three separate measurements = pH, PCO2 and PO2.
They are generally made together to evaluate acid-base status, ventilation and arterial oxygenation.
Summarise the indications for an arterial blood gas.
- Respiratory failure - both acute and chronic states
- Any illness that may lead to a metabolic acidosis - e.g. cardiac failure, liver failure, renal failure, hyperglycaemic states (DM), multiorgan failure, sepsis, burns, poisons/ toxins
- Ventilated patients
- Sleep studies
- Severely unwell patients from any cause - affects prognosis.
Identify the possible complications of an arterial blood gas.
- Local haematoma
- Arterial vasospasm
- Arterial occlusion
- Air or thrombus embolism
- Local anaesthetic anaphylactic reaction
- Infection at the puncture site
- Needle-stick injury to healthcare personnel
- Vessel laceration
Define asbestos-related lung disease (including asbestosis and mesothelioma).
Asbestosis - diffuse interstitial fibrosis of the lung as a consequence of exposure to asbestos fibres
Mesothelioma - a tumour of the mesothelial cells that usually occurs in the pleura, and rarely in the peritoneum or other organs, associated with asbestos exposure but relationship is complex
Explain the aetiology / risk factors of asbestos-related lung disease (including asbestosis and mesothelioma).
Asbestosis
- Caused by inhalation of asbestos fibers
- Commonly sued in building trade for fireproofing, pipe lagging, electrical wire insulation and roofing felt
- Degree of asbestos exposure is related to degree of pulmonary fibrosis.
- Onset occurs after 10+ years following initial exposure
- Increases risk of bronchial adenocarcinoma & mesothelioma
Risk factors:
- Occupational exposure
- Longer duration of exposure
- Smoking history
- Indirect exposure
Mesothelioma
- Long latency period (20-40 year latency)
- Few long-term survivors, high lethal malignancy
Risk factors:
- Asbestos exposure during home maintenance and renovation
- 60-85 years
- Male sex
Summarise the epidemiology of asbestos-related lung disease (including asbestosis and mesothelioma).
Asbestosis & Mesothelioma
- 90% report previous exposure to asbestos
- 20% of patients have pulmonary asbestosis
- Latent period between exposure and development of tumour is up to 45 years
- Incidence in the US is 3200 per year (for malignancy)
Recognize the presenting symptoms of asbestos-related lung disease (including asbestosis and mesothelioma).
Asbestosis
- Asymptomatic
- Shortness of breath (dyspnoea), especially on exertion
- Cough
- Presence of risk factors
Mesothelioma
- Chest pain
- Dyspnoea
- Presence of risk factors
Recognize the signs of asbestos-related lung disease (including asbestosis and mesothelioma) on physical examination.
Asbestosis
- Clubbing
- Fine end-inspiratory crackles
- Pleural plaques
Mesothelioma
- Weight loss
- Finger clubbing
- Recurrent pleural effusions
Signs of Metastasis
- Lymphadenopathy
- Hepatomegaly
- Bone pain / tenderness
- Abdominal pain /obstruction - peritoneal malignant mesothelioma
Identify appropriate investigations for asbestos-related lung disease (including asbestosis and mesothelioma) and interpret the results.
Asbestosis
- CXR (PA and lateral)
- Pulmonary function tests
- High-resolution CT chest
- Lung biopsy
- Bronchial lavage
Results:
- Pleural abnormalities
- Pleural plaques with/without calcification
- Diffuse pleural thickening
- Benign pleural effusion
- Rounded atelectasis
- In concordance with or in absence of parenchymal fibrosis
Mesothelioma
- CXR (PA and lateral)
- CT chest (with contrast)
- Histology following thoracoscopy
- Thoracentesis
- Pleural biopsy
- Video-associated thoracoscopic surgery
- Immunohistochemistry
Results:
- Pleural thickening / effusion
- Bloody pleural fluid
Define Aspergillus lung disease.
Lung disease associated with Aspergillus fungal infection.
Explain the aetiology/risk factors of Aspergillus lung disease.
Inhalation of the ubiquitous Aspergillus (usually Aspergillus fumigates) spores produce 3 different clinical pictures:
- Aspergilloma - growth of an A.fumigatus mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess)
- Allergic BronchoPulmonary Aspergillosis (ABPA)
- Invasive Aspergillosis - invasion into lung tissue and fungal dissemination (secondary to immunosuppression - e.g. neutropenia, steroids, haematopoietic stem cell/ solid organ transplantation, AIDS)
ABPA
- Aspergillus colonization of airways
- IgE and IgG mediated immune repsonses
- Proteolytic enzymes and mycotoxins released by fungi
- CD4/Th2 cells produce IL-4 and IL-5
- Eosinophilic inflammation
- IL-8 mediated neutrophilic inflammation
- Airway damage and central bronchiectasis
Summarise the epidemiology of Aspergillus lung disease.
Uncommon
Elderly
Immunocompromised
Recognize the presenting symptoms of Aspergillus lung disease.
Aspergilloma
- Asymptomatic
- Haemoptysis (may be massive)
ABPA
- Difficult to control asthma
- Recurrent episodes of pneumonia
- Wheeze
- Cough
- Fever
- Malaise
Invasive Aspergillosis
- Dyspnoea
- Rapid deterioration
- Septic picture
Recognize the signs of Aspergillus lung disease on physical examination.
- Tracheal deviation in large aspergillomas
- Dullness in affected lung
- Reduced breath sounds
- Wheeze (ABPA)
- Cyanosis (invasive aspergillosis)
Identify appropriate investigations for Aspergillus lung disease and interpret the results.
Aspergilloma
- CXR - round opacity with a crescent of air around it (in upper lobes)
- CT or MRI imaging (if CXR does not clearly delineate a cavity)
- Cultures of sputum - if no communication between cavity and bronchial tree
NB: Aspergillus is a common colonizer of an abnormal respiratory tract.
ABPA
- Immediate skin test reactivity to Aspergillus antigens
- Eosinophilia
- High serum total IgE
- High serum specific IgE and IgG to Aspergillus fumigatus or precipitating serum antibodies to Aspergillus fumigatus
- CXR
- CT - lung infiltrates, central bronchiectasis
- Lung function tests - reversible airflow limitation, reduced lung volumes/ gas transfer in progressive cases
CXR
- Transient patchy shadows
- Collapse
- Distended mucus-filled bronchi producing tubular shadows = gloved fingers
- Signs of complications
- Fibrosis in upper lobes (TB)
- Parallel-line shadows and rings (bronchiectasis)
Invasive Aspergillosis
- Detection in cultures or histologic examination (septated hyphae with acute angle branching)
- Risk factors
- Suggestive clinical findings
- Microscopic evidence of septate hyphae of examination of bronchoalveolar lavage fluid/sputum / positive serum galactomannan / beta-D-glucan assay
- Chest CT - nodules surrounded by ground-glass appearance (halo) = haemorrhage into tissue surrounding area of fungal invasion
Define asthma.
Chronic inflammatory airway disease characterized by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.
Explain the aetiology/risk factors of asthma.
Genetic Factors:
- Family history (twin studies)
- Atopy - tendency of TH2 cells to drive production of IgE on exposure to allergens
- Multiple chromosomal locations (genetic heterogeneity)
Environmental Factors:
- House dust mite
- Pollen
- Pets - e.g. urinary proteins, furs
- Cigarette smoke
- Viral respiratory tract infection
- Aspergillus fumigatus spores
- Occupation allergens (isocyanates, epoxy resins)
Early Phase (Up to 1h)
- Exposure to inhaled allergens in a pre-sensitized individual
- Cross-linking of IgE antibodies on mast-cell surface
- Release of histamine, PgD2, leukotrienes, TNF-alpha
- Smooth muscle contraction = bronchoconstriction
- Mucous hypersecretion
- Oedema
- Airway obstruction
Late Phase (After 6-12h)
- Recruitment of eosinophils, basophils, neutrophil and TH2 lymphocytes and products
- Perpetuation of inflammation and bronchial hyper-responsiveness
- Structural cells (e.g. bronchial epithelial cells, fibroblasts, smooth muscle, and vascular endothelial cells) release cytokines, profibrogenic and proliferative GFs
- Contribute to inflammation and altered function
- Contribute to the proliferation of smooth muscle cells and fibroblasts = airway remodelling
Summarise the epidemiology of asthma.
10% of children 5% of adults Increasing prevalence W > M 1000-2000 deaths from acute asthma per year
Recognize the presenting symptoms of asthma.
- Wheeze
- Breathlessness
- Cough
- Worse in the morning and at night
- Ask about interference with exercise, sleeping, days off school and work
- Acute attack - ask about whether admitted before or to ITU as a gauge of severity potential
Precipitating Factors:
- Cold
- Viral infection
- Drugs - e.g. B-blockers, NSAIDs
- Exercise
- Emotions
- History of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux, family history
Recognize the signs of asthma on physical examination.
- Tachypnoea
- Accessory muscle usage
- Prolonged expiratory phase
- Polyphonic wheeze
- Hyperinflated chest
Severe Attack:
- PEFR < 50% predicted
- Pulse >110/min
- RR >25/min
- Inability to complete sentences
Life-Threatening Attack:
- PEFR < 33%
- Chest silent
- Cyanosis
- Bradycardia
- Hypotension
- Confusion
- Coma
Identify appropriate investigations for asthma and interpret the results.
Acute
- Peak flow
- Pulse oximetry
- ABG
- CXR - to exclude pneumothorax, pneumonia etc
- FBC - high WCC if infective exacerbation
- CRP
- U&E
- Blood & sputum cultures
Chronic
- PEPR monitoring - diurnal variation (morning dip)
- Pulmonary function test - obstructive defect with improvement after trial of B2 agonist
- Blood - eosinophilia, IgE level, Aspergillus antibody titres
- Skin prick tests - identification of allergens
Generate a management plan for asthma.
Acute
- Resuscitate, monitor O2 sats, ABG, PEFR
- High-flow oxygen
- Nebulized B2-agonist bronchodilator salbutamol (5mg initially continuously, then 2-4 hourly), ipratropium (0.5mg QDS)
- Steroid therapy (100-200mg IV hydrocortisone followed by 40mg oral prednisolone for 5-7 days)
- If no improvement - IV magnesium sulphate
- Consider IV aminophylline infusion or IV salbutamol
- Summon anaesthetic if patient is getting exhausted - PCO2 increasing
- Treat any underlying cause (e.g. infection, pneumothorax)
- Give antibiotics if there is a chest infection - e.g. purulent sputum, abnormal CXR, high WCC fever
- Monitor electrolytes closely - as bronchodilators and aminophylline reduce K+
- May need ventilation in severe attacks
- If not improving or patient tiring then involve ITU early
Discharge
- PEF > 75% predicted or patient’s best diurnal variation <25%
- Inhaler technique checked
- Stable on discharge medication for 24h
- Own a PEF meter
- Steroid & bronchodilator therapy
- Arrange to follow up
Chronic Stepwise Therapy
- Review treatment every 3-6 months
STEP 1: Inhaled short-acting B2-agonist as needed, if used >1/day, move to STEP 2.
STEP 2: STEP 1 plus regular inhaled low-dose steroids (400mcg/day)
STEP 3: STEP 2 plus inhaled long-acting B2-agonist (LABA)
If inadequate control with LABA, then increase steroid dose to 800mcg/day. If no response to LABA then stop and increase steroid to 800mcg/day.
STEP 4: Increase inhaled steroid dose to 2000mcg/day, add 4th drugs (e.g. leukotriene receptor antagonist, SR theophylline or B2 agonist tablet)
STEP 5: Addition of regular oral steroids, maintain high-dose inhaled steroid, consider other treatments to minimize the use of oral steroids and refer for specialist care.
Advice
- Educate on proper inhaler technique
- Routine monitoring of peak flow
- Develop an individualized management plan with emphasis on avoidance of provoking factors
Identify the possible complications of asthma and its management.
- Growth retardation
- Chest wall deformity - e.g. pigeon chest
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death
Summarise the prognosis for patients with asthma.
Children usually improve when they grow older
Adult-onset asthma usually chronic
Define bronchiectasis.
Lung airway disease characterized by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections.
Explain the aetiology / risk factors of bronchiectasis.
Severe inflammation in the lung causes fibrosis and dilation of the bronchi. Results in pooling of mucus, predisposing to further cycles of infection, damage and fibrosis to bronchial walls.
Causes
- Idiopathic (50%)
- Post-infectious - severe pneumonia, whooping cough, TB
- Host defence defects - e.g. Kartagener’s Syndrome, cystic fibrosis, immunoglobulin deficiency, yellow-nail syndrome
- Obstruction of bronchi - e.g. foreign body, enlarged lymph nodes
- Gastric reflux disease
- Inflammatory disorders - e.g. rheumatoid arthritis
Summarise the epidemiology of bronchiectasis.
Most often arises initially in childhood.
Incidence has decreased with the use of antibiotics
1 in 1000 per year
Recognise the presenting symptoms of bronchiectasis.
- Productive cough
- Purulent sputum
- Haemoptysis
- Breathlessness
- Chest pain
- Malaise
- Fever
- Weight loss
- Symptoms begin after acute respiratory illness
Recognise the signs of bronchiectasis on physical examination.
- Finger clubbing
- Coarse crepitations - usually at the bases
- Shift with coughing
- Wheeze
Identify appropriate investigations for bronchiectasis and interpret the results.
- Sputum
- CXR
- High-Resolution CT
- Bronchography
- Other
Sputum
- Culture and sensitivity
- Common organisms = Pseudomonas aeruginosa, Haemophilis influenzae, Staphylococcus aureus, Streptococcus pneumoiae, Klebsiella, Moraxella catarrhalis, Mycobacteria
CXR
- Dilated bronchi seen as parallel lines radiating from hilum to diaphragm = tramline shadows
- Fibrosis
- Atelectasis
- Pneumonic consolidations
- Normal even
CT
- Dilated bronchi
- Thickened bronchial walls
Bronchiography
- Determine extent of disease before surgery
- Radioopaque contrast injected through the cricoid ligament or via a bronchoscope
Others
- Sweat electrolytes
- Serum immunoglobulins - 10% of adults have some immune deficiency
- Sinus X-ray - 30% have concomitant rhinosinusitis
- Mucociliary clearance study
Generate a management plan for bronchiectasis.
Acute Exacerbations
- 2 IV antibiotics - efficacy for pseudomonas
- Prophylactic antibiotics (oral or aerosolized) for those with >3 exacerbations per year
=>Inhaled corticosteroids
- e.g. Fluticasone
- Reduce inflammation and volume of sputum
- Does not affect the number of exacerbations or lung function
=>Bronchodilators
- If patients have responsive disease
=>Hydration
- Maintain with adequate oral fluid intake
=>Flu Vaccination
=>Physiotherapy
- Sputum and mucus clearance technique - e.g. postural drainage
- Position themselves so the lobe to be drained is uppermost, approx 20 min twice daily
- Reduces frequency of acute exacerbations and aids recovery
=> Bronchial Artery Embolization
- For life-threatening hemoptysis
=> Surgical
- Localized resection
- Lung or heart-lung transplantation
Identify the possible complications of bronchiectasis and its management.
- Life-threatening haemoptysis
- Persistent infections
- Empyema
- Respiratory failure
- Cor pulmonale
- Multi-organ abscess
Summarise the prognosis for patients with bronchiectasis.
Most patients continue to have symptoms after 10 years.
Define COPD.
Chronic, progressive lung disorder characterized by airflow obstruction, chronic bronchitis and emphysema.
Chronic Bronchitis - chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
Emphysema - pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles.
Explain the aetiology / risk factors of COPD.
Bronchial and alveolar damage as a result of environmental toxins - e.g. cigarette smoke.
Rare cause = alpha-1-antitrypsin deficiency (<1%)
- Young patients
- Non-smokers
- Co-presents with asthma
Chronic Bronchitis
- Narrowing of airways due to bronchiole inflammation = bronchiolitis
- Bronchi with mucosal oedema
- Mucous hypersecretion
- Squamous metaplasia
Emphysema
- Destruction and enlargement of alveoli
- Loss of elastic traction that keeps small airways open in expiration
- Larger spaces develop = bullae (>1cm)
Summarise the epidemiology of COPD.
Prevalence 8%
Middle age or later
Males
Change due to increase in female smokers
Recognise the presenting symptoms of COPD.
- Chronic cough
- Sputum production
- Breathlessness
- Wheeze
- Reduced exercise tolerance
Recognise the signs of COPD on physical examination.
Inspection
- Respiratory distress
- Use of accessory muscles
- Barrel-shaped overinflated chest
- Reduced cricosternal distance
- Cyanosis
Percussion
- Hyper-resonant chest
- Loss of liver and cardiac dullness
Auscultation
- Quiet breath sounds
- Prolonged expiration
- Wheeze
- Rhonchi and crepitations
Signs of CO2 Retention
- Bounding pulse
- Warm peripheries
- Flapping tremor of hands (asterixis)
- Late stages = signs of right heart failure (e.g. right ventricular heave, raised JVP, ankle oedema)
Identify appropriate investigations for COPD and interpret the results.
- Spirometry and Pulmonary Function Tests
- CXR
- Bloods
- ABG
- ECG and Echocardiogram - for cor pulmonale
- Sputum and Blood Cultures - acute exacerbations for treatment
- Consider alpha-1-antitrypsin Levels - in non-smokers, young patients
Spirometry & Pulmonary Function Tests
- Obstructive picture
- Reduced PEFR
- Reduced FEV1:FVC ratio - mild, 60-80%, moderate 40-60%, severe <40%)
- Increased lung volumes
- CO gas transfer coefficient reduced when significant alveolar destruction
CXR
- Normal
- Hyperinflation - >6 ribs visible anteriorly, flat hemi-diaphragms
- Reduced peripheral lung markings
- Elongated cardiac silhouette
Blood
- FBC - high Hb and PCV due to secondary polycythemia
ABG
- Hypoxia (reduced PaO2), normal or high PaCO2
Generate a management plan for COPD.
1) Stop Smoking
2) Bronchodilators
3) Steroids
4) Pulmonary Rehabilitation
5) Oxygen Therapy
Bronchodilators
- Short-acting B2 agonists - e.g. salbutamol
- Anticholinergics - e.g. ipratropium
- Delivered by inhalers or nebulizers
- Long-acting B2 agonists if >2 exacerbations per year
Steroids
- Inhaled beclomethasone if FEV1 <50% predicted or those with >2 exacerbations per year
- Regular oral steroids avoided but may be necessary
Oxygen Therapy - only if stopped smoking = long-term home oxygen therapy has been shown to improve mortality
- More economical if used for >8h /day
Indications:
- PaO2 <7.3kPa on air during a period of clinical stability
- PaO2 7.3-8.0kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension
Treatment of Acute Infective Exacerbations:
- Provide 24% O2 via non-variable flow Venturi mask
- Increase slowly if no hypercapnia and still hypoxic (ABG)
- Corticosteroids (oral or inhaled)
- Start empirical antibiotic therapy if evidence of infection - follow trust policy
- Respiratory physiotherapy essential to clear sputum
- Consider non-invasive ventilation in severe cases
- Prevention = pneumococcal and influenza vaccination
Identify the possible complications of COPD and its management.
- Acute respiratory failure
- Infections - e.g. Streptococcus pneumonia, Haemophilus influenzae
- Pulmonary hypertension
- Right heart failure
- Pneumothorax - resulting from bullae rupture
- Secondary polycythaemia
Summarise the prognosis for patients with COPD.
- High level of morbidity
- 3 year survival rate of 90% if age < 60 years and FEV1 > 50% predicted, 75% if >60 years and FEV1 40-49% predicted
Define extrinsic allergic alveolitis.
Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts.
AKA hypersensitivity pneumonitis.
Explain the aetiology / risk factors of extrinsic allergic alveolitis.
Inhalation of antigenic organic dusts containing microbes (bacteria, fungi or amoebae) or animal proteins.
Induce a hypersensitivity response = Type III antigen-antibody complex hypersensitivity reaction + Type IV granulomatous lymphocytic inflammation
Farmer’s Lung
- Mouldy hay containing thermophilic actinomycetes
Pigeon / Budgerigar Fancier’s Lung
- Bloom on bird feathers and excreta
Mushroom Worker’s Lung
- Compost containing thermophilic actinomycetes
Humidifier Lung
- Water-containing bacteria and Naegleria (amoeba)
Maltworker’s Lung
- Barley or maltings containing Aspergillus clavatus
Recognise the presenting symptoms of extrinsic allergic alveolitis.
Acute
- 4-12h after exposure
- Reversible episodes
- Dry cough
- Dyspnoea
- Malaise
- Fever
- Myalgia
- Wheeze
- Productive cough
(last 2 on repeated high-level exposures)
Chronic
- Poorly reversible manifestation
- Slowly increased breathlessness
- Reduced exercise tolerance
- Weight loss
- Exposure is usually chronic, low level and no history of previous acute episodes
Full occupational history and enquiry into hobbies and pets important.
Recognise the signs of extrinsic allergic alveolitis on physical examination.
Acute
- Rapid shallow breathing
- Pyrexia
- Inspiratory crepitations
Chronic
- Fine inspiratory crepitations
- Finger clubbing rare
Identify appropriate investigations for extrinsic allergic alveolitis and interpret the results.
- Bloods
- Serology
- CXR
- High-resolution CT-Thorax
- Pulmonary Function Tests
- Bronchoalveolar Lavage
Bloods
- FBC - neutrophilia, lymphopenia
- ABG - low PO2, low PCO2
Serology
- Precipitating IgG to fungal or avian antigens in serum
- Not diagnostic as often found in asymptomatic individuals
CXR
- Acute episodes
- Ground glass appearance
- Alveolar shadowing
- Nodular opacities
- Located in middle and lower zones
- Fibrosis prominent in upper zones in chronic cases
CT
- Early changes
- Patchy ground-glass shadowing and nodules
Pulmonary Function Tests
- Restrictive ventilatory defect = reduced FEV1, reduced FVC with preserved or increased ratio
- Reduced TLCO
Bronchoalveolar Lavage
- Increased cellularity with high CD8 + suppressor T-cells
- Lung biopsy - transbronchial or thorascopic
Summarise the epidemiology of extrinsic allergic alveolitis.
Uncommon
2% of occupational lung diseases
50% of reported cases affect farm workers (4-10 per 100,000 / year )
Marked geographical variation reflecting dependence on occupational causes
Define idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.
Inflammatory condition of the lung resulting in fibrosis of alveoli and interstitium.
Explain the aetiology / risk factors of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.
- Genetically predisposed host - e.g. with telomerase / surfactant protein mutations
- Recurrent injury to alveolar epithelial cells
- Secretion of cytokines and growth factors - e.g. TNF-alpha, IL-1, MCP-1
- Fibroblast activation, recruitment, proliferation
- Differentiation of fibroblasts into myofibroblasts
- Increased collagen synthesis and deposition
- Profibrogenic molecules (e.g. PDGF, TGF-B) secreted by inflammatory, epithelial and endothelial cells
Drugs cause a similar illness
- Bleomycin
- Methotrexate
- Amiodarone
Histological Patterns
- Usual interstitial pneumonia - e.g. patchy interstitial fibrosis, honeycomb lung
- Desquamative interstitial pneumonia - diffuse intra-alveolar accumulation of macrophages, mild thickening of alveolar septa, lymphoid aggregates
- Non-specific interstitial pneumonia
Risk Factors
- Smoking (75%)
- Occupational exposure to metal - e.g. steel, brass, lead
- Occupational exposure to wood (pine)
- Chronic microaspiration
- Animal and vegetable dusts
Summarise the epidemiology of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.
Rare
Prevalence 6 in 100,000 in UK
M:F 2:1
67y = mean age
Recognise the presenting symptoms of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.
- Gradual onset of progressive dyspnoea on exertion
- Dry irritating cough
- No wheeze
- Symptoms preceded by a viral-type illness
- Fatigue and weight loss common
- Full occupational and drug history important
Recognise the signs of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis on physical examination.
- Finger clubbing (50%)
- Bibasal fine late inspiratory crepitations
- Signs of right heart failure in advanced stages - e.g. right ventricular heave, raised JVP, peripheral oedema
Identify appropriate investigations for idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis and interpret the results.
- Blood
- CXR
- High-Resolution Ct
- Pulmonary Function Tests
- Bronchoalveolar Lavage - to exclude infections and malignancy
- Lung Biopsy - gold standard for diagnosis
- Echocardiography - to look for pulmonary hypertension
Blood
- ABG - normal in early disease, reduced PO2 on exercise
- ABG - normal PCo2 which rises in late disease
- 1/3 have rheumatoid factor or anti-nuclear antibodies
CXR
- Usually normal
- Early = small lung fields, ground glass shadowing
- Late = reticulonodular showing (at bases), signs of cor pulmonale, honeycombing
CT
- Most sensitive in early disease
- Affect mainly lower zones and subpleural areas
- Reticular densities
- Honeycombing
- Traction bronchiectasis
Pulmonary Function Tests
- Restrictive ventilatory defect (reduced FEV1, reduced FVC with preserved or increased ratio)
- Reduced lung volumes
- Reduced lung compliance
- Reduced TLCO
Define lung cancer.
Non-Small Cell
- Primary malignant neoplasm of the lung (80%)
- Squamous cell carcinoma, adenocarcinoma, large cell carcinoma, adenosquamous carcinoma
Small Cell
- Malignant neoplasm of neuroendocrine Kulchitsky cells of the lung with early dissemination
- AKA oat cell carcinoma
Explain the aetiology / risk factors of lung cancer.
Non-Small Cell
- Genetic alterations that result in neoplastic transformation
- Mainly in main or lobar bronchi
- Adenocarcinoma = more peripherally
Risk Factors
- Smoking (active or passive)
- Occupational exposure - e.g. polycyclic hydrocarbons, asbestos, nickel, chromium, cadmium, radon
- Atmospheric pollution
Small Cell
- Smoking
- Occupational and environmental exposures
Summarise the epidemiology of lung cancer.
Non-Small Cell
- Most common fatal malignancy in the West - 18% of cancer mortality
- 35,000 deaths per year UK
- 3x more common in men, but increasing in women
Small Cell
- 20% of all lung cancers
Recognize the presenting symptoms of lung cancer.
Non-Small Cell
- Asymptomatic with radiographic abnormality found (5%)
- Primary = cough, haemoptysis, chest pain, recurrent pneumonia
- Local invasion = e.g. brachial plexus (Pancoast tumour in apex of lung) causing pain in shoulder or arm, left recurrent laryngeal nerve (hoarseness and bovine cough), oesophagus (dysphagia), heart (palpitations / arrhythmias)
- Metastatic or paraneoplastic phenomena = weight loss, fits, bone pain, fractures, neuromyopathies
Small Cell
- Asymptomatic with radiographical abnormality found
- Primary tumour = cough, haemoptysis, dyspnoea, chest pain
- Metastatic disease = weight loss, fatigue, bone pain
- Parneoplastic Syndrome = weakness, lethargy, seizures, muscle fatiguability
Recognize the signs of lung cancer on physical examination.
Non-Small Cell
- No signs
- Fixed monophonic wheeze
- Signs of collapse, consolidation, pleural effusion
- Local Invasion = SVC compression (facial congestion, distension of neck veins, upper limb oedema), Brachial plexus (wasting of small muscles of hand), Sympathetic Chain (Horner’s - miosis, ptosis, anhydrosis)
- Metastases = supraclavicular lymphadenopathy, hepatomegaly
- Paraneoplastic Phenomena = hypertrophic osteoarthropathy - e.g. clubbing, painful/swollen wrists/ankles due to periosteal new bone formation, dermatological signs
Small Cell
- No signs or a fixed wheeze on auscultation of the chest
- Signs of lobular collapse or pleural effusion
- Signs of metastases - e.g. supraclavicular lymphadenopathy, hepatomegaly
- Signs of paraneoplastic syndromes
Identify appropriate investigations for lung cancer and interpret the results.
Non-Small Cell
- Diagnosis
- TNM Staging
- Bloods
- Pre-Operative
Diagnosis
- CXR - coin lesions, lobar collapse, pleural effusion, features of lymphangitis carcinomatosis
- Sputum cytology
- Bronchoscopy with brushings or biopsy
- CT or US-guided percutaneous biopsy
- Lymph node biopsy
TNM Staging
- Based on tumour size, nodal involvement and metastatic spread
- Use CT chest, CT or MRI head and abdomen or ultrasound, bone scan, PET scan
- Invasive methods - e.g. mediastinoscopy, video-assisted thoracoscopy used
Bloods
- FBC
- U&E
- Ca2+ - hypercalcaemia common
- AlkPhos - high bone metastases
- LFT
Pre-Op
- ABG
- Pulmonary function tests - FEV1 > 80% predicted to tolerate a pneumonectomy
- Lung resection is contraindicated if FEV <30% predicted
- V/Q scan
- ECG
- Echocardiogram
- General anaesthetic assessment
Small Cell
- Diagnosis - sputum cytology, bronchoscopy with brushings and biopsy, percutaneous biopsy, thoracoscopy
- Staging - CT of chest, abdomen, head, isotope boen scan
- Other - lung function tests, FBC, U&E, Ca2+, AlkPhos, LFT
Define obstructive sleep apnoea.
Characterized by recurrent collapse of the pharyngeal airway and apnoea (defined as the cessation of airflow for >10s) during sleep, followed by arousal from sleep.
AKA Pickwickian Syndrome.
Explain the aetiology/risk factors of obstructive sleep apnoea.
Occurs when the upper airway narrows because of the collapse of the soft tissues of the pharynx when tone in pharyngeal dilators decreases during sleep.
Associated with:
- Excessive weight gain
- Smoking
- Alcohol
- Sedative use
- Enlarged tonsils
- Enlarged adenoids
- Macroglossia
- Marfan’s Syndrome
- Craniofacial abnormalities
Summarise the epidemiology of obstructive sleep apnoea.
Common
5-20% of men , 2-5% of women >35 years
Prevalence increases with age.
Recognise the presenting symptoms of obstructive sleep apnoea.
- Excessive daytime sleepiness
- Unrefreshing or restless sleep
- Morning headaches or dry mouth
- Difficulty concentrating
- Irritability or mood changes
- Partner reporting snoring, nocturnal apnoeic episodes or nocturnal choking
Recognize the signs of obstructive sleep apnoea on physical examination.
- Large tongue
- Enlarged tonsils
- Long or thick uvula
- Retrognathia - pulled back jaws
- Neck circumference - >42cm in M, >40cm females
- Obesity
- Hypertension
Identify appropriate investigations for obstructive sleep apnoea and interpret the results.
- Sleep study - managed by sleep study centre for polysomnography or diagnostic sleep studies with monitoring of airflow, respiratory effort, pulse oximetry and heart rate
- Blood - thyroid function tests, ABG
Define pneumoconiosis.
Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts.
Simple - Coalworker’s pneumoconiosis or silicosis (symptom free)
Complicated - Pneumoconiosis (progressive massive fibrosis) results in loss of lung function
Asbestosis - Pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos
Explain the aetiology/risk factors of pneumoconiosis.
Caused by inhalation of particles of coal dust, silica or asbestos.
2 types:
- White asbestos
- Blue asbestos or crocidolite = more toxic
Risk Factors:
- Occupational exposure - e.g. coal mining, quarrying, iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, shipbuilders
- Depends on extent of exposure, size and shape of particles and individual susceptibility
- Co-factors = smoking, TB
Pathology
- Complicated disease - large nodules in the lung, consisting of dust particles surrounded by layers of collagen and dying macrophages
Methods of Damage:
- Direct cytotoxicity by particles
- Particle ingestion by macrophages results in activation and excessive free radical production causing lipid peroxidation and cell injury
- Proinflammatory cytokines and growth factors from macrophages and epithelial cells stimulate fibroblast proliferation and eventual scarring
Asbestosis:
- Asbestos bodies consisting of fibres coated with an iron-containing protein seen in fibrotic areas
- Seen especially in lung bases
Summarise the epidemiology of pneumoconiosis.
Incidence increasing in developing countries
Disability and mortality from asbestosis will increase for the next 20-30 years
Recognize the presenting symptoms of pneumoconiosis.
- Occupational history is very important as there may be a long latency between disease, exposure and epxression
Asymptomatic
- Picked up on routine CXR - simple coal or silica pneumoconiosis
Symptomatic
- Insidious onset
- Shortness of breath
- Dry cough
- Black sputum - melanoptysis = Coalworker’s Pneumoconiosis
- Workers exposed to asbestos may develop pleuritic chest pain may years after first exposure due to acute asbestos pleurisy
Recognize the signs of pneumoconiosis on physical examination.
- May be normal
- Decreased breath sounds in Coalworker’s Pneumoconiosis or Silicosis
- End-inspiratory crepitations
- Clubbing in asbestosis
- Signs of a pleural effusion or right heart failure (cor pulmonale)
Identify appropriate investigations for pneumoconiosis and interpret the results.
- CXR
- CT Scan - fibrotic changes visualized early
- Bronchoscopy - visualizes changes, and allows for bronchoalveolar lavage
- Lung-function Tests - restrictive ventilatory defect, impaired gas diffusion
CXR
- Simple - micronodular mottling
- Complicated (SILICOSIS) - nodular opacities (upper lobes), micronodular shadowing, eggshell calcification (hilar lymph nodes)
- Complicated (ASBESTOSIS) - bilateral reticulonodular shadowing (lower zone) and pleural plaques, white lines when calcified (diaphragmatic pleura, holly leaf patterns)
Define pneumonia.
Infection of the distal lung parenchyma.
Categories:
- Community-acquired, hospital-acquired or nosocomial
- Aspiration pneumonia, pneumonia in the immunocompromised
- Typical and atypical - e.g. Mycoplasma, Chlamydia, Legionella
Explain the aetiology / risk factors of pneumonia.
Community-Acquired:
- Streptococcus pneumonia (70%)
- COPD = Haemophilus influenzae & Morazella catarrhalis
- Contract with Birds/Parrots = Chlamydia pneumonia & Chlamydia psittaci
- Periodic epidemics = Mycoplasms pneumonia
- Anywhere with air con = Legionella
- Recent influenza infection, IV drug users = Staphylococcus aureus
- Q Fever, rare = Coxiella burnett
- TB = may present as pneumonia
Hospital-Acquired:
- Gram-negative enterobacteria = Pseudomonas, Klebsiella
- Anaerobes = aspiration pneumonia
Risk Factors:
- Age
- Smoking
- Alcohol
- Pre-existing lung disease
- Immunodeficiency
- Contact with pneumonia
Summarise the epidemiology of pneumonia.
Incidence 5-11 in 1000 (25-44 in 1000 in elderly)
Community-acquired causes >60,000 deaths/year in UK
Recognize the presenting symptoms of pneumonia.
- Fever
- Rigors
- Sweating
- Malaise
- Cough
- Sputum (yellow, green or rusty in S pneumoniae)
- Breathlessness
- Pleuritic chest pain
- Confusion - severe cases,elderly, Legionella
Atypical Pneumonia:
- Headache
- Myalgia
- Diarrhoea
- Abdominal Pain
Recognize the signs of pneumonia on physical examination.
- Pyrexia
- Respiratory distress
- Tachypnoea
- Tachycardia
- Hypotension
- Cyanosis
- Reduced chest expansion
- Dullness to percussion
- Increased tactile vocal fremitus
- Bronchial breathing - inspiration phase lasts as long as the expiration phase
- Coarse crepitations on the affected side
- Chronic suppurative lung disease (e.g. empyema, abscess): Clubbing
Identify appropriate investigations for pneumonia and interpret the results.
- Bloods
- CXR
- Sputum
- Urine
- Atypical Viral Serology
- Bronchoscopy & Bronchoalveolar Lavage
Bloods
- FBC - abnormal WCC
- U&E - low Na+, especially with Legionella
- LFT
- Blood cultures - sensitivity 10-20%
- ABG - to assess pulmonary function
- Blood film - RBC agglutination by Mycoplasma caused by cold agglutinins
CXR
- Lobar or patchy shadowing
- Pleural effusion
- Klebsiella - often seen in upper lobes
- Repeat 6-8 weeks - if abnormal suspect underlying pathology
Sputum/Pleural Fluid
- Microscopy
- Culture & sensitivity
- Acid-fast bacilli
Urine
- Pneumococcus antigens
- Legionella antigens
Atypical Viral Serology
- Increased antibody titres between acute and convalescent samples - greater than 2 weeks post onset
Bronchoscopy
- If Pneumocystis carinii pneumonia is suspected
- When pneumonia fails to resolve
- When there is clinical progression
Generate a management plan for pneumonia.
- Assess Severity - see prognosis, if >1 feature presents the manage in hospital
- Start Empirical Antibiotics
- Oral amoxicillin (0 markers)
- Oral or IV amoxicillin and erythromycin (1 marker)
- IV cefuroxime / cefotaxime / co-amoxiclav and erythromycin (>1 marker)
- Add metronidazole, if aspiration, lung abscess or empyema suspected
- Switch to the appropriate antibiotic as per sensitivity
NB: Levofloxacin and moxifloxacin can provide useful alternatives in selected hospitalized patients with community-acquired pneumonia.
- Supportive Treatment
- Oxygen - maintain PO2 > 8kPa, start with 28% O2 in COPD to avoid hypercapnia
- Parenteral fluids for dehydration or shock
- Analgesia
- Chest physiotherapy
- CPAP, BiPAP or ITU care for respiratory failure
- Surgical drainage may be needed for empyema / abscess - Discharge Planning
- Presence of two or more features of clinical instability predict a significant chance of re-admission or mortality
- Raised temperature, heart rate, respiratory rate
- Low BP, oxygen saturation, mental status and oral intake - Non-Resolving Pneumonia
- Consider other causes
Causes of Non-Resolving Pneumonia
- Unusual pathogens - e.g. Chlamydia psittaci, C.burnetti, Mycobacterium tuberculosis, Nocardia, Actinomyces israeli, fungi (Aspergillus, histoplasmosis, coccidioidomycosis, blastomycosis)
- PE
- Malignancy - e.g. bronchogenic carcinoma, bronchoalveolar cell carcinoma, lymphoma
- Inflammatory - e.g. vasculitis, Wegener’s granulomatosis, sarcoidosis, systemic lupus erythematosus
- Congestive heart failure
- Drug toxicity
- Diffuse alveolar hemorrhage
- Bronchiolitis obliterans-organizing pneumonia
- Eosinophilic pneumonia
- Acute interstital pneumonia
- Pulmonary alveolar proteinosis
- Prevention
- Pneumococcal & H.influenzae type B vaccination in vulnerable groups
- E.g. elderly, splenectomized
Identify the possible complications of pneumonia and its management.
- Pleural effusion
- Empyema (pus in the pleural cavity)
- Localized superation leading to lung abscess - seen by Staphyloccoal, Klebsiella pneumonia, presenting with swinging fever, persistent pneumonia, copious / foul-smelling sputum
- Septic shock
- ARDS
- Acute renal failure
M.Pneumonia
- Erythema multiforme
- Myocarditis
- Haemolytic anaemia
- Meningoencephalitis
- Transverse myelitis
- Guillian-Barre Syndrome
Summarise the prognosis for patients with pnuemonia.
Most resolve with treatment (1-3 weeks).
High mortality of severe pneumonia
- Community-acquired - 5-10%
- Hospital-acquired - 30%
- 50% of those in ITU
Markers of Severe Pneumonia (CURB-65 Score)
C = Confusion
U = Urea >7mmol/L
R = RR >30/min
B = BP - Systolic <90mmHg, Diastolic <60mmHg
Age >65 years.
Other markers are:
- Hypoxia <8kPa
- ECC <4 or >20 x 10^9 /mm^3
- Age >50 years
Define pneumothorax.
Air in the pleural space - the potential space between visceral and parietal pleura
Other variants depend on the substance in the pleural space - e.g. haemothorax, chylothorax (lymph)
Tension Pneumothorax - emergency when a functional valve lets air enter the pleural space during inspiration, but does not leave during expiration.
Explain the etiology / risk factors of pneumothorax.
Spontaneous
- In individuals with previously normal lungs, typically tall thin males
- Rupture of a subpleural bleb
Secondary
- Pre-existing lung disease - e.g. COPD, asthma, TB, pneumonia, lung carcinoma, cystic fibrosis, diffuse lung disease
Traumatic
- Penetrating injury to the chest
- Often iatrogenic causes - e.g. during subclavian or jugular venous cannulation, thoracocentesis, pleural or lung biopsy or positive pressure-assisted ventilation
Risk Factors:
- Collagen disorders - e.g. Marfan’s disease, Ehlers-Danlos Syndrome
Summarise the epidemiology of pneumothorax.
The annual incidence of spontaneous pneumothorax is 9 in 100,000.
20-40 year olds
4x more common in males
Recognize the presenting symptoms of pneumothorax.
- Asymptomatic if pneumothorax is small
- Sudden onset breathlessness or chest pain, especially on inspiration
- Distress with rapid shallow breathing if tension pneumothorax
Recognize the signs of pneumothorax on physical examination.
- Signs may be absent if small
- Signs of respiratory distress with reduced expansion
- Hyper-resonance to percussion
- Breath sounds reduced
Tension Pneumothorax:
- Severe respiratory distress
- Tachycardia
- Hypotension
- Cyanosis
- Distended neck veins
- Tracheal deviation away from the side of the pneumothorax
Identify appropriate investigations for pneumothorax and interpret the results.
CXR
- Dark area of film where lung markings do not extend to
- Fluid level may be seen if blood present
- Small pneumothoraces, expiratory films may make it more prominent
ABG
- Determine if hypoxaemic, particular in secondary disease
Generate a management plan for pneumothorax.
Tension Pneumothorax
- Max O2
- Insert large bore needle into 2nd ICS, MCL on side of pneumothorax to relieve pressure
- Insert chest drain soon after
Small Pneumothorax (<2cm lung-pleural margin)
- Check for underlying lung disease, pleural fluid, clincical compromise
- If none, reassure, analgesia
Moderate Pneumothorax (>2cm lung-pleural margin)
- Aspiration using large bore cannula or catheter with three-way tap
- Inserted into the 2nd ICS MCL
- 2.5L of air can be aspirated - stop if patient repeatedly coughs or resistance is felt
- Follow up CXR should be performed just after, 2h and 2 weeks later
- Advised to avoid diving
- Chest drain with water seal if the aspiration fails, or if there is fluid in the pleural cavity or after decompression of a tension pneumothorax
- Inserted into 4-6th ICS in MAL
Recurrent Pneumothoraces
- Chemical pleurodesis - visceral and parietal pleura fusion with tetracycline or talc
- Surgical pleurectomy
Advice
- Avoiding air travel until follow-up CXR confirms resolution of pneumothorax
- Avoid diving unless bilateral surgical pleurectomy
Identify the possible complications of pneumothorax and its management.
- Recurrent pneumothoraces
- Bronchopleural fistula
Summarise the prognosis for patients with pneumothorax.
After one spontaneous pneumothorax, at least 20% will have another, with the frequency increasing with repeated pneumothoraces.
Define pulmonary embolism.
Occlusion of pulmonary vessels, most commonly caused by a thrombus that has travelled to the vascular system from another site.
Explain the aetiology / risk factors of pulmonary embolism.
- Thrombus
- 95% originate from DVT of lower limbs
- Rarely from right atrium in patients with AF
- Amniotic fluid embolus
- Air embolus
- Fat emboli
- Tumour emboli
- Mycotic emboli from right-sided endocarditis
Risk factors:
- Surgical patients
- Immobility
- Obesity
- OCP
- Heart failure
- Malignancy
Summarise the epidemiology of pulmonary embolism.
Fairly common, especially in hospitalized patients
Occur in 10-20% of those with a confirmed proximal DVT.
Recognise the presenting symptoms of pulmonary embolism.
Depends on site and size.
Small - may be asymptomatic
Moderate
- Sudden onset dyspnoea
- Cough
- Haemoptysis
- Pleuritic chest pain
Large
- Sudden onset dyspnoea
- Cough
- Haemoptysis
- Severe pleuritic chest pain
- Shock
- Collapse
- Acute right heart failure
- Sudden death
Multiple Small Recurrent
- Symptoms of pulmonary hypertension
Recognize the signs of pulmonary embolism on physical examination.
Clinical Probability Assessment
- Well’s Score - >4 high probability, <3 probability
Clinically suspected DVT = 3.0 PE is most likely diagnosis = 3.0 Recent surgery (4 weeks) = 1.5 Immobilization = 1.5 Tachycardia = 1.5 History of DVT or PE = 1.5 Haemoptysis = 1 Malignancy = 1
- Raised Geneva Score - >11 high probability, 4-10 intermediate probability, <3 low probability
>65 = 1 Recent surgery or fracture (28 days) = 2 Previous DVT / PE = 3 Active maliganancy = 2 Unilateral leg pain = 3 Haemoptysis = 2 Heart Rate > 75-94/min = 3 Heart Rate >85/min = 5 Unilateral leg oedema and tenderness = 4
Small
- No clinical signs
- Tachycardia
- Tachypnoea
Moderate
- Tachycardia
- Tachypnoea
- Pleural rub
- Low O2 sats - despite O2 supplementation
Large
- Shock
- Cyanosis
- Signs of right heart strain - e.g. raised JVP, left parasternal heave, accentuated S2 heart sound
Multiple Recurrent PE
- Signs of pulmonary hypertension and right heart failure
Identify appropriate investigations for pulmonary embolism and interpret the results.
Low Probability
- D-dimer blood test - cross-linked fibrin degradation products
- Highly sensitive
- Poor specificity
High Probability
- Requires imaging
Additional:
- Bloods - ABG, thrombophilia screen
- ECG - normal, tachycardia, right axis deviation, RBBB
- CXR - exclude other differentials
NB: Classic Si, QIII, TIII pattern uncommon.
- Spiral CT Pulmonary Angiogram - 1st line, poor sensitivity for small emboli
- Ventilation-Perfusion (VQ) Scan - administration of IV 99mTc macro-aggregated albumin and inhalation of 81 krypton gas to identify areas of ventilation and perfusion mismatch
(If abnormal CXR or co-existing lung disease, do not use due to difficulty in interpretation)
- Pulmonary angiography - gold standard, invasive though
- Doppler USS of lower limb - to examine for VT
- Echocardiogram - right heart strain shown
Generate a management plan for pulmonary embolism.
Primary Prevention:
- Graduated pressure stockings (TEDs)
- Heparin prophylaxis in those at risk (e.g. undergoing surgery)
- Early mobilization and adequate hydration post-surgery
If hemodynamically stable:
- O2
- Anticoagulation with heparin or LMW heparin
- Chaing to oral warfarin therapy (INR 2-3) for a minimum of 3 months
- Analgesics for pain
If haemodynamically unstable:
- Resuscitate
- Give O2
- IV fluid resuscitation
- Thrombolysis with tPA can be considered on clinical grounds alone if cardiac arrest is imminent - 50mg bolus of tPA
Surgical or Radiological:
- Embolectomy - when thrombolysis is contraindicated
- IVC filters - Greenfield filter - may be inserted for recurrent pulmonary emboli despite adequate anticoagulation or when anticoagulation is contraindicated
Identify the possible complications of pulmonary embolism and its management, and summarise the prognosis for patients with pulmonary embolism.
- Death
- Pulmonary Infarction
- Pulmonary hypertension
- Right Heart Failure
Prognosis:
- 30% untreated motrality
- 8% with treatment - due to recurrent emboli or underlying disease
- Increased risk of future TE disease
Define tuberculosis.
Granulomatous disease caused by Mycobacterium tuberculosis.
Primary
- Initial infection may be pulmonary (acquired by inhalation from cough of the infected patient) or occasionally, gastrointestinal
Miliary TB
- Results when there is hematogenous dissemination
Post-Primary
- Caused by re-infection or reactivation
Explain the aetiology / risk factors of tuberculosis.
M.tuberculosis is an intracellular organism - AKA acid-fast bacilli
Survives after being phagocytosed by macrophages.
Summarise the epidemiology of tuberculosis.
Annual mortality of 3 million.
95% in developing countries
UK incidence annually 6000
Asian immigrants >30 times native UK white population incidence
Recognize the presenting symptoms of tuberculosis.
Primary TB
- Asymptomatic
- Fever
- Malaise
- Cough
- Wheeze
- Erythema nodosum
- Phlyctenular conjunctivitis (allergic manifestations)
Miliary TB
- Fever
- Weight loss
- Meningitis
- Yellow caseous tubercles spread to other organs - e.g. bone and kidney may remain dormant for years
Post-Primary TB
- Fever
- Night sweats
- Malaise
- Weight loss
- Breathlessness
- Cough
- Sputum
- Haemoptysis
- Pleuritic pain
- Signs of pleural effusion
- Collapse
- Consolidation
- Fibrosis
Non-Pulmonary TB
- Particularly in immunocompromised
Lymph Nodes
- Suppuration of cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin = scrofuloderma
CNS
- Meningitis
- Tuberculoma
Skin
- Lupus vulgaris - jellylike reddish-brown glistening plaques
Heart
- Percardial effusion
- Constrictive pericarditis
Gastrointestinal
- Subacute obstruction
- Change in bowel habit
- Weight loss
- Peritonitis
- Ascites
Adrenal
- Insufficiency
Bone/Joints
- Osteomyelitis
- Arthritis
- Paravertebral Abscesses
- Vertebral collapse - Pott’s disease
- Spinal cord compression from abscesses
Recognize the signs of tuberculosis on physical examination.
Primary TB
- Asymptomatic
- Fever
- Malaise
- Cough
- Wheeze
- Erythema nodosum
- Phlyctenular conjunctivitis (allergic manifestations)
Miliary TB
- Fever
- Weight loss
- Meningitis
- Yellow caseous tubercles spread to other organs - e.g. bone and kidney may remain dormant for years
Post-Primary TB
- Fever
- Night sweats
- Malaise
- Weight loss
- Breathlessness
- Cough
- Sputum
- Haemoptysis
- Pleuritic pain
- Signs of pleural effusion
- Collapse
- Consolidation
- Fibrosis
Non-Pulmonary TB
- Particularly in immunocompromised
Lymph Nodes
- Suppuration of cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin = scrofuloderma
CNS
- Meningitis
- Tuberculoma
Skin
- Lupus vulgaris - jellylike reddish-brown glistening plaques
Heart
- Percardial effusion
- Constrictive pericarditis
Gastrointestinal
- Subacute obstruction
- Change in bowel habit
- Weight loss
- Peritonitis
- Ascites
Adrenal
- Insufficiency
Bone/Joints
- Osteomyelitis
- Arthritis
- Paravertebral Abscesses
- Vertebral collapse - Pott’s disease
- Spinal cord compression from abscesses
Identify appropriate investigations for tuberculosis and interpret the results.
- Sputum / Pleural Fluid /Bronchial Washings - microscopy, culture (6 weeks), low sensitivity
- Tuberculin Tests - positive in previous exposure, strongly positive = infection (and not BCG)
- Mantoux Test - intradermal injection of PPD, induration and erythema after 72h
- Heaf Test - place drop of PPD on forearm, fire spring-loaded needled gun, read after 3-7 days, graded according to papule size and vesiculation
- Interferon-Gamma Tests - latent TB, esposure of host T-cells to TB antigens causes release of interferon (negative with BCG vaccination)
- CXR
- Primary infection - peripheral consolidation, hilar lymphadenopathy
- Miliary - fine shadowing
- Post-primary - upper lobe shadowing, streaky fibrosis, cavitation, calcification, pleural effusion, hilar lymphadenopathy - HIV Testing - to co-incident disease (2% may be HIV positive)
- CT, Lymph Nodes, Pleural Biopsy, Sampling of Other Affected Systems
Define sarcoidosis.
Multisystem granulomatous inflammatory disorder.
Explain the aetiology / risk factors of sarcoidosis.
Unknown.
Transmissibel agents - e.g. viruses, atypical mycobacterium, Propionibacterium acnes
Environmental triggers
Genetic factors
Unknown antigen presented on MHC Class II complex of macrophages to CD4 Th1 lymphocytes, which accumulate and release cytokines (IL-1, IL-2).
Formation of NON-CASEATING granulomas in a variety of organs.
Summarise the epidemiology of sarcoidosis.
Uncommon.
20-40 year olds.
Africans.
Females.
Variable prevalence
UK 16 in 100,000
Highest in Irish women.
Recognise the presenting symptoms of sarcoidosis.
General
- Fever
- Malaise
- Weight loss
- Bilateral parotid swelling
- Lymphadenopathy
- Hepatosplenomegaly
Lungs
- Breathlessness
- Cough - usually unproductive
- Chest discomfort
- Minimal clinical signs - e.g. fine inspiratory crackles
Musculosksletal
- Bone cysts - e.g. dactylitis in phalanges
- Polyarthralgia
- Myopathy
Eyes
- Keratoconjunctivitis sicca - dry eyes
- Uveitis
- Papilloedema
Skin
- Lupus pernio - red-blue infiltrations of the nose, cheeky, ears, terminal phalanges
- Erythema nodosum
- Maculopapular eruptions
Neurological
- Lymphocytic meningitis
- Space occupying lesions
- Pituitary infiltration
- Cerebellar ataxia
- Cranial nerve palsies - e.g. bilateral facial nerve palsy
- Peripheral neuropathy
Heart
- Arrhythmia
- Bundle branch block
- Pericarditis
- Cardiomyopathy
- Congestive cardiac failure
Recognise the signs of sarcoidosis on physical examination.
General
- Fever
- Malaise
- Weight loss
- Bilateral parotid swelling
- Lymphadenopathy
- Hepatosplenomegaly
Lungs
- Breathlessness
- Cough - usually unproductive
- Chest discomfort
- Minimal clinical signs - e.g. fine inspiratory crackles
Musculosksletal
- Bone cysts - e.g. dactylitis in phalanges
- Polyarthralgia
- Myopathy
Eyes
- Keratoconjunctivitis sicca - dry eyes
- Uveitis
- Papilloedema
Skin
- Lupus pernio - red-blue infiltrations of the nose, cheeky, ears, terminal phalanges
- Erythema nodosum
- Maculopapular eruptions
Neurological
- Lymphocytic meningitis
- Space occupying lesions
- Pituitary infiltration
- Cerebellar ataxia
- Cranial nerve palsies - e.g. bilateral facial nerve palsy
- Peripheral neuropathy
Heart
- Arrhythmia
- Bundle branch block
- Pericarditis
- Cardiomyopathy
- Congestive cardiac failure
Identify appropriate investigations for sarcoidosis and interpret the results.
Bloods
- High serum ACE
- Hight Ca2+
- High ESR
- WCC low due to lymphocyte sequestration in lungs
- Immunoglobulins - polyclonal hyperglobulinaemia
- LFTs - high AlkPhos & GGT
24h Urine Collection
- Hypercalciuria
CXR
- Stage 0 - may be clear
- Stage 1 - bilateral hilar lymphadenopathy
- Stage 2 - bilateral hilar lymphadenopathy with pulmonary infiltration and paratracheal node enlargement
- Stage 3 - Pulmonary infiltration and fibrosis
High-Resolution CT Scan
- For diffuse lung involvement
67-Gallium Scan
- Shows areas of inflammation (classically parotids and around eye)
Pulmonary Function Tests
- Reduced FEV1, FVC and gas transfer
- Restrictive pattern
Bronchoscopy and Bronchoalveolar Lavage
- Raised lymphocytes
- Raised CD4:CD8 ratio
Transbronchial Lung Biopsy (or Lymph Node Biopsy)
- Non-caseating granulomas composed of epithelioid cells (activated macrophages)
- Multinucleate Langhans cells
- Mononuclear cells (lymphocytes)
