Respiratory Flashcards
Learning objectives
Answer
Define acute respiratory distress syndrome
• A syndrome of acute and persistent lung inflammation with increased vascular permeability. Characterised by:
o Acute onset
o Bilateral infiltrates consistent with pulmonary oedema
o Hypoxaemia
o No clinical evidence of increased left arterial pressure (pulmonary capillary wedge pressure)
o ARDS is the severe end of the spectrum of acute lung injury
Explain the aetiology / risk factors of acute respiratory distress syndrome
Severe insults to the lungs and other organs leads to the release of inflammatory mediators. These lead to increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance . Causes o Sepsis o Aspiration o Pneumonia o Pancreatitis o Trauma/burns o Transfusion o Transplantation (bone marrow and lung) o Drug overdose/reaction There are THREE pathological stages of ARDS: o Exudative o Proliferative o Fibrotic
Summarise the epidemiology of acute respiratory distress syndrome
1 in 6000
Recognise the presenting symptoms of acute respiratory distress syndrome
- Rapid deterioration of respiratory function
- Dyspnoea
- Respiratory distress
- Cough
- Symptoms of CAUSE
Recognise the signs of acute respiratory distress syndrome on physical examination
- Cyanosis
- Tachypnoea
- Tachycardia
- Widespread inspiratory crepitations
- Hypoxia refractory to oxygen treatment
- Signs are usually bilateral but may be asymmetrical in early stages
Identify appropriate investigations for acute respiratory distress syndrome and interpret the results
• CXR - bilateral alveolar infiltrates and interstitial shadowing
• Bloods - to figure out the cause (FBC, U&Es, LFTs, ESR/CRP, Amylase, ABG, Blood Culture)
o NOTE: plasma BNP < 100 pg/mL could distinguish ARDS from heart failure
• Echocardiography
o Check for severe aortic or mitral valve dysfunction
o Low left ventricular ejection fractions = haemodynamic oedema rather than ARDS
• Pulmonary Artery Catheterisation
o Check pulmonary capillary wedge pressure (PCWP)
• Bronchoscopy
o If the cause cannot be determined from the history
Define Aspergillus Lung Disease
• Lung disease associated with Aspergillus fungal infection
NOTE: Aspergillus infection is usually caused by Aspergillus fumigatus
Explain the aetiology/risk factors for Aspergillus lung disease
Inhalation of Aspergillus spores can produce THREE different clinical pictures:
• Aspergilloma
o Growth of an A. fumigates mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess)
• Allergic Bronchopulmonary Aspergillosis (ABPA)
o Colonisation of the airways by Aspergillus leads to IgE and IgG-mediated immune responses
o Usually occurs in asthmatics
o The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage and central bronchiectasis
• Invasive Aspergillosis
o Invasion of Aspergillus into lung tissue and fungal dissemination
o This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS)
Summarise the epidemiology of Aspergillus lung disease
- UNCOMMON
* Mainly occurs in the ELDERLY and IMMUNOCOMPROMISED
Recognise the presenting symptoms of Aspergillus lung disease
• Aspergilloma o ASYMPTOMATIC o Haemoptysis (potentially massive) • ABPA o Difficult to control asthma o Recurrent episodes of pneumonia with wheeze, cough, fever and malaise • Invasive Aspergillosis o Dyspnoea o Rapid deterioration o Septic picture
Recognise the signs of Aspergillus lung disease on physical examination
- Tracheal deviation (only with very large aspergillomas)
- Dullness in affected lung
- Reduced breath sounds
- Wheeze (in ABPA)
- Cyanosis (possible in invasive aspergillosis)
Identify appropriate investigations for Aspergillus lung disease
• Aspergilloma o CXR • May show a round mass with a crescent of air around it • Usually found in the upper lobes o CT or MRI - may be used if CXR is unclear o NOTE: sputum cultures may be negative if there is no communication between the cavity colonised by Aspergillus and the bronchial tree • ABPA o Immediate skin test reactivity to Aspergillus antigens o Eosinophilia o Raised total serum IgE o Raised specific serum IgE and IgG to A. fumigatus o CXR • Transient patchy shadows • Collapse • Distended mucous-filled bronchi • Signs of complications: Fibrosis in upper lobes Bronchiectasis o CT • Lung infiltrates • Central bronchiectasis o Lung Function Tests • Reversible airflow limitation • Reduced lung volumes/gas transfer • Invasive Aspergillosis o Aspergillus is detected in cultures or by histological examination o Bronchoalveolar lavage fluid or sputum may be used diagnostically o Chest CT
- Nodules surrounded by a ground-glass appearance (halo sign)
- This is caused by haemorrhage into the tissue surrounding the fungal invasion
Define asthma
• Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
Explain the aetiology / risk factors of asthma
Genetic Factors o Family history o Atopy (tendency for T lymphocytes to drive production of IgE on exposure to allergens) Environmental Factors o House dust mites o Pollen o Pets o Cigarette smoke o Viral respiratory tract infections o Aspergillus fumigatus spores o Occupational allergens
Summarise the epidemiology of asthma
- Affects 10% of children
- Affects 5% of adults
- Prevalence appears to be increasing
Recognise the presenting symptoms of asthma
• Episodic history • Wheeze • Breathlessness • Cough (worse in the morning and at night) IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an indication of the severity of the asthma Precipitating Factors o Cold o Viral infection o Drugs (e.g. beta-blockers, NSAIDs) o Exercise o Emotions Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)
Recognise the signs of asthma on physical examination
• Tachypnoea • Use of accessory muscles • Prolonged expiratory phase • Polyphonic wheeze • Hyperinflated chest Severe Attack o PEFR < 50% predicted o Pulse > 110/min o RR > 25/min o Inability to complete sentences Life-Threatening Attack o PEFR < 33% predicted o Silent chest o Cyanosis o Bradycardia o Hypotension o Confusion o Coma
Identify appropriate investigations for asthma and interpret the results
ACUTE o Peak flow o Pulse oximetry o ABG o CXR - to exclude other diagnoses (e.g. pneumonia, pneumothorax) o FBC - raised WCC if infective exacerbation o CRP o U&Es o Blood and sputum cultures CHRONIC o Peak flow monitoring - often shows diurnal variation with a dip in the morning o Pulmonary function test o Bloods - check: • Eosinophilia • IgE level • Aspergillus antibody titres o Skin prick tests - helps identify allergens
Generate a management plan for asthma
ACUTE
o ABCDE
o Resuscitate
o Monitor O2 sats, ABG and PEFR
o High-flow oxygen
o Salbutamol nebulizer (5 mg, initially continuously, then 2-4 hourly)
o Ipratropium bromide (0.5 mg QDS)
o Steroid therapy
• 100-200 mg IV hydrocortisone
• Followed by, 40 mg oral prednisolone for 5-7 days
o If no improvement –> IV magnesium sulphate
o Consider IV aminophylline infusion
o Consider IV salbutamol
o Anaesthetic help may be needed if the patient is getting exhausted
o IMPORANT: a normal PCO2 is a BAD SIGN in a patient having an asthma attack
• This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low
• A normal PCO2 suggests that the patient is fatiguing
o Treat underlying cause (e.g. infection)
o Give antibiotics if it is an infective exacerbation
o Monitor electrolytes closely because bronchodilators and aminophylline causes a drop in K+
o Invasive ventilation may be needed in severe attacks
o DISCHARGE when:
• PEF > 75% predicted
• Diurnal variation < 25%
• Inhaler technique checked
• Stable on discharge medication for 24 hours
• Patient owns a PEF meter
• Patient has steroid and bronchodilator therapy
• Arrange follow-up
CHRONIC THERAPY
o Start on the step that matches the severity of the patient’s asthma
o STEP 1
• Inhaled short-acting beta-2 agonist used as needed
• If needed > 1/day then move onto step 2
o STEP 2
• Step 1 + regular inhaled low-dose steroids (400 mcg/day)
o STEP 3
• Step 2 + inhaled long-acting beta-2 agonist (LABA)
• If inadequate control with LABA, increase steroid dose (800 mcg/day)
• If no response to LABA, stop LABA and increase steroid dose (800 mcg/day)
o STEP 4
• Increase inhaled steroid dose (2000 mcg/day)
• Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2 agonist tablet)
o STEP 5
• Add regular oral steroids
• Maintain high-dose oral steroids
• Refer to specialist care
• Advice
o Teach proper inhaler technique
o Explain important of PEFR monitoring
o Avoid 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
- Many children improve as they grow older
* Adult-onset asthma is usually chronic
Define bronchiectiasis
Lung airways disease characterised by chronic bronchial dilation, impaired mcuociliary clearance and frequent bacterial infections
Explain the aetiology/risk factors for bronchiectasis
Chronic lung inflammation leads to fibrosis and permanent dilation of the bronchi.
This leads to pooling of mucus, which predisposes to further cycles of infection, damage and fibrosis of bronchial walls
Causes of bronchiectasis:
Idiopathic (50%)
Post-infectious (e.g. pneumonia, whooping cough, TB)
Host-defence defects (e.g. Kartagener’s syndrome, cystic fibrosis)
Obstruction of bronchi (e.g. foreign body, enlarged lymph nodes)
GORD
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
1/1000 per year
Recognise the presenting symptoms of bronchiectasis
Productive cough with purulent sputum or haemoptysis
Breathlessness
Chest pain
Malaise
Fever
Weight loss
Symptoms usually begin after an acutre respiratory illness
Recognise the signs of bronchiectasis on physical examination
Clubbing
Coarse crepitations (usually at lung bases) - these shift with coughing
Wheeze
Identify appropriate investigations for bronchiectasis
Sputum Culture and sensitivity Common organisms: Pseudomonas aeruginosa Haemophilus influenzae Staphylococcus aureus Streptococcus pneumoniae Klebsiella Mycobacteria
CXR Dilated bronchi (may be seen as parallel lines going from the hilum to the diaphragm (tramline shadows)) Fibrosis Atelectasis Pneumonic consolidations May be normal
High resolution CT
Best diagnostic method for bronchiectasis
Shows dilated bronchi with thickened walls
Bronchography - rarely used
Others: swear electrolytes (for cystic fibrosis), serum Ig, mucociliary clearance study
Generate a management plan for bronchiectasis
Treat acute exacerbations with TWO IV ANTIBIOTICS, which cover Pseudomonas aeruginosa
Prophylactic antibiotics should be considered in patients with frequent exacerbations (>3/year)
Inhaled corticosteroids (e.g. fluticasone) - reduces inflammation and volume of sputum but does NOT affect the frequency of exacerbations or lung function
Bronchodilators - considered in patients with responsive disease
Maintain hydration
Flu vaccination
Physiotherapy - enables sputum and mucus clearance. This can reduce frequency of acute exacerbations and aid recovery.
Bronchial artery embolisation - if life-tthreatening haemoptysis due to bronchiectasis
Surgical - localised resection, lung or heart-lung transplantation
Identify the possible complications of bronchiectasis
Life-threatening haemoptysis Persistent infections Empyema Respiratory failure Cor pulmonale Multi-organ abscesses
Summarise the prognosis for patients with bronchiectasis
Most patients continue to have symptoms after 10 years
Define chronic obstructive pulmonary disease (COPD)
Chronic, progressive lung disorder characterised by airflow obstruction, with the following:
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 chronic obstructive pulmonary disease (COPD)
Bronchial and alveolar damage is caused by environmental toxins (e.g. cigarette smoke)
RARE CAUSE: a1 antitrypsin deficiency
Though this is rare, consider it in young patients, who have never smoked, presenting with COPD type symptoms (and may have accomopanying symptoms of cirrhosis)
Chronic Bronchitis
Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis)
Bronchial mucosal oedema
Mucous hypersecretion
Squamous metaplasia
Emphysema
Destruction and enlargement of alveoli
Leads to loss of elasticity that keeps small airways open in expiration
Progressively larger spaces develop called bullae (diameter > 1cm)
Summarise the epidemiology of chronic obstructive pulmonary disease (COPD)
Very Common (8% prevalence) Presents in middle age or later More common in males - this may change because there has been a rise in female smokers
Recognise the presenting symptoms of chronic obstructive pulmonary disease (COPD)
Chronic cough Sputum production Breathlessness Wheeze Reduced exercise tolerance
Recognise the signs of chronic obstructive pulmonary disease (COPD) on physical examination
Inspection Respiratory distress Use of accessory muscles Barrel-shaped over-inflated chest Decreased cricosternal distance Cyanosis Percussion Hyper-resonant chest Loss of liver and cardiac dullness Auscultation Quient breath sounds Prolonged expiration Wheeze Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions. Sometimes crepitations Signs of CO2 retention Bounding pulse Warm peripheries Asterixis LATE STAGES: signs of right heart failure (cor pulmonale) Right ventricular heave Raised JVP Ankle oedema
Identify appropriate investigations for chronic obstructive pulmonary disease (COPD) and interpret the results
Spirometry and Pulmonary Function Tests
Shows obstructive picture
Reduced PEFR
Reduced FEV1/FVC
Increased lung volumes
Decreased carbon monoxide gas transfer coefficient
CXR
May appear NORMAL
Hyperinflation (> 6 anterior ribs, flattened diaphragm)
Reduced peripheral lung markings
Elongated cardiac silhouette
Bloods
FBC - increased Hb and haematocrit due to secondary polycythaemia
ABG - may show hypoxia, normal/raised PCO2
ECG and Echocardiogram
check for cor pulmonale
Sputum and Blood Cultures - useful in acute infective exacerbations
a1 antitrypsin levels - useful in young patients who have never smoked
Generate a management plan for chronic obstructive pulmonary disease (COPD)
STOP SMOKING
Bronchodilators
Short acting beta 2 agonists (e.g. salbutamol)
Anticholinergics (e.g. ipratropium bromide)
Long acting beta 2 agonists (if > 2 exacerbations per year)
Steroids
Inhaled beclamethasone considered in all patients with FEV1 < 50% of predicted
OR
> 2 exacerbations per year
Regular oral steroids should be avoided if possible
Pulmonary rehabilitation
Oxygen therapy
Only for those who stop smoking
Indicated if:
PaO2 < 7.3 kPa on air during a period of clinical stability
PaO2: 7.3 - 8 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension
Treatment of Acute Exacerbations
24 % O2 via Venturi mask
Increase slowly if no hypercapnia and still hypoxic (do an ABG)
Corticosteroids
Start empirical antibiotic therapy if evidence of infection
Respiratory physiotherapy to clear sputum
Non-invasive ventilation may be necessary in severe cases
Prevention of infective exacerbations: pneumococcal and influenza vaccination
Identify the possible complications of chronic obstructive pulmonary disease (COPD) and its management
Acute respiratory failure Infections Pulmonary hypertension Right heart failure Pneumothorax (secondary to bullae rupture) Secondary polycythaemia
Summarise the prognosis for patients with chronic obstructive pulmonary disease (COPD)
High morbidity 3 year survival of 90% if < 60 yrs, FEV1 > 50% predicted 3 year survival of 75% if > 60 yrs, 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. Also known as hypersensitivity pneumonitis.
Explain the aetiology/risk factors for extrinsic allergic alveolitis
Inhalation of antigenic dusts induce a hypersensitivity response in susceptible individuals
Antigenic dusts include microbes and animal proteins
Examples:
Famer’s Lung - caused by mouldy hay containing thermophilic actinomycetes
Pigeon Fancier’s Lung - caused by blood on bird feathers and excreta
Maltworker’s Lung - caused by barley or maltlings containing Aspergillus clavatus
Summarise the epidemiology of extrinsic allergic alveolitis
Uncommon
2% of occupational lung disease
50% of reported cases affect farm workers
Geographical variation
Recognise the presenting symptoms of extrinsic allergic alveolitis
Acute Present 4-12 hrs after exposure REVERSIBLE episodes of: Dry cough Dyspnoea Malaise Fever Myalgia Wheeze and productive cough may develop if repeat high-level exposure CHRONIC Slowly increasing breathlessness Decreased exercise tolerance Weight loss Exposure is usually chronic, low-level and there may be no history of previous acute episodes IMPORTANT: make sure you get a full occupational history and enquire about hobbies and pets
Recognise the signs of extrinsic allergic alveolitis on physical examination
ACUTE Rapid shallow breathing Pyrexia Inspiratory crepitations CHRONIC Fine inspiratory crepitations Clubbing (rare)
Identify appropriate investigations for extrinsic allergic alveolitis
Bloods FBC - neutrophilia, lymphopenia ABG - reduced PO2 + PCO2 Serology Test for IgG to fungal or avian antigens NOTE: these are not diagnostic because you may find these in normal individuals CXR Often NORMAL in acute episodes Fibrosis may be seen in chronic cases High Resolution CT-Thorax Detects early changes May show patchy 'ground glass' shadowing and nodules Pulmonary Function Tests Restrictive defect (low FEV1, low FVC) Preserved or increased FEV1/FVC ratio Reduced total lung capacity Bronchoalveolar Lavage Increased cellularity Lung biopsy can also be performed
Define idiopathic pulmonary fibrosis
Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium.
Previously known as cryptogenic fibrosing alveolitis.
Explain the aetiology/risk factors of idiopathic pulmonary fibrosis
Occurs in genetically predisposed individuals
Recurrent injury to alveolar epithelial cells results in secretion of cytokins and growth factors
This leads to fibroblast activation, recruitment, proliferation, differentiations into myofibroblasts and increased collagen synthesis and deposition
Certain drugs can produce similar illness (e.g. methotrexate, amiodarone)
Histological Patterns
Interstitial pneumonia
Risk factors
Smoking
Occupational exposure to metal or wood
Chronic microaspiration
Animal or vegetable dusts
Summarise the epidemiology of idiopathic pulmonary fibrosis
Rare
6/100,000
More common in males
Recognise the presenting symptoms of idiopathic pulmonary fibrosis
Gradual-onset, progressive dysponea on exertion
Dry irritating cough
No wheeze
Symptoms may be preceded by a viral-type illness
Fatigue and weight loss are common
IMPORTANT: take a full occupational and drug history
Recognise the signs of idiopathic pulmonary fibrosis on physical examination
Clubbing (50%)
Bibasal fine late inspiratory crackles
Signs of right heart failure in advanced stages of disease
Identify appropriate investigations for idiopathic pulmonary fibrosis
Bloods
ABG
Normal in early disease
PO2 decreases with exercise
Normal PCO2, which rises in late stage disease
ANA and Rheumatoid Factor
1/3 of patients are positive for ANA or RF
CXR
Usually NORMAL at presentation
Early disease may show ground glass shadowing
Later stage disease shows reticulonodular shadowing, signs of cor pulmonale and, eventually, honeycombing
High-resolution CT
More sensitive in early disease than CXR
Pulmonary Function Tests Restrictive features (reduced FEV1 and FVC, with preserved or increased FEV1/FVC) Decreased lung volumes Decreased lung compliance Decreased total lung capacity
Bronchoalveolar Lavage - excludes infections and malignancy
Lung biopsy - gold standard for diagnosis
Echocardiography - to check for pulmonary hypertension
Define obstructive sleep apnoea
A disease characterised by recurrent prolapse of the pharngeal airway and apnoea (cessation of airflow for >10s) during sleep, followed by arousal from sleep.
Also known as Pickwickian syndrome
Explain the aetiology/risk factors of obstructive sleep apnoea
Occurs due to narrowing of the upper airways because of the collapse of soft tissues of the pharnx
This is due to decreased tone of the pharyngeal dilators during sleep
Associated with:
Weight gain
Smoking
Alcohol
Sedative use
Enlarged tonsils and adenoids in children
Macroglossia
Marfan’s syndrome
Craniofacial abnormalities
Summary the epidemiology of obstructive sleep apnoea
Common
5-20% of men >35 years
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 Dry mouth Difficulty concentrating Irritability and mood changes Partner reporting snoring, noctural apnoeic episodes or noctural choking
Recognise the signs of obstructive sleep apnoea on physical examination
Large tongue Enlarged tonsils Long or thick uvula Retrognathia (pulled back jaws) Neck circumference More than 42cm or 40cm in males and females respectively Obesity Hypertension
Identify appropriate investigations for obstructive sleep apnoea
Sleep study Monitor airflow, respiratory effort, pulse oximetry and heart Bloods TFTs ABG
Define pneumoconiosis
Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts
Types:
Simple: Coalworker’s pneumoconiosis or silicosis (symptom-free)
Complicated: pneumoconiosis results in loss of lung function
Asbestosis: a pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos
Explain the aetiology/risk factors for pneumoconiosis
Caused by inhalation of particles of: Coal dust, silica, asbestos
Risk factors:
Occupational exposure (coal mining, quarrying, iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, ship builders)
Risk is dependent on extent of exposure and the size/shape of particles
Individual susceptibility is also important
Co-factors such as smoking and TB also contribute
Summarise the epidemiology of pneumoconiosis
Incidence is increased in developing countries
Disability and mortality from asbestosis will continue to increase for the next 20-30 years
Recognise the presenting symptoms of pneumoconiosis
Occupational history is very important
Asymptomatic - picked up on routine CXR
Symptomatic - insidious onset shortness of breath, dry cough, black sputum (melanoptysis) - produced occasionally in coalworker’s pneumoconiosis
Pleuritic chest pain (due to acute asbestos pleurisy) - in patients exposed to asbestos
Recognise the signs of pneumoconiosis on physical examination
Examination may be normal
Coalworker’s pneumoconiosis and silicosis:
Decreased breath sounds
Asbestosis:
End-inspiratory crepitations
Clubbing
Signs of pleural effusion or right heart failure (cor pulmonale)
Identify appropriate investigations for pneumoconiosis
CXR
Simple: micronodular mottling
Complicated:
Nodular opacities in upper lobes
Micronodular shadowing
Eggshell classification of hilar lymph nodes (characteristic of silicosis)
Bilateral lower zone reticulonodular shadowing and pleural plaques (in asbestosis)
CT Scan - fibrotic changes can be visualised early
Lung Function tests - restrictive pattern
Define pneumonia
Infection of distal lung parenchyma. It can be categorised in many ways: Community-acquired Hospital-acquired/nosocomial Aspiration pneumonia Pneumonia in the immunocomprised Typical Atypical (Mycoplasma, Chlamydia, Legionella)
Explain the aetiology/risk factors of pneumonia
Community-Acquired Streptococcus pneumoniae (70%) Haemophilus influenzia Moraxella catarrhalis (occurs in COPD patients) Chlamydia pneumonia Chlamydia psittaci (causes psittacosis) Mycoplasma pneumonia Legionella (air conditioning) Staphylococcus aureus Coxiella burnetii (causes Q fever) TB
Hospital-Acquired
Gram-negative enterobacteria (Pseudomonas, Klebsiella)
Anaerobes (due to aspiration pneumonia)
Risk factors Age Smoking Alcohol Pre-existing lung disease (COPD) Immunodeficiency Contact with patients with pneumonia
Summarise the epidemiology of pneumonia
5-11/1000
Community-acquired pneumonia is responsible for >60,000 deaths per year in the UK
Recognise the presenting symptoms of pneumonia
Fever Rigors Sweating Malaise Cough Sputum Breathlessness Pleuritic chest pain Confusion (in severe cases or in the elderly)
Atypical Pneumonia Symptoms: Headache Myalgia Diarrhoea/abdominal pain Dry cough
Recognise the signs of pneumonia on physical examination
Pyrexia Respiratory distress Tachypnoea Tachycardia Hypotension Cyanosis Decreased chest expansion Dull to percuss over affected area Increased tactile vocal fremitus over affected area Bronchial breathing over affected area Coarse crepitations on affected side Chronic suppurative lung disease (empyema, abscess) --> clubbing
Identify appropriate investigations for pneumonia
Bloods FBC - raised WCC U&Es LFT Blood cultures ABG Blood Film - Mycoplasma causes red cell agglutination
CXR
Lobar or patchy shadowing
Pleural effusion
NOTE: Klebsiella often affects upper lobes
May detect complications (e.g. lung abscess)
Sputum/Pleural Fluid - MC&S
Urine - Pneumococcus and Legionella antigens
Atypical Viral Serology
Bronchoscopy and Bronchoalveolar Lavage - if Pneumocystis carinii pneumonia is suspected, or if pneumonia fails to resolve
Generate a management plan for pneumonia
Assess severity using the British Thoracic Society Guidelines
Start empirical antibiotics
Oral Amoxicillin (0 markers)
Oral or IV Amoxicillin + Erythromycin (1 marker)
IV Cefuroxime/Cefotaxime/Co-‐amoxiclav + Erythromycin (> 1 marker)
Add metronidazole if:
Aspiration
Lung
abscess
Empyema
Switch to appropriate antibiotic based on sensitivity
Supportive treatment
Oxygen
IV
fluids
CPAP, BiPAP or ITU care for respiratory failure
Surgical drainage may be needed for lung abscesses and empyema
Discharge planning
If two or more features of clinical instability are present (e.g. high temperature, tachycardia, tachypnoea, hypotension, low oxygen sats) there is a high risk of re-admission and mortality
Consider other causes if pneumonia is not resolving
Prevention
Pneumococcal vaccine
Haemophilus influenzae type B vaccine
These are only usually given to high risk groups (e.g. elderly, splenectomy)
Identify the possible complications of pneumonia
Pleural effusion Empyema Localised suppuration (e.g. abscess) Symptoms of abscesses: Swinging fever Persistent pneumonia Copious/foul-smelling sputum Septic shock ARDS Acute renal failure Extra complications of Mycoplasma pneumonia Erythema multiforme Myocarditis Haemolytic anaemia Meningoencephalitis Transverse myelitis Guilliain-Barre syndrome
Summarise the prognosis for patients with pneumonia
Most resolve within treatment within 1-3 weeks
Severe pneumonia has a high mortality
The CURB-65 score is used to assess the severity of pneumonia:
Confusion <8 AMTS
Urea > 7 mmol/L
Respiratory rate >30/min
Blood pressure: systolic < 90 mmHg or diastolic < 60 mmHg
Age > 65 years
Define pneumothorax
Air in the pleural space
There are some other variants in which other substances are found in the pleural space:
Haemothorax - blood
Chylothorax - lymph
Explain the aetiology/risk factors of pneumothrax
Spontaneous
Occurs in people with typically normal lungs
Typically in tall, thin males
It is probably caused by the rupture of a subpleural bleb
Secondary
Occurs in patients with pre-existing lung disease (e.g. COPD, asthma, TB)
Traumatic
Caused by penetrating injury to the chest
Often iatrogenic (e.g. during jugular venous cannulation, thoracocentesis)
Risk factors
Collage disorders (e.g. Marfan’s syndrome, Ehler’s-Danlos syndrome)
Summarise the epidemiology of pneumothorax
Annual incidence: 9/100,000
Mainly in 20-40 years old
4 x more common in males
Recognise the presenting symptoms of pneumothorax
May be asymptomatic if the pneumothorax is small
Sudden-onset breathlessness
Pleuritic chest pain
Distress with rapid shallow breathing in tension pneumothorax
Recognise the signs of pneumothorax on physical examination
There may be no signs if the pneumothorax is small Signs of respiratory distress Reduced expansion Hyper-resonance to percussion Reduced breath sounds
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
CXR
It will show a dark area of film with no vascular markings
Fluid level may be seen if there is any bleeding
ABG - check for hypoxaemia
Generate a management plan for pneumothorax
Tension pneumothorax (emergency)
Max O2
Insert large bore needle into 2nd intercostal space MCL
Up to 2.5L of air can be aspirated
Stop if patient coughs or resistance is felt
Follow up CXR 2 hours and 2 weeks later
Chest Drain with Underwater Seal
Performed if:
Aspiration fails
Fluid in the pleural cavity
After decompression of a tension pneumothorax
Inserted in the 4th-6th intercostal space midaxillary line
Recurrent Pneumothoraces
Chemical pleurodesis (fusing of visceral and parietal pleura with tetracycline or calc)
Surgical pleurectomy
Advice
Avoid air travel until follow-up CXR confirms that pneumothorax has resolved
Avoid diving
Identify the possible complications of pneumothorax
Recurrent pneumothoraces
Bronchopleural fistula
Summarise the prognosis for patients with pneumothorax
After having one pneumothorax, at least 20% will have another
Frequency increased with repeated pneumothoraxes
Define pulmonary embolism
Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site
Explain the aetiology / risk factors of pulmonary embolism
Thrombus 95% arise from DVT in the lower limbs Rarely arises in the right atrium (in AF patients) Other causes of embolus: Amniotic fluid Air Fat Tumour Mycotic
Risk Factors Surgical patients Immobility Obesity OCP Heart failure Malignanc
Summarise the epidemiology of pulmonary embolism
Relatively COMMON (especially in hospitalised patients) Occur in 10 - 20% of patients with confirmed proximal DVT
Recognise the presenting symptoms of pulmonary embolism
Depends on the SITE and SIZE of the embolus
Small
may be ASYMPTOMATIC
Moderate Sudden onset SOB Cough Haemoptysis Pleuritic chest pain
Large (or proximal) As above and: Severe central pleuritic chest pain Shock Collapse Acute right heart failure Sudden death Multiple Small Recurrent Symptoms of pulmonary hypertension
Recognise the signs of pulmonary embolism on physical examination
Severity of PE can be assessed based on associated signs:
Small
often no clinical signs. There may be some tachycardia and tachypnoea
Moderate Tachypnoea Tachycardia Pleural rub Low O2 saturation ( despite O2 supplementation)
Massive PE Shock Cyanosis Signs of right heart strain Raised JVP Left parasternal heave Accentuated S2 heart sound
Multiple Recurrent PE
Signs of pulmonary hypertension
Signs of right heart failure
Identify appropriate investigations for pulmonary embolism and interpret the results
The Well's Score is used to determine the best investigation for PE Low Probability (Wells 4 or less) - use D dimer High Probability (Wells > 4) required imaging (CTPA)
Additional investigations:
Bloods - ABG, thrombophilia screen
ECG
May be normal
May show tachycardia, right axis deviation or RBBB
May show S1Q3T3 pattern
CXR
often NORMAL
but helps exclude other diagnoses
Spiral CT Pulmonary Angiogram FIRST LINE INVESTIGATION Poor sensitivity for small emboli VERY sensitive for medium to large emboli
Ventilation - Perfusion (VQ) Scan
Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung
Pulmonary Angiography
Invasive
Rarely necessary
Doppler US of Lower Limb
allows assessment of venous thromboembolism
Echocardiography
may show right heart strain
Generate a management plan for pulmonary embolism
Primary Prevention
Compression stockings
Heparin prophylaxis for those at risk
Good mobilisation and adequate hydration
If haemodynamically stable O2 Anticoagulation with heparin or LMWH Switch over to oral warfarin for at least 3 months Maintain INR 2 - 3 Analgesia
If haemodynamically UNSTABLE (massive PE)
Resuscitate
O2
IV fluids
Thrombolysis with tPA may be considered if cardiac arrest is imminent
Surgical or radiological
Embolectomy
IVC filters
sometimes used for recurrent PEs despite adequate anticoagulation or
when anticoagulation is contraindicated
Identify the possible complications of pulmonary embolism and its management
Death
Pulmonary infarction
Pulmonary hypertension
Right heart failure
Summarise the prognosis for patients with pulmonary embolism
30% mortality in those left untreated
8% mortality with treatment
Increased risk of future thromboembolic disease
Define sarcoidosis
• Multisystem granulomatous inflammatory disorder
Explain the aetiology/risk factors of sarcoidosis
• UNKNOWN
• Transmissible agents (e.g. viruses), environmental triggers and genetic factors have all been suggested
• Pathogenesis
o An UNKNOWN antigen is presented on MHC class 2 complexes on macrophages to CD4+ T-lymphocytes
o These accumulate and release cytokines
o This leads to the formation of non-caseating granulomas in organs
Summarise the epidemiology of sarcoidosis
- Most common in AFRICANS and SCANDINAVIANS
* Can occur at any age but tends to be in adults > 50 yrs
Recognise the presenting symptoms and the signs of sarcoidosis
• General Symptoms o Fever o Malaise o Weight loss o Bilateral parotid swelling o Lymphadenopathy o Hepatosplenomegaly • Pulmonary Symptoms o Breathlessness o Dry cough o Chest discomfort o Minimal clinical signs • Musculoskeletal Symptoms o Bone cysts (e.g. dactylitis) o Polyarthralgia o Myopathy • Eye Symptoms o Keratoconjunctivitis sicca (inflammation of the conjunctivitis and surrounding tissues due to the eyes being dry)
o Uveitis
o Papilloedema
• Skin Symptoms
o Lupus pernio (red-blue infiltrations of the nose, cheeks, ears and terminal phalanges)
o Erythema nodosum o Maculopapular eruptions • Neurological Symptoms o Lymphocytic meningitis o Space-occupying lesions o Pituitary infiltration o Cerebellar ataxia o Cranial nerve palsies o Peripheral neuropathy • Cardiac Symptoms o Arrhythmia o Bundle branch block o Pericarditis o Cardiomyopathy o Congestive cardiac failure
Identify appropriate investigations for sarcoidosis
• Bloods o High serum ACE o High calcium o High ESR o FBC - WCC may be low due to lymphocyte sequestration in the lungs o Immunoglobulins - polyclonal hyperglobulinaemia o LFTs - high ALP + GGT • 24 hr Urine Collection o Hypercalciuria • CXR o Stage 0 - may be clear o Stage 1 - bilateral hilar lymphadenopathy
o Stage 2 - stage 1 with pulmonary infiltration and paratracheal node enlargement
o Stage 3 - pulmonary infiltration and fibrosis
• High-Resolution CT Scan
o Check for diffuse lung involvement
• Gallium Scan - shows areas of inflammation
• Pulmonary Function Tests
o Low FEV1
o FVC shows restrictive picture
• Bronchoscopy and Bronchoalveolar Lavage
o High lymphocytes
o High CD4: CD8 ratio
• Transbronchial Lung Biopsy (or lymph node biopsy)
o Shows non-caseating granulomas consisting of:
• Epithelioid cells (activated macrophages)
• Multinucleate Langerhans cells
• Mononuclear cells (lymphocytes)
Define Tuberculosis
Granulomatous disease caused by Mycobacterium tuberculosis
Primary TB: initial infection may be pulmonary or more rarely gastro
Miliary TB: results from haematogenous dissemination of TB
Post-Primary TB: caused by reinfection or reactivation
Explain the aetiology/risk factors of tuberculosis
Mycobacterium tuberculosis is an intracellular organism
It survives after being phagocytosed by macrophages
Summarise the epidemiology of tuberculosis
Annual mortality = 3 million (95% in developing countries)
Annual UK incidence = 6000
Asian immigratns are the highest risk group in the UK
Recognise the symptoms and signs of tuberculosis
Primary TB: Mostly Asymptomatic Fever Malaise Cough Wheeze Erythema Nodosum Phlyctenular conjuctivits
Miliary TB: Fever Weight loss Meningitis Yellow caseous tubercles spread to other organs
Post-primary TB Fever/night sweats Malaise Weight loss Breathlessness Cough Sputum Haemoptysis Pleuritic chest pain Signs of pleural effusion Collapse Consolidation Fibrosis
Non-pulmonary TB - occurs mainly in the immunocompromised
Lymph nodes - suppuration of cervical lymph nodes leading to abscesses or sinuses
CNS - meningitis, tuberculoma
Skin - lupus vulgaris (jelllylike reddish-brown glistening plaques)
Heart - pericardial effusion, constrictive pericarditis
GI Subacute obstruction Change in bowel habit Weight loss Peritonitis Ascites
Genitourinary UTI symptoms Renal failure Epididymitis Endometrial or tubal involvement Infertility
Adrenal insufficiency
Bone/Joint - osteomyelitis, arthiritis, vertebral collapse (Pott’s disease), spinal cord compression from an abscess
Identify appropriate investigations from tuberculosis
Sputum/Pleural Fluid/Bronchial Washings -MC&S
Note: culturing TB takes a long time (around 6 weeks)
Tuberculin Tests
Positive if the patient has had previous exposure to M.tuberculosis or BCG
Mantoux Test
A purified protein derivative is injected intradermally
Erythema occurs after 72 hours
Heaf Test Place a drop of PPD on the forearm Fire a spring-loaded needle gun Check again after 3-7 days Graded according to papula size and vesiculation
Interferon Gamma Tests
Useful in latent TB
Exposure of host T cells to TB antigens leads to release of interferon
CXR
Primary Infection - Peripheral consolidation & Hilar lymphadenopathy
Miliary Infection - Fine shadowing
Post-Primary - Upper lobe shadowing, Streaky fibrosis and cavitation, Calcification, Pleural effusion, Hilar lymphadenopathy
HIV Testing
CT, lymph nodes, pleural biopsy, sampling of other affected systems
