Respiratory Flashcards
What is the survival and mortality from lung cancer?
- 10% 10 year survival for lung cancer - lowest survival outcome of any cancer
- Low survival usually due to late diagnosis or comorbidities
- Age that lung cancer survival is highest: 15-39 years
- Commonest cause of death from malignant disease - 21% of cancer deaths
- 50% of deaths occur in over 75s
- More common in people living in deprived aras
Describe the aetiology of lung cancer
Smoking is the main cause of lung cancer
Other risk factors
> Environmental tobacco soke
> Ionising radiation: radon, uranium
> Air pollution
> Asbestos
> others: fibrosing conditions of the lung, human papilloma virus, hereditary (polymorphisms in cytochrome p450)
What are the signs and symptoms of lung cancer?
- Cough
- Haemoptysis
- Shortness of breath
- Anorexia / weight loss
- General malaise
Central: usually squamous or small cell carcinoma
> Haemoptysis
> Bronchial obstruction: obstruction pneumonia
> Cough
Peripheral: usually adenocarcinomas
> Few symptoms
> Chest pain if pleura or chest wall involved
How does lung cancer spread locally?
- Pleura: haemorrhagic effusion
- Hilar lymph nodes
- Adjacent lung tissue (may involve large vessels leading to haemoptysis)
- Pericardium: pericardial effusion with subsequent involvement of pericardium
- Mediastinum:
> Superior vena caval obstruction
» Headache, oedema of face & arms, raised JVP
> Recurrent laryngeal nerve: hoarseness if invaded
> Phrenic nerve paralysis e.g. paralysis of right hemidiaphragm, can compromise lung volume
What is a pancoast tumour?
- Tumour that invades apical structures of the lung
- Involvement of the brachial plexus gives sensory & motor symptoms
- Severe pain in the shoulder, scapula, arm
- Weakness in the hands
- Horner’s syndrome aka oculosympathetic play
> Invasion of cervical sympathetic chain
> Symptoms: pupillary constriction, ptosis, enophthalmos, hemifacial anhydrosis (same side of tumour)
How does lung cancer spread distantly?
- Haematogenous: common due to invasion of pulmonary veins
> Liver, bone, brain, adrenal - Lymphatic: cervical lymph nodes
List the non-metastatic effects of lung cancer
- ACTH secretion
> Leads to adrenal hyperplasia
> Raised blood cortisol leads to Cushing’s syndrome - ADH secretion
> Retention of water
> Dilutional hyponatraemia - SIADH - Parathyroid hormone related peptide (PTHrP) secretion
> Osteoclastic activity leads to hypercalcaemia - Other non-metastatic effects
> Encephalopathy
> Cerebellar degeneration
> Neuropathy
> Myopathy
> Eaton Lambert myasthenia-like syndrome
> Cancer-associated retinopathy
List the different pathological types of lung cancer
- Non-small cell lung cancer (NSCLC)
> Adenocarcinoma
> Squamous cell carcinoma
> Large cell carcinoma - Small cell lung cancer (SCLC)
- Other
> Inflammatory myofibroblastic tumour - mesenchymal tissue
> Adenoid cystic carcinoma - salivary gland-type tumours
> Tumours of ectopic origin: germ cell tumours
> Carcinoid
> Lymphoma
Describe the appearance and main characteristics of adenocarcinoma
- Common in females; also seen in non-smokers (but still associated with smoking)
> 2/3 arise in the periphery - Appearance:
> Glandular, solid, papillary or lepidic (lines up along alveolar walls)
> Mucin production - Screened for EGFR mutations: ALK, PD-L1, ROS-1
Describe the appearance and main characteristics of squamous cell carcinoma
- Arises centrally from major bronchi
> Often within dysplastic epithelium following squamous metaplasia - Slow growing and metastasise late (good for surgery)
- May undergo cavitation
- May block bronchi leading to retention pneumonia or collapse
Appearance: malignant epithelial tumour showing keratinization and intercellular bridges
In situ squamous cell carcinoma may be seen in adjacent airway mucosa
Describe the appearance and main characteristics of large cell carcinoma
- Diagnosis of exclusion
- Usually arises centrally
- Undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC & glandular or squamous differentiation
Describe the appearance and main characteristics of small cell lung cancer
Usually advanced at diagnosis - most aggressive form of lung cancer
> Metastasises early and widely
Responds to chemotherapy but most patients relapse
Appearance
> Oval to spindle shaped cells
> Inconspicuous nucleoli
> Scant cytoplasm
> Nuclear moulding
Describe the appearance and main characteristics of carcinoid tumours
- Neuroendocrine tumour, classified as typical or atypical
- Can be central or peripheral & can metastasise but much better prognosis than other lung cancers
- Histology
> Polypoid nodule in bronchus
> Well-circumscribed outline
> Lymphoma (purple)
Describe the pathogenesis of lung cancer
Lung cancer is a multi-step process which involves the chronic irritation of cells by carcinogens
> There is increased cell turnover and progressive accumulation of genetic abnormalities in molecules involved in cell cycle, signalling & angiogenesis pathways
Phenotypic changes are potentially reversible but genotypic alterations persist
> Normal tissue > hyperplasia > metaplasia > dysplasia > carcinoma in situ > invasive cancer > metastasis
Describe the targeted therapies used in non-small cell lung cancers
Non-squamous non-small cell lung cancer:
EGFR receptor mutations: tyrosine kinase inhibitors
EML4-ALK gene fusions: ALK inhibitors
ROS-1 oncogenic fusion
KRAS mutations: sotorasib
BRAF mutations: BRAF inhibitors
All NSCLC:
PD-L1: PD-L1 inhibitors
List cancers that frequently metastasise to the lung
Breast
Colon
Head & neck
Kidney - cannonball metastases
Testicular carcinoma
Sarcoma
Name the stain used in TB to identify AAFB (acid alcohol fast bacilli)
Ziehl-Neelsen stain
Describe the cause, characteristics and histology of mesothelioma
Mesothelioma is a primary pleural tumour (also occurs in peritoneum, pericardium & tunica vaginalis)
Cause: asbestos exposure
> Asbestos bodies can be found in the lung (bronchial washings) - macrophages try to eat refractile fibre and release free radicals
Very long lag period before disease develops
Histology: either epithelioid or sarcomatoid appearance or both (biphasic)
Malignant mesothelioma: compression of the lung causes respiratory compromise
> Characteristic feature: invasion of horizontal fissure
List signs and symptoms of pleural effusion
Symptoms
- Dyspnoea
- Fever
- Sputum
- Cachexia
- Fatigue
- Haemoptysis
- Chest pain
- Cough
Signs
- Fingernail clubbing
- Ascites
- Lymphadenopathy
- Chest: coarse crackles, stony dullness on percussion, reduced breath sounds
- decreased vocal resonance and decreased vocal fremitus
How do you differentiate between a transudate and an exudate?
Light’s criteria
Any 1 of 3: exudate
Protein level > 30g/l
Fluid protein:serum protein ratio > 0.5
Fluid LDH:serum LDH ratio >0.6 or Fluid LDH > 2/3 maximum serum normal
List the causes of pleural effusion
Transudate
> Heart failure
> Cirrhosis
> Renal failure - nephrotic syndrome
> Hypothyroidism
> Hypoalbuminaemia
> Peritoneal dialysis
> Protein losing enteropathy
Exudate
> Malignancy
> Infection
> Empyema
> TB
> Haemothorax
> PE
> Pancreatitis
> Drug induced
> Post-CABG
Which investigations are used to diagnose a pleural effusion?
CXR - meniscus sign
CT scan
Ultrasound
Bloods: CRP, WCC
Sampling: never drain undiagnosed effusion, limits diagnosis
> Local anaesthetic thoracoscopy: direct visual examination of pleural with a thoracoscope (used in undiagnosed cytology negative pleral effusion)
How are pleural effusions managed?
Management is symptom-driven (i.e. only treat if symptomatic, like dyspnoea)
> Chest drain +/- talc pleurodesis
> Talc pleurodesis sticks lung to chest wall, removing space between lung & chest wall so fluid does not build up between layers
Indwelling pleural catheter is an option if talc fails or lung is trapped
Describe the different types of pleural infection and their management
50% of pneumonias have an associated effusion
> Complex parapneumonic effusion
> pH < 7.2
> LDH > 1000
> Glucose <2.2
> Loculated on ultrasound
> Drain
> Empyema
> Presence of pus or bacteria: quickly drain, severe condition
Management
> Drainage 12-16F
> IV antibiotics
> Fibrinolytics
> Surgery
Describe the pathophysiology of allergy
Immediate:
Recognition of antigen by APC & T cells
IgE & mast cell mediated
> production of IL-4 & IL-13
Delayed:
Mediated by reactive T cells
Production of IL-12 & interferon gamma
Define asthma
Allergic inflammation of the airway characterised by reversible obstruction and diurnal variation
Describe the pathophysiology of asthma
Characterised by invasion of macrophages & T lymphocytes
Scabby epithelium and thickened basement membrane
Thickened smooth muscle with mast cells within
> Contain granules with histamine and leukotrienes which trigger smooth muscle constriction
Mucociliary impairment leads to sputum production
Turbulent airflow caused by expiratory phase narrowing leads to wheeze and breathlessness
Bronchial hyperreactivity and hypersensitivity
List asthma triggers
- Exercise
- Cold
- Allergen exposure (dust mites, cats)
- Chemical exposure: salicylates/aspirin, spicy food, perfume, NSAIDs, beta blockers
- Viral infections
Describe the tests used in the diagnosis of asthma
- Peak flow measurements: diurnal variation
- Methacholine or histamine challenge: bronchial hyperresponsiveness
» Drop of >20% FEV1 by <8 mg/ml methacholine (may also use histamine or mannitol) - Spirometry: reversible airflow obstruction - improvement >15% in FEV1 after 5mg nebulised salbutamol
- Skin scratch test: allergens
Describe the management of asthma
- Short acting beta agonist: salbutamol
- Corticosteroids: beclomethasone, budesonide
- Long acting beta agonist: salmeterol
- Leukotriene receptor antagonists: montelukast
- Long acting muscarinic antagonist: ipratropium
- Biological therapy
> Anti-IgE: omalizumab
> Anti-TNF: infliximab
> IL-5: mepolizumab
> IL-13: - Interventional: bronchial thermoplasty, vagus nerve ablation
List the features of acute severe and life-threatening asthma
Severe asthma
> Peak expiratory flow: 33-50% of normal
> Can’t complete sentences in one breath
> Respiratory rate > 25 breaths per minute
> Pulse >110 bpm
Life-threatening
> PEFR <33% predicted
> SpO2 <92%
> Silent chest, cyanosis, feeble respiratory effort
> Arrhythmia or hypotension
> Exhaustion, altered consciousness
> ABG: severe hypoxia, lowered pH
Describe the management of an acute severe asthma attack
Oxygen to maintain SpO2 94-98%
Salbutamol 5mg or terbutaline 10mg via an oxygen-driven nebuliser
Prednisolone (oral) 40-50mg
> Or hydrocortisone IV 100mg if unable to take oral
If life-threatening features are present
> IV magnesium sulphate 1.2-2g infusion over 20 minutes
> Nebulised beta 2 agonist more frequently e.g. salbutamol 5mg up to every 15-30 minutes
> If patient is still not improving senior clinical may consider use of IV salbutamol or aminophylline or progression to mechanical ventilation
After discharge: treatment with oral prednisolone (40-50mg until recovery, minimum 5 days) & ICS
Describe extrinsic allergic alveolitis (EAA) and its triggers
aka hypersensitivity pneumonitis
Acute illness due to type III reaction - serum sickness or immune complex sickness
Subacute: days to weeks
> Type IV: T-cell mediated reaction
Triggers
> Each one has an antibody that can be measured in serum e.g. avian precipitans
- Bird dander
- Mushroom worker’s lung
- Farmer’s lung: fungal spores (Micropolyspora faeni) - secondary to exposure to mouldy hay in stables
- Aspergillus lung
- Cheese workers or mollusc shell workers
- Malt worker’s lung or humidifier lung
Describe the clinical presentation of EEA
4-6h after exposure
- Wheeze
- Cough
- Fever
- Chills
- Headache
- Myalgia
- Malaise
- Fatigue
Describe the pathophysiology of EEA
Immune complex disease: acute inflammation, neutrophils, consolidation
Impairment of lung function
> Thickening of septae, filling alveoli with fluid
> Passive movement of gas by diffusion is reduced: type 1 respiratory failure
> Measured by carbon monoxide gas transfer during full PFTs
> Airspace shadowing on CXR
> Biopsy shows a granuloma with giant cells
> CT scan: bilateral ground glass changes
Chronic exposure
> Pulmonary fibrosis: interstitial scarring from chronic tissue remodelling / repair pathways
> Emphysema: interstitial destruction from neutrophilic enzyme release
Describe the management of EEA
- Allergy: avoid trigger
- Inflammation
> Corticosteroids - Oxygen supplementation
Describe how interstitial lung disease presents on pulmonary function tests
- Restrictive effects
> Reduced RV & TLC
> Reduced FEV1 & FVC but normal or even increased FEV1/FVC ratio on spirometry
Gas exchange
> Decreased PaO2 and increased A-a O2 gradient: decreased DLCO and V/Q mismatch
> PaCO2 is normal: eucapnia maintained by increased VE until late
Define and list the risk factors for idiopathic pulmonary fibrosis (IPF)
IPF is a form of chronic fibrosing interstitial lung disease of unknown aetiology; it is limited to the lung and worsens over time
Risk factors
> Smoking: current or ex-smokers 1.6x more likely
> Male sex
> Heartburn (acid reflux): treat with PPI
> Age: age of onset >50 years
> Genetics: 2-5% of IPF cases are familial
List the signs and symptoms of IPF
- Progressive dyspnoea: gradual onset
- Fingernail clubbing (2/3)
- Productive cough
- Cyanosis
- Crackles
> Fine bilateral, bibasal
> End-inspiratory crackles - Progression over months-years
Describe the pathophysiology of IPF
- Repeated cycles of injury and repair - an unidentified agent causes epithelial injury
> Dysregulated repair process leads to fibrosis - Reduced compliance, lung capacity & gas exchange
- Harder breathing is required to take up oxygen & oxygen levels fall with time
List the investigations used in IPF
- Spirometry: restrictive
- CXR: reticular pattern
> Tends to affect periphery & lower zones
> Bibasal + posterior
> Honeycomb change reflects true fibrotic process - Surgical lung biopsy
> Usual interstitial pneumonia (UIP) is the histopathological appearance
> Fibroblast foci & honeycomb cysts - High resolution lung CT
What is the prognosis for IPF?
Gradual deterioration, median survival 3-5 years, 10 year survival <15%
Acute exacerbation
> Clear increase in symptoms over 30 days or less
> New X-ray changes in both lungs (absence of infection or other causes)
> High risk
» In-hospital mortality >50%
» 1 Year survival is 22%
» No difference between subtypes of ILD (IPF v non-IPF)
Describe the treatment for IPF
Anti-fibrotic drugs
> Pirfenidone and nintadenib: slow deterioration of IPF
Oxygen
> Home and portable oxygen if in respiratory failure
Pulmonary rehabilitation
> Improvement in dyspnoea but must be continued to sustain benefits
Lung transplant
> <65 years
Immunosuppressive treatment is not beneficial
Define and list the signs and symptoms of sarcoidosis
Sarcoidosis is a multi-system granulomatous disorder of unknown cause characterised by the classic triad of bilateral hilar lymphadenopathy, erythema nodosum (shin rash) and arthritis
Other signs
- fatigue
- fever
- weight loss
- dry cough
- dyspnoea
- chest discomfort
- sweats
- lungs involved in 90% of cases
- female > male, peak age 20-39 years
Which investigations are used in sarcoidosis?
CXR
Bilateral hilar lymphadenopathy progresses to bilateral hilar lymphadenopathy + parenchymal changes and eventually pulmonary fibrosis
Bronchoscopy
> Cytology or biopsy to confirm diagnosis
> exclude lymphoma, TB or lung cancer
Bronchoalveolar lavage (BAL)
> Lymphocytic alveolitis
Transbronchial lung biopsy (TBLB)
> Non-necrotising granuloma
Transbronchial needle aspirate (TBNA)
> Needle aspirate of mediastinal lymph node
> Giant cells present in non-necrotising granuloma
Lung function
> Restrictive usually (but obstructive also possible)
Blood tests
> Hb mildly reduced
> ESR elevated
> Calcium is elevated (altered vitamin D metabolism)
> Increased gamma globulins
> ACE increased in 60%
Describe the treatment of sarcoidosis, its prognosis and associated causes of death
Most cases need no treatment - steroids if declining lung function
Prognosis
> mainly good, >50% resolve by 3 years
> progressive fibrosis in 25%
> <5% die
Causes of death: fibrotic lung disease or complications of cardiac or neurological sarcoid
Define COPD and list causes
- Characterised by progressive airflow obstruction
- Not fully reversible - does not change markedly over several months
- Causes
- Smoking
- Burning biomass fuels (wood-burning stoves)
- Coal mining
Air pollution
Explore the pathogenesis of COPD, focusing on the effects of cigarette smoking
- Reduced cilial motility, airway inflammation, mucus hypertrophy and hypertrophy of goblet cells: increased sputum production leads to chronic cough
- Increased protease activity, anti-proteases inhibited
- Oxidative stress - increased free oxygen radicals (hydrogen peroxide)
- Squamous metaplasia - higher risk of lung cancer
> Also increases epithelial permeability, facilitating carcinogen diffusion from alveoli into bloodstream
> Increases risk of other cancers e.g. bladder, oesophageal cancer & cardiovascular risk
How do host genetics impact on the development of COPD?
Alpha 1 antitrypsin deficiency
> Serine proteinase inhibitor
> M alleles: normal variant
> SS and ZZ homozygotes: clinical disease
> Unable to counterbalance destructive enzymes in lung
> Non-smokers get emphysema, smokers get emphysema much earlier
Describe emphysema and the different types
Emphysema is the destruction of lung parenchyma
> Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
> Patients may present with weight loss - too breathless to eat & make meals
» Leads to hypoxaemia and pulmonary hypertension in end-stage disease
Types
- Centri-acinar: damage around respiratory bronchioles, more in upper lobes
- Pan-acinar: uniformly enlarged from the level of the terminal bronchioles distally; can get large bullae
- Paraseptal: does not cause airflow obstruction, subpleural - individuals are prone to pneumothorax as bullae can rupture
Describe the pathophysiology of chronic bronchitis
> Production of sputum on most days for at least 3 months in at least 2 years
> Small airway disease
> Bronchiolitis in airways of 2-3mmm (early feature of COPD)
> Narrowing of bronchioles due to mucus plugging, inflammation and fibrosis
Infiltration of airways with neutrophils, CD4+ & CD8+ lymphocytes, macrophages
> Release inflammatory mediators
» TNF, IL-8
» Neutrophil elastase, proteinase 3, cathepsin G (from activated neutrophils)
> Elastase & MMPs (from macrophages)
> Reactive oxygen species
- Squamous metaplasia
- Mucus gland hyperplasia - mucus plugging
Describe the mechanisms of airflow obstruction in COPD
- Loss of elasticity and alveolar attachments due to emphysema
> Airway collapse on expiration
> Causes airtrapping & hyperinflation > increased work of breathing > breathlessness
> Dynamic hyperinflation: worsening with exercise due to shorter respiratory cycles
> Goblet cell metaplasia with mucus plugging of lumen
> Thickening of the bronchiolar wall: smooth muscle hypertrophy and peribronchial fibrosis
Describe the investigations used in COPD
CXR
> Black lung fields due to decreased vascular markings
> Hyperinflation
> blackened hemidiaphragms
> Heart appears long & thin
> Increased number of anterior rib ends above diaphragm
Spirometry
> Obstructive pattern: FEV1/FVC ratio < 70% (both reduced)
> Flow volume loop shows classical church and steeple pattern: severe airflow obstruction
Stage 1: mild, 80% predicted FEV1
Stage 2: moderate, 50-79% predicted FEV1
Stage 3: severe, 30-49% predicted FEV1
Stage 4: very severe, <30% predicted FEV1
Describe the management of COPD
- Smoking cessation: only intervention which slows progression
- Inhaled bronchodilators
> Short-acting beta agonists: salbutamol (SABA)
> Long-acting beta agonists: salmeterol (LABA)
> Long-acting muscarinic antagonists: tiotropium (LAMA) - Inhaled corticosteroids
> Budesonide and fluticasone - combination inhalers - Oxygen therapy (severe patients)
> If respiratory failure at rest - Oral theophyllines
> Controversial - Mucolytics - carbocysteine
> Thin sputum
> Ease cough - Nebulised therapy
Usually reserved for exacerbations
Describe the “blue bloater” COPD patient
- Low respiratory drive
- Type 2 respiratory failure: low oxygen, high CO2
- Cyanosis
- Warm peripheries
- Bounding pulse
- Flapping tremor
- Confusion, drowsiness
Right heart failure - oedema, raised JVP
Describe the “pink puffer” COPD patient
- High respiratory drive - pulmonary stretch receptors
- Type 1 respiratory failure: low oxygen, low CO2
- Desaturates on exercise
- Pursed lip breathing
- Use accessory muscles
- Wheeze
- Indrawing of intercostals
- Tachypnoea
Compare COPD & asthma
COPD
- Cells: CD8 T lyphocytes, macrophages, neutrophils
- Caused by noxious agent
- Progressive & irreversible
Asthma
- Cells: CD4 T lymphocytes, eosinophils
- Caused by a sensitising agent
- Completely reversible
- Spirometry: >400ml responsibility on spirometry following inhaler
Describe the presentation, assessment and DDX of an acute exacerbation of COPD
- Presentation
- Increased dyspnoea
- Worsening cough
- Increasing sputum volume / purulence
- Asessment / monitoring
- CXR
- ECG
- FBC, U&Es, LFTs & CRP
- Sputum miscroscopy & culture
- Oxygen saturations
- ABG
- DDX
- Pneumonia
- Pneumothorax
- PE
- Left ventricular failure
Lung cancer
Describe the treatment of an acute exacerbation of COPD
Oxygen 28% via venturi mask at 4L/min or 1.2L/min via nasal cannula if SpO2 <88%
Corticosteroids
> Prednisolone oral 25g-40mg each morning for 5 days
○ If patient unable to take oral treatment
> Hydrocortisone IV 100mg immediately
> Then 50mg 6 hourly if need to continue
Bronchodilators
> Nebulisation should be with air
> Supplementary oxygen via nasal cannula during nebulisation
> 1-6L/min to maintain oxygen saturation 88-92%
Salbutamol 2.5-5mg nebules 4x daily
Ipratropium 0.5mg nebules 4x daily (add if poor response to salbutamol)
IV bronchodilators
> Aminophylline infusion may be considered if no response to nebulised therapy
Non-invasive mechanical ventilation (NIMV)
> If worsening repiratory acidosis or hypercapnia despite achieving target oxygen & adequate immediate therapy
Antibiotics
> Indicated in the presence of increased sputum purulence, raised inflammatory markers or focal radiological changes
Mucolytic therapy
Aid sputum clearance: acetylcysteine oral 600mg once daily
If one mass is identified on CXR, what is the DDX?
- Tumour
> Malignant most likely: lung cancer, carcinoid / lymphoma
> Benign: pulmonary hamartoma
- Infection
> Abscess or TB
» Fever, cough, spit, night sweats - Inflammation
> Sarcoid or rheumatoid nodules
If more than one mass is identified on CXR, what is the DDX?
Metastases - weight loss
Infection - fever, cough
Describe the appearance of large abscesses on CXR
Cavity results in appearance of an air-fluid level as lung parenchyma has liquefied
Describe the appearance of different stages of TB on CXR
Primary
- Asymptomatic
- Fever, cough, blood stained spit
- Non-specific infection appearance on CXR
- Right hilar nodes
Post primary
- Reactivation - years later, reduced immunity
- Cavities mainly in upper segments
Miliary
- Haematogenous spread
- Immune compromised
- Poor prognosis
Chronic changes
- Calcification of lungs and nodes
- Scarring of upper zones
List the causes of consolidation and signs of consolidation on CXR
Consolidation consists of replacing air with a collection of substances
> Pus: pneumonia
> Fluid: pulmonary oedema
> Blood: haemorrhage
> Cells: tumour
Air bronchogram: hallmark of consolidation - appearance of solid background instead of air allows contrast & visualisation of airways
- Silhouette sign: loss of normal structures & their silhouettes
- Lingular consolidation: loss of left heart border
- Right lower lobe collapse: loss of silhouette of right diaphragm
- Right middle lobe: loss of right heart border
- Left upper lobe: veil-like opacity, loss of left heart border
- Left lower lobe: loss of left hemidiaphragm border, sail sign (triangular shape seen behind heart)
Define a pneumothorax and describe its causes
A breach of the pleural space leads to free air in the pleural cavity and collapse of the elastic lung
Causes
- Spontaneous
> Primary: no underlying lung disease; risk factors include male, smoker, tall - rupture of subpleural blebs/bullae
> Secondary: underlying disease, emphysema, asthma, pulmonary fibrosis
- Iatrogenic: CT-guided lung biopsy, transbronchial lung biopsy, pleural aspirate
- Traumatic: rib fracture, penetrating chest wall injury/stab wound
Describe the signs and symptoms of pneumothorax
- Symptoms
- Pleuritic chest pain
- Breathlessness
- Respiratory distress
- Signs
- Hyperresonant percussion
- Reduced breath sounds
- Reduced vocal resonance
Describe the diagnosis and treatment of a pneumothorax
- Diagnosis
CXR
○ Tracheal deviation + mediastinal shift to the opposite side
○ Depressed hemidiaphragm - Treatment
Pneumothorax
○ Observation or aspiration or intercostal chest drain (with underwater seal)
○ Depends on size of pneumothorax, symptoms, presence of coexisting lung disease
Tension pneumothorax
○ Immediate needle decompression by inserting a large bore needle (venflon) into the 2nd intercostal space in the midclavicular line
○ Then needs formal intercostal chest drain inserted
○ Don’t wait for CXR to treat
Describe the risks of a tension pneumothorax
One way valve: increased intrapleural pressure
○ Decreased venous return
○ Decreased cardiac output
○ Decreased blood pressure
○ Decreased oxygen saturation
○ PEA arrest without intervention
Pushes other structures: tracheal deviation, compression of great vessels & heart
Which score determines the likelihood of a PE? Include its criteria and management steps
- Wells score
- Pre-test probability score
○ Criteria: haemoptysis, pulse rate, previous VT events
○ > 4 points: PE likely
» Perform CT pulmonary angiogram (CTPA)
□ CTPA positive: anticoagulate > Risk stratification □ CTPA negative > PE suspected: proximal leg vein ultrasound scan > PE not suspected
○ < 4 points: PE unlikely
> Quantitative D dimer test
□ Positive: perform CTPA
□ Negative: unlikely PE
Describe the risk stratification process for PE
High risk - haemodynamic instability
> Systolic BP < 90mmHg or drop >40mmHg for more than 15 mins in absence of other cause
> Cardiac arrest
Intermediate
> Intermediate-high: haemodynamically stable but PESI III-V, RV dysfunction and elevated troponin
> Intermediate-low: haemodynamically stable but PESI III-V, of RV dysfunction and elevated troponin one or none positive
Low: no risk factors
Describe the treatment algorithm for a patient with suspected PE and haemodynamic instability
Assess RV with TTE
> No RV dysfunction: search for other causes of instability
> RV dysfunction: perform CTPA
> > Positive CTPA: treat high risk PE
> Haemodynamic support
> Reperfusion therapy
> > Negative CTPA: search for other causes of instability
What haemodynamic support would be provided to a patient with PE?
Volume optimisation: 500ml saline bolus
Vasopressors and inotropes
Norepinephrine: increased RV inotropy and systemic BP
Dobutamine: increased RV inotropy
Mechanical circulatory support– ECMO: rapid short-term support combined with oxygenator
Discuss the options for reperfusion therapy for PE patients
- Systemic thrombolysis:
> Agents: rtPA (alteplase, tenecteplase), streptokinase, urokinase
> Indication: high risk (massive) PE
- Catheter-directed thrombolysis
> EKOS system, safer in terms of bleeds, lower doses used & allows for direct clot retrieval; however, not readily available and takes time to set up - Surgical embolectomy: rarely performed, high risk
Describe the management of an intermediate and low risk PE
Intermediate risk
- RV dyfunction
- PESI class III-V
- Cardiac troponin
> Elevated: intermediate-high
> > No clear strategy
Monitor closely
Rescue reperfusion is available
Routine use of thrombolysis is not recommended
> Normal: intermediate-low
> Hospitalisation
> Anticoagulation
>Observation to ensure stabilisation
>Routine use of thrombolysis is not recommended
Low risk
> Routine use of thrombolysis is not recommended
Describe the severity score used in pulmonary embolism
PESI score - Pulmonary Embolism Severity Index
> Risk factors for mortality risk
> Age
> Cardiorespiratory disease
> Cancer
> Pulse rate
> Blood pressure
> Oxygen saturation
List complications following a PE
- RV dysfunction
- Right ventricle cannot cope with increased afterload
- Post-thrombotic syndrome
Chronic Thromboembolic Pulmonary Hypertension (CTEPH)
How is residual lung volume measured?
- Unable to measure residual volume in spirometry
- 2 methods
- Helium dilution - inspire known quantity of inert gas
- Body plethysmography
○ Respiratory manoeuvres in a sealed box leads to changes in air pressure
○ Can derive lung volumes
○ Archimedes principles - Lung volumes reduced in restrictive lung diseases
- Increased RV and RV/TLC in obstructive lung disease
List the causes of type 1 and type 2 respiratory failure
- Type 1: low oxygen, normal/low PaCO2
- Aim SpO2 94 - 98%
- Causes
○ Pneumonia
○ Pulmonary embolism
○ Pulmonary oedema
○ Pulmonary fibrosis
- Type 2: low oxygen, high PaCO2
- Aim SpO2 88 - 92%
- Causes
> COPD
> Neuromuscular disease / severe kyphoscoliosis
> Obesity hypoventilation
> Opiate overdose
Describe the formula used to calculate an anion gap and its interpretation
- Calculate for metabolic acidosis differential diagnosis
- Anion gap = [Na+] - ([Cl-] + [HCO3-])
- Normal anion gap 8 - 16 mmol/L
- Acidaemia = high [H+] or low HCO3
- Raised anion gap: making too much H+ or can’t get rid of it
- Renal failure
- Diabetic or other ketoacidosis
- Lactic acidosis
- Toxins e.g. salicylate
- Normal anion gap: losing too much HCO3
- Renal tubular acidosis
- Diarrhoea
- Carbonic anhydrase inhibitors
Ureteric diversion
Define obstructive sleep apnoea
- Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia & sleep fragmentation
- Obstructive sleep apnea syndrome (OSAS) manifests as excessive daytime sleepiness
Describe the mechanisms behind OSAS
Often patients are obese with large neck circumference
- During periods of low muscle tone such as sleep, there is pharyngeal narrowing resulting in negative thoracic pressure
- This results in arousal during sleep, including waking & sleep fragmentation
- If untreated, this leads to
> Blood pressure surge (increased sympathetic activity)
> Increased endothelial damage predisposes patients to cardiovascular & cerebrovascular disease
> > > Heart attacks
Strokes
Right heart strain
Cardiovascular disease
- Sleep disruption
○ Daytime sleepiness
○ Reduced quality of life
○ Road traffic accidents
List risk factors and symptoms of OSAS
Risk factors
- Male sex
- Age >40
- Obesity
- Often overlaps with COPD
Symptoms
- Snoring
- Witnessed apnoeas
- Disruptive sleep - nocturia / choking / dry mouth / sweating
- Unrefreshed sleep
- Daytime somnolence
- Fatigue
- Low mood
- Poor concentration
Describe the assessment of daytime sleepiness in OSAS
Epworth Sleepiness Score
> 0-5 lower normal daytime sleepiness
> 6-10 normal daytime sleepiness
> 11-12 mild excessive daytime symptoms
> 13-15 moderate excessive daytime symptoms
> 16-24 severe excessive daytime symptoms
STOP-BANG questionnaire
Berlin questionnaire
Describe the investigations used in OSAS
Limited polysomnography - limited sleep study
> 5 channel home study
> Oxygen saturations
> Heart rate
> Flow
> Thoracic and abdominal effort (via 2 bands)
> Position
In-patient full polysomnography
> EEG: sleep staging
> Video + audio
> Thoracic & abdominal bands
> Position
> Flow
> Oxygen saturations
> Limb leads
> Snore
Transcutaneous Oxygen Saturations and Carbon dioxide Assessment (TOSCA)
> Home or inpatient
> Indicated for headaches: possibility of CO2 retention overnight
Describe apnoea, hypopnoea, respiratory effort-related arousals and oxygen desaturation (ODI)
- Apnoea
- Cessation (or near cessation) of airflow
- 4% oxygen desaturation lasting >10 secs
- Hypopnoea
Reduction of airflow to a degree insufficient to meet criteria for apnoea - Respiratory effort-related arousals
Arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea - Oxygen desaturation (ODI)
The number of times per hour of sleep that the SpO2 falls >4% from baseline
Describe the Apnoea-Hypopnoea Index (AHI)
- Calculated by adding the number of apnoeas and hypopnoeas and dividing by the total sleep time (in hours)
- AHI >15 is diagnostic of OSA
- OR AHI 5-15 with compatible symptoms
- AHI <5 : normal
- AHI 5-15 : mild
- AHI 16-30 : moderate
AHI >30 : severe
Describe the Apnoea-Hypopnoea Index (AHI)
- Calculated by adding the number of apnoeas and hypopnoeas and dividing by the total sleep time (in hours)
- AHI >15 is diagnostic of OSA
- OR AHI 5-15 with compatible symptoms
- AHI <5 : normal
- AHI 5-15 : mild
- AHI 16-30 : moderate
AHI >30 : severe
Describe the treatment of OSAS
- Treat the symptomatic OSAS - daytime sleepiness
- AIM: improve daytime somnolence and quality of life
- Explain OSAS
- Weight loss
- Avoid triggering factors - alcohol
- Treat underlying conditions
- Tonsils
- Hypothyroidism
- Nasal obstruction
- Continuous positive airway pressure (CPAP)
- Splints airway open
- Stops snoring
- Stops sleep fragmentation
- Improves daytime sleepiness + QOL
> Not necessary if no daytime sleepiness
- Mandibular advancement device (MAD)
- Mild-moderate OSAS unable to tolerate CPAP
- Needs good dentition
- Maxillary-mandibular surgery
- Problematic patients
- Severe retrognathia/micrognathia
- Sleep position trainers
- Supine OSA
- Device vibrates when patient lies on back
- Weeks to change sleeping position
Describe the issues OSAS patients may have with driving
- OSAS (day time sleepiness) - likely impairment of driving, inform DVLA
- Patient’s responsibility to inform the DVLA if diagnosed
- OSA without DTS - do not need to stop driving or contact DVLA unless previous history of MVC
- OSAS can hold a Cat I driving license if compliant with treatment and DTS improved
- Assessed every 3 years
Cat 2 licence holders should be assessed within 4 weeks, annual monitoring by DVLA
