Respiratory Flashcards
Define chronic obstructive pulmonary disease
Non-reversible long-term deterioration in air flow through the lungs caused by damage to lung tissue (almost always due to smoking).
2 main types:
* Chronic bronchitis: clinical diagnosis. Daily productive cough for 3+ months, in at least 2 consecutive years. Hypertrophy and hyperplasia of mucous glands, chronic inflammation cells infiltrate bronchi > hypersecretion, ciliary dysfunction, luminal narrowing.
* Emphysema: pathological diagnosis. Permanent enlargement and destruction of airspaces distal to the terminal bronchiole. Destruction of elastin layer causes trapped air distal to blockage (large air sacs = bullae). Centriacinar emphysema = respiratory bronchioles only, smokers. Panacinar emphysema = A1AT deficiency.
Describe the epidemiology for COPD
40-60 years, smokers, males, miners/coal workers
Describe the aetiology for COPD
Smoking, pollution, genetics (A1AT)
Describe the risk factors for COPD
Smoking, increasing age, second-hand smoke exposure, occupational exposure (mining, dust, cotton, wool), pollution (heating fuel, outdoor pollutants), genetics (alpha-1-antitrypsin deficiency)
Describe the pathophysiology for COPD
Obstructed airflow through airways > difficulty ventilating the lungs > shortness of breath and prone to infection. Unlike asthma, not reversible with a bronchodilator.
Patients may experience exacerbations; if due to infections they are called infective exacerbations (H. influenza, S. pneumonia.)
What are the key presentations for COPD
Long-term smoker, shortness of breath, cough, sputum, wheeze, recurrent respiratory infections.
Barrel chest/hyperinflation, hyper-resonance on percussion, distant breath sounds on auscultation.
Describe the clinical manifestations for COPD
Signs: Chronic bronchitis: ‘blue bloaters’, chronic productive cough, purulent sputum, dyspnoea, cyanosis, peripheral oedema, haemoptysis, obesity
Emphysema: ‘pink puffers’, dyspnoea/tachypnoea, minimal cough, pink skin, pursed lip-breathing, accessory muscle breathing, cachexia (body/muscle wasting), hyperinflation (barrel chest), weight loss
What is the gold standard investigation for COPD
Clinical presentation + spirometry (FEV1/FVC <0.7 = obstruction. Bronchodilator irreversible = COPD. Bronchodilator reversible = asthma)
Describe the first line investigations for COPD
Spirometry (FEV1/FVC < 0.7 = shows obstruction. Overall lung capacity is better than their ability to forcefully expire air quickly).
DLCO (diffusion capacity of CO across lung. COPD = low). Pulse oximetry (low O2)
Chest x-ray (hyperinflation, exclude lung cancer/other pathology)
ABG (type 2 respiratory failure – raised pCO2, low pO2).
FBC (chronic hypoxia > polycythaemia). BMI (weight loss - lung cancer). ECG. Serum alpha-1-antitrypsin levels. Sputum culture.
Other: Grades: MRC dyspnoea scale
Grade 1: breathless on strenuous exercise
Grade 2: breathless walking up a hill
Grade 3: breathless that slows on the flat
Grade 4: stop to catch breath after 100m walking on flat
Grade 5: unable to leave house due to breathlessness
What are the differential diagnosis for COPD
Asthma, bronchiectasis, fibrosis, congestive heart failure, lung cancer
Describe the management for COPD
General: stop smoking!! Pneumococcal vaccine, annual flu vaccine
1st line – SABA short acting beta agonist (e.g., salbutamol or terbutaline) OR SAMA short acting muscarinic antagonist (e.g., ipratropium bromide)
2nd line – if no asthmatic/steroid response: LABA long-acting beta agonist (salmeterol), LAMA long-acting muscarinic antagonist (tiotropium). If asthmatic/steroid response: LABA long-acting beta agonist (salmeterol), ICS inhaled corticosteroids (budesonide)
3rd line – LTOT long term oxygen therapy
Describe the complications for COPD
Infective exacerbations: acute worsening of symptoms – SOB, cough, wheeze, sputum. Triggered by infection (H. influenza, S. pneumonia). ABG – raised CO2 > acidosis. Type 2 respiratory failure (raised pCO2, low pO2).
Treatment: steroids (hydrocortisone/prednisolone) + nebulised bronchodilators (salbutamol/ipratropium bromide) + antibiotics (amoxicillin).
Other complications: cor pulmonale, recurrent pneumonia, depression
Define asthma
Chronic, inflammatory condition causing episodes of reversible airway obstruction, airway hyperresponsiveness and inflamed bronchioles, due to bronchoconstriction and excessive secretion production.
Describe the aetiology for asthma
Hypersensitivity of the airways, triggered by: cold air, exercise, cigarette smoke, air pollution, allergens (pollen, cats, dogs, mould), time of day (early morning, night)
Describe the risk factors for asthma
Allergens, atopy, smoking, previous respiratory tract infection, hygienic hypothesis: Growing up in very hygienic environment
Describe the pathophysiology for asthma
Overexpressed TH2 cells in airways exposed to trigger > TH2 cytokine release, IgE production, eosinophil recruitment > IgE mast cell degranulation releasing histamines, leukotrienes, tryptase. Eosinophilia: release of toxic protein > bronchial constriction, mucus hypersecretion
Define Atopic triad and Samter’s triad
Atopic triad: atopic rhinitis, eczema, asthma. Samter’s triad: asthma, aspirin allergy, nasal polyps.
What are the key presentations of asthma
Episodes of wheeze (widespread, polyphonic – multiple musical notes starting and ending at same time), breathlessness, chest tightness and dry cough.
Atopy (family/personal history of eczema/asthma/hayfever).
Diurnal variability (typically worse at night).
What is the gold standard investigation for asthma
Spirometry with reversibility testing. Obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7. Bronchodilator reversible (>12% FEV1 improved).
Describe the first line investigations for asthma
FeNO (fractional exhaled nitric oxide - raised), spirometry (obstruction FEV1:FVC <0.7), peak flow measurement, chest x-ray (normal/hyperinflated), FBC (raised eosinophils or neutrophils)
What are the differential diagnosis for asthma
Cystic fibrosis, COPD, bronchiectasis, alpha-1-antitrypsin deficiency
Describe the management for asthma
Management 1st line – SABA short acting beta 2 adrenergic receptor agonists (salbutamol) – bronchodilation
2 – add ICS inhaled corticosteroids (budesonide) – reduce inflammation and reactivity of airways
3 – add LRTA leukotriene receptor antagonist (montelukast) – block leukotriene effects (inflammation, bronchoconstriction, mucus secretion)
4 – add LABA long-acting beta agonist (salmeterol)
5 – increase ICS dose
For exacerbations OSHITME: oxygen, SABA salbutamol, Hydrocortisone (ICS), Ipratropium bromide, Theophylline, MgSO4, escalate (ventilation – BiPAP bilevel positive airway pressure)
Describe the complications for asthma
Exacerbation, airway remodelling, oral candidiasis/dysphonia (voice disorders) from inhaled steroids
Define tuberculosis
Infectious granulomatous caseating disease caused by mycobacterium tuberculosis bacteria
Describe the epidemiology for tuberculosis
Majority of cases in Africa and South Asia, cause of death for most people with HIV
Describe the aetiology for tuberculosis
Mycobacterium tuberculosis complex (TB causing): M. tuberculosis, M. africanum, M. microtis, M. bovis
Describe the risk factors for tuberculosis
Living/travel to TB area, immunocompromised (e.g. HIV), homeless/crowded housing, IVDU, smoking, alcohol, increasing age
Describe the pathophysiology for tuberculosis
Aerobic, non-motile, non-sporing slightly curved bacilli with a thick waxy mycolic acid capsule. Acid-fast bacilli – stains red/pink with Ziehl Neelsen stain. Slow growing. Resistant to phagolysosomal killing and able to remain dormant by granuloma formation.
TB spreads via respiratory droplets. TB phagocytosed but resists phagolysosomal killing and forms caseating granuloma > T cells recruited and central region of granuloma undergoes caseating necrosis to form Ghon focus in upper lungs > Ghon focus spreads to nearby lymph nodes forming Ghon complex > if TB spreads systemically = miliary TB, if infection in containing within granulomas (dormant, asymptomatic) it is latent TB.
What are the key presentations for tuberculosis
Productive cough (sputum), cough > 3 weeks, haemoptysis, breathlessness, chest pain, lymphadenopathy
Weight loss, low grade fever, anorexia, night sweats, malaise, pyrexia
Describe the clinical manifestations for tuberculosis
Signs of bronchial breathing, dullness on percussion, decreased breathing, fever, crackles.
Extrapulmonary: meningitis, skin changes (erythema nodosum), TB pericarditis symptoms, joint pain (spinal TB – Pott’s disease of spine)
What is the gold standard investigation for tuberculosis
Sputum culture (positive)
Describe the first line investigations for tuberculosis
Chest x-ray (fibronodular opacities on upper lobes), sputum acid-fast bacilli smear 3x (Ziehl Neelsen stains red/pinkusing Lowenstein Jensen culture), biopsy (shows caseating granuloma), sputum culture (positive), FBC (raised WBCs), NAAT (positive for M. tuberculosis)
Diagnosing latent TB: tuberculin skin test ‘Mantoux’ (tuberculin injected in skin and look for induration – thickening/hardening - of 5mm or more), interferon gamma release assay (mixing blood with TB antigens, if a person has already had TB, their WBCs will release interferon gamma)
What are the differential diagnosis for tuberculosis
Covid-19, community acquired pneumonia, lung cancer, sarcoidosis
Describe the management for tuberculosis
Acute TB intensive phase therapy:
* R: rifampicin – 6 months, bactericidal > blocks protein synthesis, SE: red urine, hepatitis
* I: isoniazid – 6 months, bactericidal > blocks cell wall synthesis, SE: neuropathy, hepatitis Give pyridoxine/vit B6 to reduce neuropathy side effects
* P: pyrazinamide – 2 months, bactericidal initially, less effective after, SE: gout, arthralgia, rash, hepatitis
* E: ethambutol – 2 months, bacteriostatic > blocks cell wall synthesis, SE: optic neuritis
Latent TB treatment: isoniazid and rifampicin
All cases must be notified to Public Health England. BCG vaccine available (live attenuated TB)
Describe the complications for tuberculosis
Transmission of TB, ARDS, pneumothorax, emphysema, bronchiectasis
Define pneumonia
Inflammation of the substance of the lungs. It is an acute lower respiratory tract infection. Bacterial infection of the distal airways and alveoli with the formation of an inflammatory exudate.
Community-acquired (pneumonia acquired outside hospital or healthcare facilities),
Hospital-acquired (acute lower respiratory tract infection defined by acquired after at least 48 hours of hospital admission and is not incubating at the time of admission),
Atypical pneumonia (bacterial pneumonia caused by organisms that are not detectable on gram stain and cannot be cultured using standard methods)
Pneumonia in immunocompromised patients (e.g., pneumocystis jirovecii pneumoniae in HIV patients)
Describe the epidemiology for pneumonia
CAP: extremes of ages, Pneumocystis pneumonia is most common in HIV
Describe the aetiology for pneumonia
Bacterial infection:
Community acquired – 1. Streptococcus pneumoniae, 2. Haemophilus influenzae, 3. Mycoplasma pneumoniae.
Hospital acquired – aerobic gram-negative bacilli, e.g., pseudomonas aeruginosa, E. coli, Klebsiella pneumoniae.
Atypical – mycoplasma pneumoniae, Chlamydophila pneumoniae, listeria pneumophila.
Also, viral (influenza, covid-19, CMV) and fungi infection (pneumocystis jirovecii).
Describe the risk factors for pneumonia
Age, smoking, COPD, residence in healthcare setting, poor hygiene, multidrug-resistant bacteria
Describe the pathophysiology for pneumonia
Lower airways should always be sterile in a healthy person.
Invasion and overgrowth of a pathogen in lung parenchyma > overwhelming of host immune defences > production of intra-alveolar exudates and sputum
What are the key presentations for pneumonia
Fever, productive cough (purulent sputum), pleuritic chest pain, dyspnoea, rigors, confusion, haemoptysis, night sweats.
Rusty sputum is characteristic of strep pneumoniae.
Atypical pneumonia: headache, low grade fever, dry cough, malaise
Describe the clinical manifestations for pneumonia
Signs: Increased respiratory rate and heart rate, hypotension.
Dullness to percussion, decreased air entry, bronchial breath sounds (harsh breathing sounds on inspiration and expiration), coarse crackles.
Symptoms: Dyspnoea, tachypnoea, malaise, cough, myalgia, fatigue, headache
What is the gold standard investigation for pneumonia
Chest x-ray shows consolidation: air that fills lung airways is replaced with something else (fluid or solid). Air bronchogram – fluid filled alveoli.
* Pneumonic lesions: multi-lobar – s. pneumonia, s. aureus, legionella.
* Multiple abscesses: s. aureus.
* Upper lobe: Klebsiella but exclude TB first
Describe the first line investigations for pneumonia
FBC (raised WCC), CRP raised, pulse oximetry/ABG (low arterial O2), U&Es (raised urea), blood culture (organism growth), sputum culture and gram stain (growth),
Chest x-ray (consolidation, multi-lobar: s. pneumoniae, s. aureus. Multiple abscesses: s. aureus)
Other: CURB-65 score (to assess severity, 1 point for each):
* Confusion (abbreviated mental test score <8)
* Urea > 7
* Respiratory rate > 30
* BP < 90 systolic AND/OR <60 diastolic
* Age > 65
Score: 0-1 (outpatient treatment), 2 (short-stay inpatient treatment OR hospital-supervised outpatient treatment), 3-5 (manage as high-severity pneumonia)
What are the differential diagnosis for pneumonia
Covid-19, bronchitis, COPD exacerbation, congestive heart failure, tuberculosis
Describe the management for pneumonia
Maintaining O2 saturation between 94-98% (88-92% in COPD patients), analgesia (NSAIDs or paracetamol), IV fluids
CURB-65 guided treatment:
0-1: oral amoxicillin at home
2: consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin, erythromycin)
3+: consider ITU, IV co-amoxiclav + macrolide (clarithromycin + erythromycin)
Atypical pneumonia: 1st line – clarithromycin. Pneumocystis jirovecii pneumonia – co-trimoxazole (trimethoprim/sulfamethoxazole)
Describe the complications for pneumonia
Sepsis, pleural effusion, empysema, lung abscess, ARDS
Describe the prognosis for pneumonia
5-20% mortality
Define cystic fibrosis
Autosomal recessive condition affecting CFTR gene (cystic fibrosis transmembrane conductance regulatory gene on chromosome 7) which codes for chloride channels. Mutation affects mucus glands, resulting in thick mucus plugs.
Describe the epidemiology for cystic fibrosis
Most diagnosed in childhood, 90% before 8 yo
Describe the aetiology for cystic fibrosis
Autosomal recessive mutation in cystic fibrosis transmembrane conductance regulatory (CFTR) gene on chromosome 7 (delta-F508)
Describe the risk factors for cystic fibrosis
Family history, both parent carriers, Caucasians
Describe the pathophysiology for cystic fibrosis
Mutation in CFTR gene leads to a defect in chloride secretion and sodium absorption across airway epithelium. Normal CFTR secretes Cl- and Na+ (+H20) into ductal secretions making them thin and watery. Defect causes thicker secretion due to Cl- and Na+ retention.
Also impaired mucociliary clearance as mucus is thicker > increases stagnation > increases infection risk and difficulty breathing, and increased risk of bronchiectasis.
What are the key presentations for cystic fibrosis
Respiratory: Productive cough and mucus plugs, dyspnoea, recurrent infection (pseudomonas aeruginosa), bronchiectasis, pneumothorax.
Neonates: meconium ileus (bowel obstruction – baby’s first poo is thicker and stickier so causes blockage), failure to thrive.
GIT: thick secretions, exocrine pancreatic insufficiency (malabsorption, steatorrhea), bowel obstruction.
Other: males = atrophy of vas deferens (infertility), very salty sweat.
Describe the clinical manifestations for cystic fibrosis
Low weight and height, nasal polyps, finger clubbing, crackles and wheezes on auscultation, abdominal distention.
What is the gold standard investigation for cystic fibrosis
Sweat test (>60mmol/L Cl-): pilocarpine applied to skin, electrodes send small current causing sweat production, sweat is absorbed and sent to lab for chloride concentration. Diagnostic = over 60mmol/L
Describe the first line investigations for cystic fibrosis
Sweat test (>60mmol/L Cl-)
Chest x-ray (bronchiectasis, hyperinflation)
Faecal elastase decreased (normally elastase produced by pancreas and found in faeces – pancreatic exocrine insufficiency and bowel obstruction decreases it)
Genetic testing (CFTR mutation chromosome 7 – delta-F508) by amniocentesis or chorionic villous sampling
Other: Newborn bloodspot test
What are the differential diagnosis for cystic fibrosis
Primary ciliary dyskinesia, asthma, GORD, coeliac disease
Describe the management for cystic fibrosis
1st line - Respiratory physiotherapy (mobilise mucus from walls – vibrating chest wall devices, positive expiratory pressure devices)
Inhaled mucolytics (dornase alfa), inhaled bronchodilator (salbutamol), empirical antibiotics for infection (tobramycin), anti-inflammatory (azithromycin, ibuprofen), pancreatic enzyme supplementation, CFTR modulator (ivacaftor)
Describe the complications for cystic fibrosis
Infections: s. aureus, h. influenza, p. aeruginosa. Male infertility, chronic respiratory failure, diabetes mellitus, arthritis.
Define bronchiectasis
Chronic inflammation of bronchi/bronchioles resulting in permanent dilation
Describe the aetiology for bronchiectasis
Post-infection (most common): TB, pneumonia, H. influenzae, S. pneumoniae
Other: cystic fibrosis, asthma, HIV, ABPA (allergic bronchopulmonary aspergillosis)
Describe the risk factors for bronchiectasis
Cystic fibrosis, immunosuppressed, previous infections, congenital bronchial airway disorders
Describe the pathophysiology for bronchiectasis
Irreversible dilation and loss of cilia > mucus hypersecretion which increased risk of infection due to decreased muco-ciliary clearance.
Usually affects lower lobes
What are the key presentations for bronchiectasis
Chronic, productive, foul-smelling cough with lots of sputum. Dyspnoea, recurrent respiratory tract infections
Describe the clinical manifestations for bronchiectasis
Signs: Finger clubbing, coarse inspiratory crackles, wheeze, haemoptysis, rhinosinusitis
Symptoms: Fever, fatigue, weight loss
What is the gold standard investigation for bronchiectasis
High resolution chest CT (thickened, dilated bronchi – signet ring sign - and cysts at the end of bronchioles. Big broncho:arterial ratio)
Describe the first line investigations for bronchiectasis
Sputum culture (H. influenzae, S. pneumoniae, P. aeruginosa),
spirometry (obstructive FEV1:FVC <0.7),
chest x-ray (cystic shadows, thickened bronchial walls),
FBC (raised WCC), low serum immunoglobulins
Other: Cystic fibrosis sweat test as bronchiectasis is common in CF, primary ciliary dyskinesia testing
What are the differential diagnosis for bronchiectasis
COPD, asthma, pneumonia
Describe the management for bronchiectasis
Conservative = Respiratory physiotherapy to clear secretions (e.g., postural drainage). Airway pharmacotherapy (mucolytics, inhaled corticosteroids, inhaled bronchodilator)
Antibiotics if infection (H. influenzae and S. pneumoniae = amoxicillin. P. aeruginosa = piperacillin/tazobactam).
Describe the complications for bronchiectasis
Empyema, lung abscess, respiratory failure, cor pulmonale
Define pleural effusion
Fluid collects between visceral and parietal pleural surfaces of the thorax
Describe the aetiology for pleural effusion
Transudate (protein <25g/L) = due to increased hydrostatic pressure or low oncotic pressure. E.g., congestive heart failure, liver cirrhosis, nephrotic syndrome, hypalbuminaemia
Exudate (protein >35g/L) = due to inflammation causing increased vascular permeability. E.g., cancer, TB, pneumonia, rheumatoid arthritis
Describe the risk factors for pleural effusion
Congestive heart failure, pneumonia, malignancy, pulmonary embolism
Describe the pathophysiology for pleural effusion
Rate of fluid formation > rate of fluid removal. Normal pleural space has some fluid for lubrication.
Exudate effusion: alteration of local factors like inflammation leading to capillary leakage of high protein (>35g/L) and LDH fluid into pleural space
Transudate effusion: mediated by systemic factors like elevated portal pressure from cirrhosis, heart failure or hypalbuminaemia, leading to low protein (<25g/L) and LDH fluid in pleural space
What are the key presentations for pleural effusion
Dyspnoea, dullness to percussion (due to increased fluid), cough, quieter breath sounds, pleuritic chest pain
Describe the signs of pleural effusion
Tracheal deviation away from effusion if it is massive
What is the gold standard investigation for pleural effusion
Chest x-ray (decreased costophrenic angles – blunting. Excess fluid appears white. Fluid in lung fissures. Tracheal and mediastinal deviation)
Describe the first line investigations for pleural effusion
Chest x-ray (blunting of costophrenic angle), pleural ultrasound (pleural fluid), thoracocentesis (identifies underlying cause. Sample pleural fluid: protein, LDH, pH, lactate, microscopy, WCC. Transudate – translucent. Exudate - cloudy)
What are the differential diagnosis for pleural effusion
Pneumothorax (hyper-resonant percussion), congestive heart failure, pulmonary embolism
Describe the management for pleural effusion
1st line - Chest drain/pleural aspiration. If recurrent, pleurodesis – surgical fusing of pleural layers to prevent fluid build-up.
Congestive heart failure – loop diuretics (furosemide, bumetanide), infection – empirical antibiotics (co-amoxiclav, metronidazole), malignant – therapeutic thoracocentesis
Describe the complications for pleural effusion
Empyema, pleural fibrosis, lobar collapse, pneumothorax following thoracocentesis
Define pneumothorax
Air in pleural space, causing ipsilateral collapse.
Classification: Spontaneous (without trauma or precipitating event),
Traumatic (penetrating or blunt injury to chest),
Iatrogenic (accidental consequence of medical interventions, e.g., central line, mechanical ventilation),
Lung pathology,
Tension pneumothorax (emergency, one way valve – air enters pleural space but cannot exit)
Describe the epidemiology for pneumothorax
Tall thin males, connective tissue disorder, smokers, trauma
Describe the aetiology for pneumothorax
Spontaneous or secondary to trauma, iatrogenic, lung pathology
Describe the risk factors for pneumothorax
Smoking, family history, male, tall and slender build, young age, presence of underlying lung disease
Describe the pathophysiology of pneumothorax
Normally intrapleural pressure is negative. Pleural space is a vacuum (no air). Breach in pleura causes abnormal connection between pleural space and airways.
Tension PTX – air enters pleural space but cannot exit. Increased positive pressure in chest. Collapse of ipsilateral lung and compression of contralateral lung, trachea, heart and other structures.
What are the key presentations for pneumothorax
Stable patient. Sudden onset one-sided pleuritic chest pain, dyspnoea, or cough. Hyper-resonant percussion. Decreased ipsilateral breathing sounds.
Tension PTX: cardiopulmonary deterioration – hypotension (imminent cardiac arrest), respiratory distress, low sats, tachycardia, shock. Severe chest pain. Increasing intrapleural pressure, worse with every breath
Describe the signs of pneumothorax
Evidence of trauma or tension pneumothorax on examination (tracheal deviation to contralateral side, ipsilateral reduced breath sounds, reduced air entry on ipsilateral side hyperresonance on percussion, hypoxia)
What is the gold standard investigation for pneumothorax
Chest x-ray (excess air appears black. Tracheal deviation to contralateral side. Reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall)
Describe the first line investigations for pneumothorax
Erect chest x-ray (reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall)
Bloods – clotting abnormalities. Chest USS. CT chest. ABG is stats <92% on room air.
What are the differential diagnosis for pneumothorax
Pulmonary embolism, myocardial infarction, asthma/COPD exacerbation
Describe the management for pneumothorax
Small primary spontaneous pneumothorax (visible rim <2cm) and not SOB: self-healing, consider discharge and follow-up chest x-ray.
Large primary spontaneous pneumothorax (visible rim >2cm) and/or SOB: needle aspiration and remove air with syringe, if not <2cm on repeat chest x-ray insert chest drain and supplemental O2 if needed. Chest drain triangle of safety: 5th intercostal space, midaxillary line, anterior axillary line.
If recurrent, pleurodesis (surgical fusion of pleura to stop pleural space filling)
Tension PTX: cardiac arrest call, high flow O2, immediate decompression. Unless due to trauma: insert large bore cannula into pleural space through 2nd intercostal space at midclavicular line. Hiss sound confirms diagnosis.
Describe the complications for pneumothorax
Effusion, haemorrhage, empyema, respiratory failure, cardiac arrest
Describe the prognosis for pneumothorax
Tension pneumothorax fatal if treatment delayed
Define tension pneumothorax
Caused by trauma to the chest wall that creates a one-way valve that lets air in but not out. Can lead to tracheal deviation away from side of the pneumothorax .
Describe the management of tension pneumothorax
Insert a large bore cannula into the second intercostal space in the midclavicular line
Define empyema
Presence of pus in pleural space
Describe the aetiology for empyema
Bacterial pneumonia
Describe the risk factors for empyema
Pneumonia, iatrogenic intervention in pleural space, alcohol, diabetes mellitus
Describe the pathophysiology for empyema
End-stage process of pleural inflammation. Pleural fluid accumulation > bacterial invasion > formation of pus
What are the key presentations for empyema
Infection and significant pleura effusion, recent pneumonia, pyrexia and rigors. Productive cough, pleuritic chest pain, dyspnoea.
What is the gold standard investigation for empyema
CT chest
Describe the first line investigations for empyema
Blood cultures, WBC and CRP raised, chest x-ray (blunting of costophrenic angle, effusion on affected side), thoracocentesis (pleural fluid sample: protein, LDH, pH, glucose, WCC, culture)
What are the differential diagnosis for empyema
Pleural effusion, pneumothorax, pneumonia
Describe the management for empyema
1st line – urgent chest drain.
Prolonged course of antibiotics (cefuroxime/ceftriaxone, metronidazole, co-amoxiclav)
Describe the complications for empyema
Sepsis, respiratory failure
Describe the prognosis for empyema
15-20% mortality
Define interstitial lung disease and idiopathic pulmonary disease
Interstitial lung disease: conditions that affect lung parenchyma causing inflammation and fibrosis. Idiopathic pulmonary fibrosis: Formation of scar tissue in lungs with no known cause.
