Respiratory Flashcards
Asthma
Chronic inflammatory disorder of the airways characterised by reversible airflow limitation, airway hyperresponsiveness & inflammation of the bronchi
Asthma aetiology
Atopy - genetic predisposition to IgE-mediated allergen sensitivity
Hygiene hypothesis - reduced exposure to infectious pathogens at a young age predisposes individuals to such diseases
Aspirin-induced asthma - asthma, aspirin sensitivity & nasal polyps (Samter’s triad)
Occupational asthma
Exercise-induced asthma
Asthma pathophysiology
Early phase - inhalation of allergens results in an immediate (type 1) hypersensitivity reaction in the airways, sensitisation occurs causing release of IgE antibodies from plasma cells -> bind to mast cells, subsequent exposure to antigens cause mast cell degranulation -> smooth muscle contraction & bronchoconstriction
Late phase - recruitment of a variety of inflammatory cells
Chronicity - airways lay down fibrous tissue due to persistent chronic inflammation, airway remodelling occurs and manifests as fixed airway obstruction
Asthma symptoms
Cough (worse at night)
Dyspnoea
Chest tightness
Poor sleep
Asthma signs
Expiratory wheeze
Prolonged expiratory phase
Tachypnoea
Harrison’s sulcus: groove at the inferior border of the rib cage that may be seen in children with chronic severe asthma (seen in rickets too)
Asthma grading
Moderate - increasing symptoms of asthma, O2 >/= 92%, PEFR >/= 50-70%
Severe - can’t complete sentences, HR >/= 110, RR >/= 25, O2 >/= 92%, PEFR 33-50%
Life-threatening - silent chest, cyanosis, exhaustion, confusion, poor respiratory effort, PaO2 < 8kPa, O2 < 92%, PEFR < 33%
Near-fatal - raised PaCO2 or requires mechanical ventilation with raised inflation pressures
Asthma investigations
Spirometry - measures the flow and volume of air during inhalation and exhalation
-FVC may be normal but often reduced
-FEV1 is reduced
-FEV1/FVC < 70%
-Reversibilty after the administration of a bronchodilator
PEFR
-Demonstrates characteristic variability on PEFR diaries
FeNO - typically offered same time as spirometry, newer way of testing for eosinophilic airway inflammation
-FeNO > 40ppb = supports asthma diagnosis
-FeNO 25-39ppb = suggestive of asthma
-FeNO < 25ppb = does not support asthma diagnosis
Asthma management
1) SABA PRN (if doses > 3 week, step up treatment)
2) ICS - fluticasone and beclomethasone
3) + LABA - MART is a combined inhaler eg. fostair which contained formoterol/beclometasone, should be used daily as maintenance (should not be prescribed a SABA with this)
4) increase ICS/LTRA - consider increasing ICS to medium dose/adding a leukotriene receptor antagonist
5) consider specialist referral
Acute asthma management
Initial management
-Salbutamol nebulisers - 2.5-5mg driven by oxygen & may be repeated every 15 to 30 minutes
-Oxygen - should be started immediately in severe attacks & titrated to saturations of 94-98%, ABG considered if sats < 92% or life-threatening features
-Steroids - PO with prednisolone 40-50mg daily/IV hydrocortisone 100mg six hourly, continued for at least 5 days
-Ipratropium bromide - nebulisers, 0.5mg 4-6 hourly, are given to most patients with acute asthma attack
Second line therapies
-Magnesium sulphate
-Beta 2 agonist infusion
-Aminophylline
Asthma follow-up
All patients with a peak flow <50% of best/predicted on admission require prednisolone 40-50mg/day until recovery
Check inhaler technique & will need GP follow-up within two days of discharge and referral to asthma specialist nurse clinic
If admitted to hospital, they will require a respiratory clinic appt. within four weeks
COPD
Progressive, obstructive airway disease that is not fully reversible, results from disease of the airways and parenchyma in the form of chronic bronchitis and emphysema
Chronic bronchitis and emphysema
Chronic bronchitis - clinical term relating to a chronic productive cough for at least 3 months over two consecutive years
Emphysema - structural lung changes, abnormal airspace enlargement distal to terminal bronchioles with evidence of alveoli destruction & no obvious fibrosis
COPD aetiology
Smoking
Alpha-1 antitrypsin deficiency - autosomal recessive disorder
A1A is a protease inhibitor (made in the liver) and acts in the lung parenchyma to oppose the action of elastase
Elastase is a protease that causes the breakdown of elastin, a protein important to the structural integrity of alveoli -> causes emphysema
COPD chronic bronchitis aetiology
Chronic bronchitis - inflammation of the bronchi, defined as a chronic productive cough for 3 or more months in two consecutive years
-Characterised by chronic inflammation with neutrophilic infiltration, CD8+ T lymphocytes & macrophages
-Leads to
–Goblet cell hyperplasia
–Mucus hypersecretion
–Chronic inflammation and fibrosis
–Narrowing of small airways
COPD emphysema aetiology
Emphysema - permanent enlargement of airspaces distal to the terminal bronchiole when interstitial pneumonias are excluded, destruction of the lung parenchyma results in a reduced area for gas exchange and chronic hypoxia
-Loss of elastin has two effects
–Collapse - alveoli are prone to collapse
–Dilation & bullae formation - alveoli dilate and may eventually join with neighbouring alveoli forming bullae
COPD cor pulmonale aetiology
Cor pulmonale - refers to right ventricular impairment secondary to pulmonary disease (COPD is most common cause)
-Chronic hypoxia causes vasoconstriction of pulmonary arteries -> elevated pulmonary arterial pressure
-Chronic elevation of pulmonary arterial pressure -> right heart failure
COPD symptoms
Chronic cough
Sputum production
Breathlessness
Frequent episodes of bronchitis
Wheeze
COPD signs
Dyspnoea
Pursed lip breathing
Wheeze
Coarse crackles
Loss of cardiac dullness
Downward displacement of liver
Signs of CO2 retention - drowsy, asterixis, confusion
Signs of cor pulmonale - peripheral oedema, left parasternal heave, raised JVP, hepatomegaly
COPD investigations
Spirometry - confirm diagnosis
Bedside - observations, BMI, sputum cultures, ABG, ECG
Bloods - FBC, alpha-1 antitrypsin levels
Imaging - CXR, CT scan, ECHO
CXR - hyperexpanded, flattened hemidiaphragms, hypodense, saber-sheath trachea
MRC dyspnoea scale
1) breathlessness on strenuous exercise
2) breathlessness on hurrying/slight hill
3) walks slower than contemporaries on ground level due to breathlessness OR have to stop to catch breath when walking at own pace
4) stops to catch breath after 100 metres OR a few minutes of walking
5) breathlessness on minimal activity/unable to leave the house due to breathlessness
COPD severity
Mild - >/= 80
Moderate - 50-79
Severe - 30-49
Very severe - < 30
(based on predicted FEV1 %)
COPD management (non-pharmacological)
Education
Smoking cessation
Vaccination - seasonal influenza vaccine & pneumococcal vaccine
Pulmonary rehab - multidisciplinary programme that aims to optimise the physical and social performance of patients
Self-management plans - helping patients manage their symptoms including how to manage acute exacerbations
Management of comorbidities
COPD management pharmacological
1) offer a SABA/SAMA to use on PRN basis
2) offer LABA+LAMA if no evidence of steroid responsiveness or asthma features OR offer LABA+ICS if evidence of steroid responsiveness/asthmatic features
3) offer escalation to triple therapy (LABA+LAMA+ICS)
-If already on LABA+LAMA:
–Struggling with quality of life - add ICS (3 month trial)
–1 severe/2 moderate acute exacerbations within one year - add ICS
-If already on LABA+ICS:
–Add LAMA if struggling with QoL/exacerbations
Oral pharmacological options
-Corticosteroids - mainstay of treatment in acute exacerbations
-Theophylline - (some bronchodilator action through inhibition of phosphodiesterase): used in difficult to treat COPD
-Mucolytics - used in patients with a chronic productive cough to reduce frequency & sputum production
-Antibiotics - used for acute exacerbations & prophylactically in certain situations
COPD acute management
Oxygen - any known/new evidence of CO2 retention then a sats target of 88-92% should be used
-NIV for patients who require high levels of O2 to prevent hypoxia but are at high risk of hypercapnic respiratory failure
-Venturi masks - allow an exact fraction of inspired oxygen to be administered
Bronchodilators - usually given as nebulisers
-Salbultamol 2.5mg nebulised
-Ipratropium 500mcg nebulised
Corticosteroids - prednisolone 30mg once daily should be given for 5 days
Antibiotics - doxycycline/co-amoxiclav
IV theophylline may be considered in severe cases
LTOT
Arterial PaO2 < 7.3kPa
Arterial PaO2 < 8kPa with any of
-Pulmonary hypertension
-Peripheral oedema
-Secondary polycythaemia
COPD complications
Respiratory failure
Pneumonia
Pneumothorax
Polycythaemia/anaemia
Depression
PE aetiology
One or more emboli usually arising from a thrombus break off and obstruct within the pulmonary arteries
Usually arises from a DVT
PE pathophysiology
Predominant therapy of development of VTE is Virchow’s triad
-Venous stasis
-Endothelial injury
-Hypercoagulable state
Occlusion of one or more of the pulmonary arteries leads to absence of perfusion to that area of the lung
-V/Q mismatch because ventilation is unaffected
-May lead to hypoxia and clinical features of breathlessness
-Area of lung may undergo infarction (usually prevented by the bronchial circulation)
PE symptoms
Dyspnoea
Pleuritic chest pain
Cough
Haemoptysis
Dizziness
Syncope
Leg pain and swelling
PE signs
Tachycardia (> 100 bpm)
Low grade fever (>37.5)
Hypoxia (sats < 94%)
PE investigations
Routine bloods
D-dimer
ECG - sinus tachycardia, S1Q3T3 pattern
CXR, V/Q scan, lower limb USS, echo
CTPA
PE Wells score
PE - series of seven criteria are used that given a score between 0-12.5
Clinical signs and symptoms of DVT (+3)
PE is #1 diagnosis/equally likely (+3)
HR > 100 (1.5)
Immobilisation at least 3 days or surgery in the previous 4 weeks (+1.5)
Previous, objectively diagnosed PE/DVT (+1.5)
Haemoptysis (+1)
Malignancy with treatment within 6 months/palliative (+1)
PE likely (score > 4) = straight to CTPA, if not available, interim anticoagulation if safe
PE unlikely (score < 4) d-dimer blood test within 4 hours, if positive = CTPA
PE management anticoagulation
Stable - offer apixaban/rivaroxaban
Haemodynamic instability - consider thrombolysis & heparin-based anticoagulation according to local guidelines
Active cancer - consider DOAC (edoxaban)
Renal impairment - if CrCl 15-50ml/min, offer apixaban/rivaroxaban or LMWH for 5 days then edoxaban/warfarin, if CrCl <15ml/min, offer LMWH/UFH as per local guidance
PE management thrombolysis
Thrombolysis - use of recombinant tissue plasminogen activator (fibrinolytic drug that breaks down clots)
-Cardiac arrest with confirmed or suspected PE
-Confirmed PE with deterioration despite anticoagulation
-Haemodynamic instability & high clinical suspicion of PE/confirmed PE within 14 days
PE long-term management
Long-term management - patients are advised to continue anticoagulation for a minimum period of 3 months
After this patients should be referred to a specialist anticoagulation clinic & discuss whether to continue anticoagulation
PE complications
High mortality (20%) in patients with haemodynamic instability
Maternal death in pregnancy
Chronic thromboembolic pulmonary hypertension & associated right sided HF
TB (different types)
Caused by bacteria of the mycobacterium tuberculosis complex & is one of the world’s most common and deadly infective diseases
Latent TB - refers to individuals infected with TB, who suppressed the initial infection, have no active diseases & not infectious
Active TB - refers to symptomatic/progressive disease
Primary TB - initial infection, often subclinical, suppressed in the majority of individuals
Progressive-primary TB - primary infection is not suppressed & prolonged infection occurs
Post-primary TB - occurs in patients with latent TB, frequently due to immunocompromised (may be pulmonary/extra-pulmonary)
TB pathophysiology
Inhaled bacilli find their way into alveoli & begin dividing
In some individuals -> may be immediately cleared, in others primary TB develops
Once a critical mass is reached a host immune response is elicited with mycobacterium producing a strong immune response
Ghon complex may develop
-Ghon focus - small caseating granuloma
-Ipsilateral mediastinal lymph node
After 2-10 weeks a sufficient cell-mediated response halts the proliferation of the bacilli in the majority of individuals - these patients develop latent TB (may have a Ranke complex = calcified Ghon’s complex)
Small proportion of patients do not halt the primary infection & develop primary-progressive TB (linked to patients with inadequate T-cell immunity)
TB symptoms and signs
Pulmonary TB - cough, fever, weight loss
Lymph node - enlarged, firm, non-tender (most commonly affects cervical and supraclavicular nodes)
Genitourinary TB - sterile pyuria, salpingitis, epididymo-orchitis, renal abscess
Miliary TB - disseminated haematogenous spread of bacilli
CNS TB - TB meningitis: fever, malaise and headache
TB investigations
CXR - demonstrate consolidation, cavitation (typically upper lobe) & effusion
-Miliary TB - appearance of millet seeds throughout the lung fields
Latent TB
-Mantoux test - intradermal injection of tuberculin
-If patient has had exposure to TB they exhibit a delayed hypersensitivity reaction
-Previous BCG vaccination affects results
Interferon-gamma release assay - assays detect the bodies cellular immune response (tests for the T-cell interferon-gamma response to M. tuberculosis)
-Unaffected by previous BCG and non-tuberculous mycobacterium
Active TB
-Microbial - microscopy & culture, cytology & histology, nucleic acid amplification
-Imaging
TB management
Latent TB - advise treatment in those younger than 65
-6 months of isoniazid with pyridoxine OR
-3 months of isoniazid and rifampicin
Active TB - combination antibiotics for 6-12 months
-Without CNS involvement - managed with isoniazid (with pyridoxine), rifampicin, pyrazinamide & ethambutol for 2 months followed by rifampicin and isoniazid for 4 months
-With CNS involvement - treated with isoniazid & rifampicin for 12 months whilst pyrazinamide & ethambutol are given for the first 2 months
–Adjunctive steroids - offered dexamethasone or prednisolone at the start of treatment which is then weaned over 4-8 weeks
Bronchiectasis
Irreversible and abnormal dilatation of the airways
Bronchiectasis aetiology
Immune deficiency
Mechanical obstruction
Mucociliary clearance dysfunction
Congenital airway defects
Other causes - rheumatic diseases, allergic bronchopulmonary aspergillosis, COPD, inflammatory bowel disease
Bronchiectasis pathophysiology
Infective insults combined with defective mucociliary clearance, airway obstruction or impaired host immunity
Infective pathogens promote an inflammatory response involving the activation of neutrophils and release of inflammatory mediators -> results in damage to elastic & muscular components of the airway -> dilated airways
Abnormal dilatation of the airways further predispose patients to infections -> leads to a cycle of infection & worsening bronchiectasis
Bronchiectasis symptoms
Persistent sputum production
Persistent cough
Dyspnoea
Haemoptysis
Weight loss
Bronchiectasis signs
Crackles
High pitched inspiratory squeaks
Wheeze
Clubbing (rare)
Bronchiectasis investigations
Bloods - FBC, renal function, serum immunoglobulins
Cultures - sputum cultures, blood cultures
Imaging - CXR (tram track airways & ring shadows), thin section CT (signet ring)
Aspergillus fumigatus - serum total IgE, sensitisation assessment
Bronchiectasis management
1) airway clearance - respiratory physiotherapist will teach airway clearance techniques
2) mucoactives - (help the clearance of mucus from the airways), isotonic and hypertonic saline may be used & have been shown to improve quality of life
3) prophylactic antibiotics - patients with recurrent exacerbations (> 3 per year) should be considered for long term abx
P. aeruginosa: inhaled colistin & gentamicin, oral azithromycin/erythromycin can be considered in those who don’t tolerate inhaled therapy
Non-P. aeruginosa: azithromycin/erythromycin may be used
4) bronchodilators
5) surgery - lung resection may be considered in patients with localised disease with uncontrolled symptoms
Bronchiectasis complications
Infective exacerbation
Chronic respiratory failure
Haemoptysis
Cor pulmonale
Pneumothorax
Chest pain
CF
Autosomal recessive multi-system disease predominantly characterised by respiratory features
CF aetiology
Caused by mutations to the cystic fibrosis transmembrane conductance regulator (CFTR) gene found on chromosome 7
CFTR gene encodes for a epithelial chloride channel regulated by cyclic AMP
CF pathophysiology
In the lungs, CFTR channels are found on the apical surface of epithelial cells
Defects in normal ion transport leads to dehydration & depletion of airway surface liquid
Resultant mucociliary dysfunction causes reduced mucus clearance, airway obstruction & predisposition to infection
Recurrent infection leads to chronic bronchitis, damage to the bronchi and eventual bronchiectasis -> permanent dilation of bronchi secondary to damage to the elastic and muscular components of the bronchial wall
CF symptoms and signs
Respiratory disease - productive cough & recurrent chest infections
-Children - staph aureus & haemophilus influenza
-Older age groups - colonisation with pseudomonas aeruginosa
-Recurrent infections -> bronchiectasis
Pancreatic disease - fatty stools, malabsorption, diabetes, recurrent acute pancreatitis & eventual chronic pancreatitis
-Thick secretions block the outflow of exocrine digestive enzymes
-Autolysis destroys the pancreatic islets
Gastrointestinal disease - meconium ileus in infants, constipation, DIOS
Malignancies - increased risk of gastrointestinal malignancies
-Large and small bowel
-Pancreas
-Biliary tract
-HCC
CF investigations
Diagnosis is now commonly made after a positive heel prick test (newborn screen) followed by confirmatory testing
-Immuno-reactive trypsin test - used at newborn screening, a positive test is indicative but further confirmation testing is needed
-Sweat test - can be used in children of any age
Sweat chloride > 60mmol/L is considered positive for CF, 30-59mmol/L is inconclusive & <30mmol/L is considered negative
-Genetic testing - common mutations are screening for, where not found, sequencing of the entire CFTR gene may be completed
CF pulmonary disease management
Pulmonary disease - encouraging clearance of secretions & treating/preventing infections
-Airway clearance techniques
-Mucoactive agents - rhDNase, hypertonic sodium chloride, mannitol dry powder for inhalation
-Pulmonary infection
–Staph aureus - oral flucloxacillin can be offered as prophylaxis up to 6
–Pseudomonas aeruginosa - patients with a new infection are treated with eradication therapy with oral/IV antibiotics & inhaled antibiotics
–Other infections - specific treatments
-Lung transplantation
CF extra-pulmonary disease management
Nutrition and pancreatic insufficiency
-Nutritional assessment forms a key part of the management
-Pancreatic insufficiency is common resulting in malabsorption and steatorrhoea -> patients with CF should be tested for this
Liver disease
-Should be screened regularly for liver disease thorough history, examination & LFTs
-Ursodeoxycholic acid may be given to those with abnormal liver function with the aim to improve biliary flow
CF-related diabetes
-Often results in diabetes through damage to the pancreatic islets
-Screen annually from the age of 10 & at any times where symptoms are suggestive or the clinical situation demands
ILD
Family of conditions with shared characteristics of interstitial inflammation, fibrosis and/or cellular changes in the absence of infection and malignancy
Idiopathic pulmonary fibrosis = progressive pulmonary fibrosis with no clear cause
IPF aetiology
Majority of cases of IPF occur spontaneously without known cause
Familial pulmonary fibrosis
Hermansky-pudlak syndrome
Telomeropathies
IPF symptoms
Exertional dyspnoea
Dry cough
Fatigue
IPF signs
Bilateral inspiratory crackles
Clubbing
Acrocyanosis
IPF investigations
(for ILD - HRCT ‘ground glass’ appearance)
Bloods - FBC, renal function, LFTs & CRP
Lung function tests - spirometry, lung volumes and diffusing capacity of the lung for carbon monoxide (DLCO)
Imaging
-CXR - key investigation in any patient presenting with shortness of breath/chronic cough
-High resolution CT - honeycombing, reticular opacities, traction bronchiectasis, emphysema and loss of lung volume -> changes predominantly seen in the bases & peripheries
Biopsy and cytology
-Bronchoalveolar lavage and/or transbronchial biopsy
-Surgical lung biopsy
IPF management
Supportive care
Pulmonary rehab
Oxygen therapy
Disease modifying medical therapies - pirfenidone & nintedanib
-Pirfenidone = anti-inflammatory & anti-fibrotic whose mechanism of action is incompletely understood
-Nintedanib = acts on 3 growth factor receptors implicated in the development of IPF
Lung transplant
NSCLC types
Adenocarcinoma
SCC
Large cell
Lung cancer aetiology
Smoking
Exposure
-Asbestos - more strongly associated with mesothelioma, asbestos is linked with adenocarcinoma of the lung
-Radon gas, released from naturally occurring uranium, is also a recognised cause of lung cancer
Lung cancer types
Non-small cell lung cancer
-Adenocarcinoma - cancer of the mucus-secreting cells
–Tends to occur in lung peripheries
-Squamous cell - second most common form of lung cancer
–Second most common form of lung cancer
–Typically occurring in the central parts of the lungs -> can present with pneumonia secondary to an obstructed bronchus
-Large cell - undifferentiated neoplasms accounting for 5% of lung cancers, tend to metastasise
Small cell lung cancer
-Fast doubling time, aggressive nature & early metastasis
-Cancer of the APUD cells, a neuroendocrine cell
Lung cancer symptoms
Fever
Malaise
Nausea
Cough
Haemoptysis
Hoarseness (due to involvement of the recurrent laryngeal nerve)
Weight loss
Lung cancer signs
Lymphadenopathy
Stridor
Wheeze
Clubbing
Hypertrophic pulmonary osteoarthropathy (fibrovascular proliferation that results in periostitis of the long bones, arthralgia and clubbing)
Signs of pleural effusion (exudative)
Dull (‘stony dull’) percussion
-Reduced vocal fremitus
-Reduced breath sounds
Lung cancer SVC obstruction features
Causes engorgement of vessels in the neck and face, shortness of breath & ‘fullness’ of the head
Pancoast tumour features
Horner’s syndrome
Pain in the shoulder that radiates into the arm and hand
Atrophy of muscles of the upper limb
Oedema of the upper limb
Lung cancer metastasis features
Bone - bone pain, raised ALP
Brain - focal and non-focal neurology
Liver - abnormal LFTs
Adrenal glands - normally asymptomatic
Lung cancer paraneoplastic syndromes
Hypercalcaemia - bony metastasis, tumour secretion of PTHrP or calcitriol
-50% SCC, 20% adenocarcinoma, 15% small cell carcinoma
SIADH
-10% small cell lung cancer
Cushing’s syndrome - lung cancers produced ectopic ACTH driving an increase in glucocorticoids
Lambert-eaton syndrome - antibodies to voltage-gated calcium channels
-1-3% of small cell lung cancer
-Characterised by both proximal and ocular muscle weakness
Hypertrophic osteoarthropathy
-Clubbing and periostitis
-Symmetrical, painful arthropathy affecting the distal joints
Lung cancer investigations
Bloods
Imaging
-CXR - focal lesion, pleural effusion, widened mediastinum
-CT chest - solitary pulmonary nodule, lymph node involvement
-PET-CT - radioactive tracer taken up preferentially into more metabolically active cells
-CT/MRI brain - ordered to exclude cerebral metastasis
Bronchoscopy
Lung function tests
Histology & cytology
Lung cancer 2WW and urgent CXR criteria
2 week wait referral for:
Suggestive CXR findings
Unexplained haemoptysis and aged over 40
Urgent CXR for:
Persistent/recurrent chest infection
Clubbing
Supraclavicular lymphadenopathy/persistent cervical lymphadenopathy
Chest signs indicative of lung cancer
Thrombocytosis
OSA
Characterised by episodes of complete or partial upper airway obstruction during sleep
OSA pathophysiology
Occurs if the upper airway at the back of the throat is sucked closed when the patient breathes in
Occurs during sleep because the muscles that hold the airway open are hypotonic
Airway closure continues until the patient is woken up by the struggle to breathe against a blocked throat
OSA symptoms and signs
Apnoea episodes during sleep
Snoring
Morning headache
Waking up unrefreshed from sleep
Daytime sleepiness
Concentration problems
Reduced oxygen saturation during sleep
OSA investigations
Polysomnography (PSG) - ENT specialist perform sleep studies: monitor their oxygen sats, HR, RR & breathing, extent of snoring
Portable multichannel sleep tests
Awake fiberoptic endoscopy
OSA epworth scale
Epworth sleepiness scale = how likely they are to fall asleep in eight specific situations
Sitting and reading
Watching TV
Sitting in a public place
Sitting in a care as a passenger without a break
Lying down to rest
Sitting and talking to someone
Sitting quietly after lunch without alcohol
In a car, while stopped for a few minutes in traffic
OSA management
Correct reversible risk factors - stop drinking, stop smoking and lose weight
Continuous positive airway pressure (CPAP) - provides a continuous pressure to maintain the patency of the airway
Surgery - surgical restructuring of the soft palate and jaw (uvulopalatopharyngoplasty)
OSA complications
Hypertension
Ischaemic heart disease
Cerebrovascular disease
Pulmonary hypertension
AF
Depression
Pleural effusion
Abnormal collection of fluid within the pleural space
Pleural effusion transudate vs exudate
Transudate - fluid with minimal protein or cellular content, occurs due to alteration in hydrostatic and oncotic pressures leading to the fluid being ‘squeezed’ into the pleural space
Exudate - fluid with a high protein and cellular content, develops due to a variety of inflammatory conditions that affect vessel permeability and/or lymphatic drainage
Transudate examples
Heart failure
Hypoalbuminaemia
Cirrhosis
Constrictive pericarditis
Nephrotic syndrome
Peritoneal dialysis
Meigs’ syndrome - ascites and pleural effusion in association with a benign ovarian tumour
Exudate examples
Parapneumonic effusion (secondary to pneumonia)
Malignancy (breast/lung)
Tuberculosis
Pulmonary embolism
Pancreatitis
Radiation pleuritis
Systemic inflammatory condition (eg. SLE, RA)
Trauma
Pleural effusion symptoms
Breathlessness
Non-productive cough
Pleuritic pain
Extra-pulmonary symptoms based on underlying caus
Pleural effusion signs
Reduced chest expansion
Reduced breath sounds
Stony dull percussion
Reduced vocal resonance
Trachea deviation
Extra-pulmonary signs - depending on the underlying cause
Pleural effusion pathophysiology
Increased fluid entry
-Increased vasculature permeability - loss of fluid and macromolecules from ‘leaky’ vessels
-Increased microvascular pressure - increased venous pressure affects hydrostatic pressure forcing fluid out
-Decreased plasma oncotic pressure - hypoproteinaemia -> favour accumulation of the fluid in the pleural space
Decreased fluid exit
-Alteration in lymphatic drainage
-Intrinsic factors - inflammatory mediators, infiltration, damage
-Extrinsic factors - physical compression, limitation by respiratory motion, decreased intrapleural pressure
Pleural effusion investigations
CXR - PA with approximately 200ml of pleural fluid, blunting of the costophrenic angle, meniscus
Ultrasound, CT and MRI
Pleural paracentesis and analysis
Pleural aspiration - biochemistry, microbiology, cytology
Pleural effusion Light’s criteria
Pleural fluid is an exudate if one or more of the following criteria are met:
Pleural fluid protein divided by serum protein is > 0.5
Pleural fluid LDH divided by serum LDH is > 0.6
Pleural fluid LDH > ⅔ the upper limits of laboratory normal value for serum LDH
Pleural effusion management
Address underlying cause
Pleural aspiration and/or chest drains
-Therapeutic paracentesis - involves the removal of 1-1.5L of pleural fluid via a special drainage kit
-Chest drain insertion - involves the insertion of a tube into the pleural space to allow drainage over hours to days
–Connected to an underwater seal to prevent backflow of air/fluid into the pleural space
–Complications: re-expansion pulmonary oedema, pneumothorax, infection, bleeding, damage to thoracic viscera, subcutaneous emphysema
Pleurodesis - procedure to obliterate the pleural space and prevent re-accumulation of fluid or air
Surgical intervention
Pneumothorax
A collection of air within the pleural space
Spontaneous - occurring without prior trauma, normally in older patients with underlying lung disease/younger patients with apical blebs
Traumatic - occuring in the setting of trauma, may be open or closed
Pneumothorax aetiology
Primary spontaneous pneumothorax - occur spontaneous in a previously non-pathological lung, typically seen in tall thin young men
Secondary spontaneous pneumothorax - occur in previously diseased lungs (common causes = COPD & asthma)
Pneumothorax clinical features
Symptoms
Dyspnoea
Pleuritic chest pain - pain worse on deep inspiration, usually unilateral
Signs
Normal
Tracheal deviation
Reduced chest expansion
Reduced breath sounds
Hyperresonant percussion
Absent tactile fremitus (vibration intensity)
Absent vocal resonance (sound intensity)
Pneumothorax investigations
eCXR - allows size of pneumothorax to be estimated
USS - therapeutically may be used to aid drain placement
CT chest - can be considered the gold standard
Primary spontaneous pneumothorax management
Large (>2cm) or breathless:
Active intervention
Needle aspiration (14-16G needle) is typically advised first (stop after 2.5L has been aspirated)
If needle aspiration fails, small bore chest drain can be inserted
Small (<2cm) and asymptomatic:
Observation with outpatient follow-up
Advised to return if they develop breathlessness
Secondary spontaneous pneumothorax management
Large (>2cm) or breathless:
Small bore chest drain
Size 1-2cm:
Needle aspiration is typically advised first
Size < 1cm
Admit and observe for at least 24h, consider supplemental oxygen
Tension pneumothorax management
Administer high flow oxygen and carry out urgent needle decompression, imaging should not be awaited
Placing a large-bore cannula in the 2nd intercostal space midclavicular line
T1RF & T2RF
Type 1 respiratory failure - characterised by hypoxaemia and a normal or low CO2
Type 2 respiratory failure - characterised by hypoxaemia and hypercapnia
T1RF causes
Pneumonia
COPD
Asthma
Pulmonary oedema
Pneumothorax
PE
Obesity
T2RF causes
COPD
Asthma
Chronic neurological disorders
Chronic neuromuscular disorders
Chest wall diseases
Obesity hypoventilation syndrome
When should a chest tube be placed in a pleural infection?
All patients with a pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling
- if the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage
- if the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed
