Respiratory (Free)

Respiratory (Free)

🫁 Respiratory

‣
😤 Airway

Many of these diseases affect multiple pieces of anatomy; these are clarified within the disease section. However, to help your understanding, they’re classified within the primary piece of anatomy they affect.

‣
Diagram: Airways
UNSHAW, CC BY-SA 4.0
UNSHAW, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Classifying by anatomy:

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Upper airways (Nasopharynx & Trachea)
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Obstructive sleep apnoea (OSA)
‣
What is this?
  • Obstructive sleep apnoea occurs due to the relaxation of the throat muscles, blocking your airway during sleep.
    • Collapse of the pharyngeal airway.
    • Apnoea episodes are where the individual will stop breathing for up to a few minutes.
‣
What scale is used to assess sleepiness?
  • Epworth Sleepiness Scale
‣
What features may suggest this?
  • Snoring
  • Daytime sleepiness
  • Apnoea episodes (often reported by the partner)
  • Waking up not feeling refreshed from sleep
  • Concentration problems
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How is this managed?
  1. Sleep studies with ENT specialist / at a sleep clinic
    2. ‣
    What do these involve?

    Sleeping while monitoring the:

    1. Oxygen saturation
    2. Heart rate
    3. Respiratory rate
    4. Breathing
  2. Lifestyle: Stop smoking, drinking alcohol and lose weight
  3. Continuous positive airway pressure (CPAP)
  4. Surgery: Uvulopalatopharyngoplasty (UPPP)
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Epiglottitis
‣
What is it?
  • Haemophilus influenza type B infection causing swelling of the epiglottis.
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What would you see on lateral neck X-ray?
  • Thumbprinting sign: Shadowing caused by the swollen epiglottis
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How do you manage it?
  • ABCDE
  • Immediate escalation to anaesthetics to secure the airway, this may be through intubation if possible or by tracheostomy as the swollen epiglottis may make intubation impossible.
  • IV antibiotics (see local guidelines)
  • Steroids, e.g. dexamethasone

Management:

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Non-invasive ventilation: What’s the difference between BiPAP and CPAP?
  • CPAP: Pushes only.
    • Provides a fixed positive pressure on the airways through inspiration and expiration, maintaining airway patency.
  • BiPAP: Pushes & pulls. Used in T2RF.
    • This is used in CO₂ retainers when they can no longer maintain their respiratory drive. It pulls the CO₂ from the lungs as well as pushing O₂ in.
      • ‣
      What conditions can indicate BiPAP?
      • COPD with respiratory acidosis
      • Hypercapnic respiratory failure: Chest wall deformity, neuromuscular disease
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Bronchi / bronchioles
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Asthma

Asthma is a chronic respiratory condition causing inflammation and narrowing of the bronchi.

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Acute exacerbation
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Presentation
‣
Name the common triggers.
  1. Dust
  2. Exercise
  3. Infection
  4. Time of day: Night or early morning
  5. Cold/damp
‣
What features suggest asthma?
  1. Occurring in episodes
  2. Diurnal variation: Often worse at night.
  3. Wheeze
  4. Shortness of breath
  5. Atopy: Eczema, hayfever, food allergies
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Grading

What makes up the following grades:

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Moderate
  • PEFR: 50-75%
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Severe
  • PEFR: 33-50%
  • RR ≥ 25
  • HR ≥ 110
  • Unable to complete sentences
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Life-threatening
  • PEFR < 33%
  • SpO2 < 92%
  • Cyanosis
  • Hypotension
  • Exhaustion - PaCO₂ normal/high
  • Silent chest
  • Tachyarrhythmias
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Near-fatal
  • pCO2 > 6 (Normal - represents exhaustion)
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Management
‣
Step 1: Initial
  1. ABCDE
  2. Nebulised salbutamol 5mg & ipratropium bromide
    3. ‣
    What bloods should you monitor because of this?
    • K⁺ as can be ↓
  3. Steroids: PO prednisolone / IV hydrocortisone
  4. Antibiotics (if you suspect this is secondary to an infection)
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Step 2: If non-responsive
  • IV aminophylline
  • IV salbutamol
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Step 3: Life-threatening
  1. IV magnesium sulphate
  2. Admission to HDU/ITU for intubation & ventilation

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After an acute asthma attack, when can the patient be discharged?
  • Stable on salbutamol inhaler for 24 hours
  • PEFR > 75% predicted
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Chronic

Investigation:

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What are the first-line investigations?
  1. Fractional exhaled NO (FeNO): ↑ in airway inflammation
  2. Spirometry with reversibility
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What are the second-line investigations?
  • Peak flow variability: measure peak flow multiple times a day for 2-4 weeks looking for variability throughout the day.
  • Direct bronchial challenge test (with histamine or methacholine).
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What can be seen on histology in asthma?
  • Curschmann spirals: Shed epithelium becomes whirled mucus plugs
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Diagnostic protocol: What do you need for diagnosis?

Note: Ask at your University which guideline protocol they follow in exams.

  • BTS (2016):
    • If high probability of asthma based on clinical picture, try treatment.
    • If unsure, use spirometry with reversibility testing to confirm.
    • If low probability, consider referring for other causes.
  • NICE (2017):
    • Advise not to make a diagnosis based on clinical picture.
    • Always investigate at a diagnostic hub.

Management:

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How do the following drugs work:
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β-2 adrenergic receptor agonists (SABA/LABA)
  • Activate beta 2 adrenergic receptors on the smooth muscle that surrounds the airways → Smooth muscle to relaxation → Bronchodilation.
    • SABA: Work within minutes, last several hours.
    • LABA: Lasts at least 12 hours.
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Inhaled corticosteroids (ICS)
  • Reduce airway inflammation, preventing or reducing asthma attacks → Prevents airway smooth muscle hypertrophy secondary to chronic inflammation.
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Muscarinic antagonists (SAMA/LAMA)
  • Block acetylcholine receptors blocking the parasympathetic effect of bronchoconstriction, indirectly causing bronchodilation.
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Leukotriene receptor antagonists
  • Leukotrienes → Inflammation, bronchoconstriction & mucus secretion.
  • Blocking these prevents this.
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What are the stages of management for adults (≥ 17 years)? (8)

Based on NICE Guidelines (2017):

  1. SABA
  2. Add regular low-dose ICS
  3. Add LTRA (review in 4-8 weeks)
  4. Add LABA (discuss if LTRA has helped at all, if not stop it)
  5. MART (maintenance & reliever therapy): Combined ICS (low-dose) & fast-acting LABA
  6. MART with moderate dose ICS
  7. Increase ICS to high-dose OR add PO theophylline OR add LAMA.
  8. Refer to specialist
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Give examples of each type of inhaler. (6)
  • SABA - Salbutamol
  • SAMA - Ipratropium
  • ICS - Beclometasone, budesonide, fluticasone, mometasone
  • LTRA - Montelukast
  • LABA - Salmeterol, formoterol
  • LAMA - Tiotropium
  • MART - Turbohaler, spiromax
  • ICS & LABA - Symbicort, fostair, seretide
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What drugs can be used in pregnancy?
  • Inhaled drugs, theophylline and prednisolone can be taken as normal during pregnancy and breast-feeding.
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Atelectasis

Atelectasis is the complete or partial collapse of the entire lung, or a lobe of the lung due to airway obstruction.

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How can you classify this?
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Obstructive: Airway blockage
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What are the 3 common causes of this?
  1. Mucus plug
    2. ‣
    Why does this commonly occur post-operatively?
    • Secretions build up in airways due to reduced movement and because you can’t cough → Airrway obstruction → Bibasal lung collapse → Reduced lower lobe breath sounds
    ‣
    Name 2 other causes.
    1. Cystic fibrosis
    2. Asthma
  2. Foreign body: Inhaled object (e.g. peanut)
  3. Lung tumour within the airway
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Non-obstructive: From pressure from outside the lung
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What could cause this?
  • Pleural effusion
  • Pneumonia
  • Pneumothorax
  • Lung tissue scarring of lung tissue due to injury, lung disease or surgery.
  • Tumor (non-airway) causing external compression
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How is it managed?
  1. Position patient upright
  2. Chest physiotherapy
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Bronchiectasis
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What is this?
  • Damage and scarring of the large airways due to recurrent infection and resulting inflammation from immune response.
  • Leads to mucus buildup and dysfunction of the mucociliary escalator.
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What is seen on CXR?
  • Multiple thin walled cystic space (ring opacities), several of which have air-fluid levels.
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What are the key features on CT?
  1. Tram track sign
  2. Signet ring sign
  3. Cluster of grapes sign
Mcgfowler, CC BY-SA 3.0
Mcgfowler, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons
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Chronic obstructive pulmonary disease (COPD)

COPD is chronic inflammation of the airways causing bronchitis (airway inflammation & narrowing) and emphysema (alveoli destruction).

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Presentation
‣
What else may they present with?
  • Shortness of breath.
  • Cough.
  • Wheeze.
  • Recurrent LRTI.
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What are the two main presentations?
  1. 'Pink puffer': Predominantly emphysema.
    • Compensate for damaged alveoli by hyperventilating.
    • High VQ ratio.
  2. 'Blue bloater': Predominantly bronchitis.
    • Compensate for lack of air getting to the alveoli by increasing cardiac output.
    • Low V/Q ratio.
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How do you assess the impact of their breathlessness?
  • MRC dyspnoea scale. Scale of 1-5, useful to remember the extremes:
    • SOB on strenuous exercise = 1.
    • Unable to leave house = 5.
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Investigations
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What would you look for on spirometry?
  • Obstructive picture: FEV1/FVC ratio < 0.7
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How do you assess the severity (stage) of the exacerbation?

Using FEV1:

  1. Stage 1: FEV1 > 80% predicted
  2. Stage 2: FEV1 50-79% predicted
  3. Stage 3: FEV1 30-49% predicted
  4. Stage 4: FEV1 <30% predicted
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How do you assess if somebody is a CO₂ retainer?
  • ABG: ↑ HCO₃⁻ → Chronic retainer
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What are the TLCO & KCO?
  • TLCO: Total lung diffusion capacity
  • KCO: Diffusion capacity of a single alveolus

What would they be in the following diseases:

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COPD
  • Both low
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Pneumonectomy/atelectasis
  • KCO high (compensatory), TLCO reduced
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Lung fibrosis/fluid
  • Both low
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Myasthenia gravis with respiratory muscle weakness
  • KCO high, TLCO low
  • Lack of lung expansion → Higher pressures in alveoli → More diffusion
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What other investigations would be helpful for management?
  • Bedside:
    • Sputum culture: Tailor antibiotic regimen later.
    • ECG
  • Bloods:
    • FBC: WCC to assess if infective cause, Hb to look for secondary polycysthaemia.
    • Serum ɑ-1 antitrypsin
  • Imaging:
    • Chest X-ray: Exclude other causes.
    • CT thorax: Exclude fibrosis and cancer.
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Management
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Exacerbation
‣
What is the typical management of an exacerbation if sending the patient home?
  1. Prednisolone 30mg OD for 7-14 days
  2. Antibiotics (if infective cause)
  3. Regular inhalers
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If they require admission, how are they managed?
  1. Inhaled: Nebulised salbutamol and ipratropium
  2. Steroids: IV hydrocortisone or PO prednisolone
  3. Antibiotics (if likely infective cause)
  4. Chest physiotherapy to help clear sputum
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If they are on O₂ and they are becoming more acidotic and are also deteriorating, what do you need to do?
  • Non-invasive ventilation (BiPAP), may also need IV aminophylline
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Long-term management
‣
What are the stages of long-term management?
  1. Stage 1: SABA (salbutamol)/SAMA (ipratropium)
  2. Stage 2:
    • No steroid features: LABA & LAMA
    • Steroid features: LABA & ICS
  3. Stage 3:
    • Triple therapy: LABA & LAMA & ICS (Trelegy ellipta, trimbo)
  4. Advanced management
    5. ‣
    What surgical management is available & when is it indicated?
    • Bullectomy (removing the dilated airspaces)
    • Lung volume reduction surgery
    • Indicated in if on maximal medical therapy and still have marked ADL restriction. Must have:
      • FEV1 > 20% predicted
      • Upper lobe predominant emphysema
    ‣
    What are the indications for long-term O2 therapy?
    1. PaO2 of < 7.3 kPa (measured when the patient is clinically stable, on two occasions, at least 3 weeks apart)
    2. PaO2 of 7.3 - 8 kPa & one of the following:
      • Nocturnal hypoxaemia (SaO2 < 90%)
      • Secondary polycythaemia
      • Pulmonary hypertension (pulmonary artery pressure > 25mmHg)
      • Peripheral oedema
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What should they all have?
  • Annual pneumococcal & flu vaccine
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Lung cancer
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What are your differentials for a lung nodule on CXR? (6)
  • Malignancy - 1° or 2°
  • Foreign Body
  • Abscess / cyst
  • Granuloma - Sarcoid / TB
  • Pulmonary hamartoma / AVM
  • Skin tumor
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Classifying lung cancer
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Primary
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NSCLC (85%): What are the types?
  1. Adenocarcinoma (~ 40%)
      2. ‣
      How is this presentation different to the rest?
      • Presents in non-smoking women (but still in smokers too)
    1. Best prognosis
  2. Squamous cell carcinoma (~ 30%)
    • Present in the mediastinum, develop from the bronchi
      • ‣
      What is it associated with?
      • Hypercalcaemia - Secretes PTH
      • Hypertrophic pulmonary osteoarthropathy (affects hands & feet)
  3. Large cell carcinoma (~ 10%)
    • Likely to metastasise
  4. Carcinoid
    5. ‣
    What is this?
    • Neuroendocrine tumour secreting serotonin, histamine & bradykinin
    ‣
    What are the features?
    • Bradykinin → Facial flushing
    • Histamine → SOB
    • Serotonin → Diarrhoea, asthma & SOB
    ‣
    How do you investigate it?
    • Urinary 5-HIAA
    • Octreotide scan
    ‣
    How do you manage it?
    • Somatostatin analogues: Octreotide
  5. Mesothelioma
    6. ‣
    What is this?
    • Pleural tumour associated with asbestos exposure with a long latent period of up to 45 years between exposure and cancer development.
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SCLC (~ 20%)
  • Aggressive, quickly metastasise, strongly related to smoking.
  • Release neuroendocrine hormones, meaning they commonly cause paraneoplastic syndromes.
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Secondary
  • Metastases from other sites
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Paraneoplastic syndromes

Name the paraneoplastic syndrome & tumour causing it:

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Hoarse voice
  • Recurrent laryngeal nerve palsy
  • Upper lung tumour
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Pemberton's sign is positive
  • SVCO
  • Upper lung tumour
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Ptosis, miosis & anhidrosis
  • Horner's syndrome
  • Pancoast (apical) tumour compressing the sympathetic ganglion
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Severe hyponatraemia
  • SIADH
  • SCLC secreting ADH causing dilutional hyponatraemia
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Striae, weight gain, easy bruising, T2DM, interscapular fat pad, spinal tenderness, HTN
  • Cushing's syndrome
  • SCLC secreting ACTH
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Bone pain, renal stones, abdominal pain, confusion
  • Hypercalcaemia
  • Squamous cell carcinoma secreting PTHrP
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Proximal muscle weakness that improves on exercise, diplopia & ptosis
  • Lambert-Eaton syndrome
  • SCLC

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How might they present?
  • Cough
  • Shortness of breath
  • Weight loss
  • Haemoptysis
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How do you investigate a suspected lung cancer?
  1. CXR:
    • Pleural effusion (usually unilateral - exudative)
    • Mass
    • Atelectasis
  2. Contrast-enhanced CT thorax, abdomen, pelvis (CT TAP):
    • Confirm diagnosis & staging
    • PET-CT may also allow us to more clearly see metastases
  3. Bronchoscopy with EBUS (endobronchial USS) with transbronchial needle aspiration for histology
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What are the management options & indications for each?
  • Lifestyle:
    • Smoking cessation
  • Medical:
    • Chemotherapy: Metastases
    • Radiotherapy: Can be definitive in adenocarcinoma (but surgery is preferred)
  • Surgical:
    • Lobectomy/segmentectomy → Localised disease (T1/2 N0 M0)
    • Pneumonectomy/bi-lobectomy → Extensive disease
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Alveoli
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Pneumonia

Infection of the lung tissue.

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What is the pathophysiology of consolidation?
  • Bacteria infect alveoli → Pulmonary membrane inflammation → Increased permeability → Blood & fluid entering alveoli causing consolidated appearance (filled with liquid)
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How do you assess the severity?

CURB-65 (1 point for each of the following):

  • Confusion: New disorientation to time, place or person
  • Urea > 7
  • RR ≥ 30 bpm
  • BP < 90/60 mmHg
  • > 65 years
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How do you classify pneumonia?
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Typical
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Community-acquired pneumonia (CAP)
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What are the common causes?
  1. S. pneumonia (50%)
  2. H. influenzae (20%)
    3. ‣
    What is shown on culture?
    • Gram ⊖ coccobacilli
  3. Moraxella catarrhalis
    4. ‣
    Who presents with this?
    1. Immunocompromised patients
    2. Chronic pulmonary disease patients

Cases:

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A patient has signs of pneumonia and the following rash:
‣
What is the rash called and the underlying pathogen?
  • Rash: Herpes labialis
  • Pathogen: S. pneumoniae (Gram ⊕ diplococci)
‣
How can you confirm this diagnosis?
  • Pneumoncoccal urinary antigen
  • CXR: Lobar consolidation
Speifensender, CC BY-SA 3.0
Speifensender, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
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What is the most common cause of an infective exacerbation of COPD?
  • H. influenzae (Gram ⊖ coccobacilli)
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Patient presents with headache, fever, myalgia and cough, chest clear. What is this likely to be?
  • Influenza
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A patient with cystic fibrosis presents with pneumonia. What organism could this be?
  • Pseudomonas aeruginosa (Gram ⊖ bacilli)
  • Staphylococcus aureus (Gram ⊕ cocci)
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Hospital-acquired pneumonia (HAP)

Lower respiratory tract infection (LRTI) developing > 48 hours after admission to hospital.

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What are the common causes of HAP? (4)
  1. P. aeruginosa (Gram ⊖ bacilli) - Associated with mechanical ventilation
  2. S. aureus (Gram ⊕ cocci)
  3. Enterobacteria:
    1. E. coli (Gram ⊖ bacilli)
    2. Klebsiella (Gram ⊖ bacilli)

Cases:

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A patient with leukaemia recently had the flu and now has a bacterial pneumonia. What is the cause?
  • S. aureus: Associated with flu, lymphoma/leukaemia, IVDU
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An alcoholic presents fever, red currant sputum & bronchial breathing in the upper zones. What is the cause?
  • Klebsiella
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Aspiration
‣
Who is at risk of this?
  1. Stroke
  2. Myasthenia gravis
  3. Bulbar palsy
  4. Alcoholics
  5. Epileptics due to post-ictal state
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What are they at risk of developing?
  • Lung abscess causing recurrent fever, finger clubbing and foul smelling breath
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Atypical

Pneumonia caused by an organism that cannot be cultured or detected using a gram stain.

‣
Name the 5 of them.

"Legion of psittaci MCQ"

  1. Legionella
  2. Chlamydia psittaci
  3. Mycoplasma pneumoniae
  4. Chlamydydophila pneumoniae
  5. Q fever (coxiella burnetii)

Cases:

‣
A patient presents with pneumonia but also has a rash made up of circular lesions across the body, her LFTs also show high bilirubin. Diagnosis?
  • Mycoplasma pneumonia. Rash → Erythema multiforme.
    • ‣
    Why has she got raised bilirubin?
    • Cold AIHA (see haematology) → ↑ RBC breadown → ↑ Bilirubin
    ‣
    What is the diagnostic test for this?
    • Mycoplasma serology
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A patient returns from holiday feeling SOB and with pleuritic chest pain. She has deranged LFTs and hyponatraemia. Diagnosis?
  • Legionella
    • ‣
    Why do they have hyponatraemia?
    • Legionella → SIADH
    ‣
    How is this diagnosis confirmed?
    • Urinary legionella antigen
    ‣
    How is it managed?
    • Clarithromycin
‣
A patient has D&V, dry cough, fever & polyarthralgia. He works at a local zoo cleaning bird cages. Pathogen?
  • Chlamydia psittaci
‣
Farmer who has been exposed to the bodily fluids of all of his animals presents with a flu-like illness. Pathogen?
  • Coxiella burnetii
‣
Fungal
‣
A patient with HIV presents with exertional dyspnoea. Likely pathogen?
  • Pneumocystis jiroveci (see Infectious disease)
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Management

For all of these, the antibiotic choice depends on local guidelines. However, these are more commonly used.

‣
How is CAP managed? (Depending on CURB-65)
  • 0-1: Home, PO amoxicillin / clarithromycin 5 days
  • 2: Admit, PO/IV amoxicillin & clarithromycin 7 days
    • Penicillin allergy: PO/IV clarithromycin
  • ≥ 3: ITU, IV co-amoxiclav/ceftriaxone/tazocin & clarithromycin
‣
How is HAP managed?
  1. < 5 days from admission: Co-amoxiclav
  2. > 5 days from admission: Tazocin / ciprofloxacin
‣
What complications can occur?
  1. Sepsis
  2. Pleural effusion (exudative)
  3. Lung abscess

Case:

‣
Patient with pneumonia and pleural effusion is on IV antibiotics and yet still has a fever. Pleural fluid aspirate shows pH < 7.2. Diagnosis & management?
  • Empyema → Chest drain & antibiotics
‣
Pulmonary oedema

Fluid collection within the alveoli.

‣
What are the 2 types & the differences between them?
  1. Cardiogenic
    • ↑ hydrostatic pressure in the pulmonary vessels (due to overload) → Transudative fluid in alveoli
      • ‣
      What is the cause of this?
      • Heart failure
  2. Non-cardiogenic
    • Acute lung inflammation → ↑ vascular permeability & ↑ hydrostatic pressure (due to vascular resistance) → Exudative fluid in alveoli
      • ‣
      What are the causes of this?
      1. ARDS: Sepsis, trauma, pancreatitis
      2. High altitude
      3. Opioid/salicylate toxicity
      4. PE
‣
What are you looking for on CXR?
  1. Bats wing airspace shadowing
    2. Frank Gaillard, CC BY-SA 3.0
    Frank Gaillard, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
  2. Signs of heart failure:
    • Alveolar oedema
    • Kerley B lines
    • Cardiomegaly
    • Upper lobe diversion
    • Pleural effusion
      • Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
      Mikael Häggström, CC0, via Wikimedia Commons. No changes were made.
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🍇 Interstitium

The interstitium is the tissue surrounding the alveoli, the tissue that oxygen moves across when passing from the alveoli to the blood, including alveolar epithelium, pulmonary capillary endothelium and basement membrane.

‣
Diagram: Anatomy
Anatomyclassproj1, CC BY-SA 4.0
Anatomyclassproj1, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Diseases:

‣
Interstitial lung disease (ILD)
‣
Types:
‣
Upper lobe pulmonary fibrosis: Causes?
  1. Coal worker's lung
  2. Hypersensitivity pneumonitis
    3. ‣
    What is this?
    • Type III hypersensitivity to environmental allergen causing tissue inflammation (extrinsic allergic alveolitis).
    ‣
    What do you see on bronchoalveolar lavage?
    • Lymphocytes
    • Mast cells
    ‣
    Name 3 examples.
    1. Bird-fanciers lung → Bird droppings
    2. Farmer's lung → Hay mold spores
    3. Malt workers lung → Mould on barley
  3. Ankylosing spondylitis
  4. Radiation
  5. Tuberculosis
  6. Sarcoidosis
‣
Lower lobe pulmonary fibrosis: Causes?
  1. Idiopathic
    2. ‣
    What are 2 common exam findings?
    • Bibasal fine crackles
    • Finger clubbing
    ‣
    How is it managed?
    1. Pirfenidone: Antifibrotic & inflammatory
    2. Nintedanib
  2. Connective tissue disorders (except ankylosing spondylitis)
    3. ‣
    Examples?
    • SLE
    • RA
    • Systemic sclerosis
  3. Drug-induced: 
    4. ‣
    Examples?
    • Methotrexate
    • Cyclophosphamide
    • Amiodarone
    • Bleomycin
  4. Asbestosis
    5. ‣
    What happens here?
    • Asbestos is fibrinogenic (so induces fibrosis in the tissues) & oncogenic
    • There is a gap between exposure & mesothelioma
‣
How do you investigate this?
  1. CT: "Ground glass appearance" / "Honeycombing"
  2. Lung biopsy
‣
Sarcoidosis
‣
What is this?
  • Build up of inflammatory cells in the tissues forming non-caseating granulomas.
  • It’s triggered by the immune system reacting to foreign substances (viruses, bacteria, chemicals)
‣
Presentation:
‣
What is this associated with?
  • Erythema nodosum (painful)
  • Parotid gland swelling
  • Lymphadenopathy
‣
What electrolyte abnormality does it cause?
  • Hypercalcaemia: Macrophages inside the granulomas causing an increased conversion of vitamin D to its active form.
‣
What are the less common features?
  • Neurological: Bilateral facial nerve palsies
  • Ocular: Anterior uveitis
  • Cardiovascular: Heart block/arrhythmia
  • Gastrointestinal: Hepatomegaly
  • Dermatological: Lupus pernio
‣
Investigations:
‣
What are your initial investigations? (6)
  • Bedside:
    • Spirometry: Restrictive picture
    • ECG: Checking for heart involvement
  • Bloods:
    • FBC: Lymphopenia due to lymphocytes all clustered in tissues
    • U&E: Abnormal if renal stones
    • LFTs: Cholestasis or cirrhosis
    • Calcium: Hypercalcaemia
    • Serum ACE (Raised in 50%)
  • Imaging:
    • CXR
‣
How is it staged based on CXR?
  • Stage 0: No changes
  • Stage 1: Bilateral hilar lymphandenopathy
  • Stage 2: Lymphadenopathy with pulmonary infiltrates (presence of a substance denser than air)
  • Stage 3: Pulmonary infiltrates alone
  • Stage 4: Fibrosis
Jmh649, CC BY-SA 3.0
Jmh649, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
How is it definitively diagnosed?
  • Biopsy showing non-caseating granulomas
‣
Management:
‣
How is it managed based on stage?
  • Stage 1 (hilar lymphandenopathy):
    1. Conservative
  • Stage 2 (pulmonary infiltrates):
    1. Prednisolone (40mg)
    2. Methotrexate / azathioprine
‣
What is the prognosis?
  • 60% of patients with pulmonary sarcoidosis have symptom resolution at 2 years.
  • 20% respond to steroids.
  • 20% show no improvement.
‣
🌽 Pleura

The pleura is a double-layered serous membrane that covers each lung (visceral), and lines the thoracic cage (parietal). The pleural space sits between them contains a small amount of serous fluid.

‣
Diagram: Anatomy
Cancer Research UK, CC BY-SA 4.0
Cancer Research UK, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.

Diseases:

‣
Pneumothorax

This is an abnormal collection of air in the pleural space between the lung and the chest wall.

‣
Simple pneumothorax
‣
What are the important history points and investigations to determine the management?
  1. Do they have an underlying lung condition?
    • Cystic fibrosis, asthma, COPD.
  2. Are they short of breath?
  3. CXR: Size of pneumothorax
‣
How do you investigate for this?
  • Erect CXR
    • ‣
    How do you assess the size of the pneumothorax?
    • At the level of the hilum, measure horizontally from the chest wall to the lung edge.

Cases:

‣
What is the cause of the following pneumothorax?
‣
Answer
  • Right-sided rib fractures
James Heilman, MD, CC BY-SA 4.0
James Heilman, MD, CC BY-SA 4.0 creativecommons.org/licenses/by-sa/4.0, via Wikimedia Commons. No changes were made.
‣
Primary: No underlying cause

How are the following patients managed:

‣
Not SOB & CXR shows pneumothorax < 2cm on CXR?
  • Conservative
‣
SOB or pneumothorax > 2cm on CXR?
  1. Aspirate with a 16-18G cannula under local anaesthetic
  2. Insert chest drain
‣
Secondary: Underlying lung condition

How are the following patients managed:

‣
Not SOB AND the pneumothorax is < 1cm on CXR?
  • Conservative
‣
Not SOB and the pneumothorax is 1-2 cm on CXR?
  1. Aspirate
  2. Chest drain
‣
SOB OR the pneumothorax is > 2 cm on CXR?
  • Chest drain
‣
Tension pneumothorax
‣
How does this differ from a simple pneumothorax?
  • Tension pneumothorax occurs when there is a one-way valve that allows air into the pleural space, but does not allow it out. This causes the pressure to build up and is a very severe, life-threatening condition.
‣
What can you see on the following CXRs?
‣
Answer
  • Tracheal deviation.
  • Absence of lung markigs in the left upper zone.
  • Collapse of the left lung secondary to the pressure exerted by the pneumothorax.
Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D.Consent note: Written informed consent was obtained from the individual, including online publication., CC0, via Wikimedia Commons. No changes were made.
Mikael Häggström, M.D. Author info - Reusing images- Conflicts of interest: NoneMikael Häggström, M.D.Consent note: Written informed consent was obtained from the individual, including online publication., CC0, via Wikimedia Commons. No changes were made.
‣
How is this acutely managed?
  1. ABCDE
  2. Needle decompression using a 16-gauge cannula (gray) inserted at the second intercostal space, mid-clavicular line.
    • Insert just above the third rib to avoid damage to neurovascular bundle
  3. Chest drain
‣
What definitive management will stop the pressure from building up again?
  • Chest drain, sited within the triangle of safety.
    • Triangle of safety borders: 5th intercostal space, mid axillary line, anterior axillary line.
‣
Pleural effusion

A buildup of fluid within the pleural space.

‣
Where do you insert a chest drain?
  • Triangle of safety: Space between the base of the axilla, lateral edge pectoralis major, 5th intercostal space and the anterior border of latissimus dorsi
    • ‣
    What are the contraindications?
    • INR > 1.3
    • Platelet count < 75
    • Pulmonary bullae
    • Pleural adhesions
‣
How do you investigate pleural effusion & what do you test for?
  • Thoracocentesis (aspirate fluid):
    • Exudate vs transudate
      • Protein < 25 → Transudate. Protein > 35 → Exudate
      • LDH: Pleural fluid LDH is > 2/3 the upper reference limit for serum LDH in exudative
    • Culture
    • Cytology (Malignancy)
    • Glucose (↓ in RA)
    • NT-proBNP (↑ in HF)
‣
How does investigation of a unilateral effusion differ from bilateral?
  • Unilateral always requires thoracocentesis whereas if bilateral is with HF symptoms & signs then it is only done if medical therapy is unsuccessful.
    • HF would be investigated with a transthoracic ECHO
‣
What are the causes of:
‣
Exudate (6)
  1. Infection (most common exudate): Pneumonia, TB, subphrenic abscess
  2. Connective tissue disease: RA, SLE
  3. Neoplasia: Lung cancer, mesothelioma, metastases
  4. Pancreatitis
  5. PE
  6. Dressler's syndrome
‣
Transudate (4)
  1. HF (most common transudate)
  2. Hypoalbuminaemia: Liver disease, nephrotic syndrome, malabsorption
  3. Hypothyroidism
  4. Meigs' syndrome: Ovarian tumour
‣
When would you request pleural fluid cytology?
  • ? malignant pleural effusion
‣
🩸 Pulmonary Circulation

This is the system of transportation, taking de-oxygenated blood from the heart to the lungs to be re-saturated with oxygen before being dispersed into the systemic circulation.

‣
Diagram: Anatomy
OpenStax College, CC BY 3.0
OpenStax College, CC BY 3.0 creativecommons.org/licenses/by/3.0, via Wikimedia Commons. No changes were made.

Diseases:

‣
Pulmonary embolism (PE)

Thrombus within the pulmonary arteries.

‣
What is Virchow's triad?

Triad of factors contributing to thrombosis:

  1. Endothelial injury
  2. Blood flow stasis
  3. Hyper-coagulability: Malignancy, thrombophilia, previous VTE, polycythemia
‣
How do we prevent VTE in hospital?
  1. LMWH (depends on local guidelines as to which one)
    2. ‣
    When do we avoid giving this?
    1. Active bleeding
    2. Already anticoagulated, e.g. on warfarin
  2. Compression stockings: TEDS

Presentation:

‣
How symptoms are key to look for in PE?
  1. SOB
  2. Haemoptysis
  3. Pleuritic chest pain
‣
What scoring system is used to assess if somebody is likely to have a VTE?

Investigations & Management:

‣
How would you investigate a potential PE? (8)
  • Bedside:
    • ECG
      • ‣
      What are you looking for?
      • Sinus tachycardia
      • May have S1Q3T3 (but less common)
  • Bloods:
    • ABG
      • ‣
      What would you find?
      • T1RF / Respiratory alkalosis (hyperventilation)
    • FBC, U&E, CRP
    • Clotting
  • Imaging:
    • CXR: Likely normal, important to rule out differentials including cancer and pneumonia.
    • CT pulmonary angiogram (CTPA)
    • VQ scan
    • Lower limb duplex scan - DVT (first-line in pregnancy)
    • Echocardiogram - If massive PE causing right heart strain
‣
How does a CTPA work?
  • CT chest with IV contrast that allows us to identify clots within the pulmonary arteries
    • James Heilman, MD, CC BY-SA 3.0
    James Heilman, MD, CC BY-SA 3.0 creativecommons.org/licenses/by-sa/3.0, via Wikimedia Commons. No changes were made.
‣
Whilst waiting for investigations to confirm diagnosis, what should you administer?

NICE guidelines (March 2020) recommend:

  • Apixaban/rivaroxaban
  • Low molecular weight heparin (LMWH) may be used depending on local guidelines
‣
Thrombolysis
‣
Who is considered eligible for thrombolysis?

Massive PE causing:

  • Haemodynamic instability
  • Right heart strain
‣
How does it work & what are the risks?
  • Alteplase breaks down fibrin in the clots, rapidly dissolving them. This puts them at increased risk of bleeding elsewhere, e.g. intracranially.
‣
Long-term management:
‣
What are the options?
  1. Warfarin
    2. ‣
    Target INR?
    • 2-3
  2. DOAC
  3. LMWH
    4. ‣
    When is this used?
    • Active cancer
    • Pregnancy
‣
When would you anticoagulate for 3 months?
  • Provoked VTE, cause is identifiable.
‣
When would you anticoagulate for 6 months then review?
  • Unprovoked VTE due to unknown cause or irreversible cause.
    • Active cancer
    • Thrombophilia
‣
Pulmonary hypertension

Increased pressure within the pulmonary arteries.

‣
Name 5 causes.
  • Primary pulmonary hypertension / connective tissue disease, e.g. SLE
  • Heart failure (left): Poor LV function causes back pressure
  • Chronic lung disease, e.g. COPD.
  • Pulmonary vascular disease, e.g. PE.
  • Sarcoidosis / haematological disorders
‣
How would they present?
  1. Progressive SOB, fatigue,
  2. Syncope: Ventricular wall stress can cause vasovagal syncope
  3. Signs of right heart failure
‣
How do you investigate it?
  1. ECG: Right axis deviation, RBBB
  2. CXR: RVH
  3. Echocardiogram: Look at RV function & estimate pulmonary pressures
  4. Right heart catheterisation: Diagnostic
    • ≥ 25 mmHg
‣
How do you manage it?
  • IV prostanoids, powerful vasodilators acting through prostaglandin system (e.g. epoprostenol).
  • Phosphodiesterase-5 inhibitors, prolonging the action of nitrous oxide causing vasodilation (e.g. sildenafil).
‣
CO poisoning
‣
How would they present?
  1. Confusion
  2. N&V
  3. Cherry red skin
‣
How do you investigate it?
  1. ABG: Carboxyhaemoglobin > 20% (diagnostic)
  2. CXR: ARDS
‣
How are they managed?
  1. 100% O₂
  2. Hyperbaric (higher pressure than normal) O₂

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