Respiratory Flashcards
1
Q
Overview of Acute bronchitis
A
Overview
- Self-limiting LRTI char. by inflammation of the bronchi
- 90% caused by a virus
- Usually follows an upper RTI
- Presents with cough, can be in comb. with sputum, runny nose, headache, malaise
- Mx with adequate hydration & possibly NSAIDs for Sx relief
- ABx not indicated unless at risk of 2nd bacterial infection
2
Q
Aetiology & Clinical Features of Acute Bronchitis
A
Aetiology
- Viruses (>90%)
- Influenza A & B
- Parainfluenza
- Adenovirus, RSV, Rhinovirus, Coronavirus
- Bacteria, environmental aetiologies
Clinical features
- Cough > 5 days
- Resolves in 2-3 weeks
- Sputum (50%), esp as infection progresses
- Represents sloughing of cells from the tracheobronchial epithelium + inflammatory cells
- Runny nose & sore throat
- Chest pain, dyspnea
- Headache
- Malaise
- Myalgia
- Fever uncommon
3
Q
DD of Acute Bronchitis
A
- Bronchiolitis
- Pneumonia
- DD of acute cough
- DD of chronic cough (if cough persisting ≥ 8 weeks)
4
Q
Treatment of Acute Bronchitis
A
- Rest & adequate hydration
- NSAIDs (myalgia, chest pain, headache)
- ABx not recommended
- Unless ^ risk of bacterial infection
- Smokers
- Elderly
- Immunocompromised
- Pts with lung disease
- Pts with suspected DD
- Unless ^ risk of bacterial infection
- Antitussives, expectorants & bronchodilators generally not recommended
- Generally self-limiting
5
Q
Overview of Anthrax
A
Overview
- Rare, infectious disease by Bacillus anthracis
- A gram-positive spore-forming non-motile rod found in soil
- Zoonotic infection, primarily infects cows, goats, sheep
- Human infection usually from infected livestock or animal products (e.g. wool, meat)
- An occupational hazard for pts handing livestock & process potentially infected animal materials
- Person-to-person infection usually doesn’t occur
- Three clinical syndromes
-
Inhalation anthrax
- Results in haemorrhagic mediastinitis
- Fever, acute, nonproductive cough
- Retrosternal chest pain
- And/or pleural effusion
- Results in haemorrhagic mediastinitis
-
Cutaneous anthrax (most common)
- Starts with papular lesion > later vesicular > necrotic eschar
-
Gastrointestinal anthrax (very rare)
- Causes GI ulceration
- Haematemesis
- Bloody diarrhoea
- Causes GI ulceration
-
Inhalation anthrax
- High mortality, but swift Rx with ABx can increase survival
- Better prognosis for cutaneous than for inhalation & GI
6
Q
Pathophysiology of Anthrax
A
Pathogen
-
Bacillus anthracis
- Gram-positive, spore-forming, non-motile rod
- Edge of colony shows irregular comma-shaped outgrowths on blood agar (‘Medussa head’)
-
Antiphagocytic capsule (poly-D-glutamate)
- Only bacterium with a polypeptide capsule, protects from lysis following phagocytosis
Anthrax toxin
- Responsible for the local and systemic manifestation of anthrax
- Made up of A and B subunits
-
A subunit - 2 components
- ED (edema factor) > cell edema
-
LF (lethal factor)
- A metalloprotease which destroys MAPKK (mitogen-activated protein kinase) > cell death
-
B subunit
- Binds to epithelial receptors > facilitates entry of the A subunit into the host cell
-
A subunit - 2 components
7
Q
Clinical Features of Anthrax
A
Cutaneous
- Incub period typically 5-7 days
- Pruritic papules > vesicle > ulcer with surrounding oedema (black eschar)
Inhalation
- Incub period typically 1-3 days
- Prodromal phase - nonspecific Sx (fever, malaise)
- Fulminant phase
- Substernal chest pain
- High-grade fever
- Progressive dyspnoea
- Hypoxia
- Shock
- Haemorrhagic mediastinitis (mediastinal widening)
- CT
- Mediastinal widening
- Perihilar interstitial pneumonia
- Haemorrhagic pleural effusion
Gastrointestinal
- Incub period 2-5 days
- N&V
- ABdo pain
- Severe, bloody diarrhoea
- Haematemesis
- Haemorrhagic lymphadenitis
Bloods
- Leukocytosis
- ^ AST, ALT
8
Q
Treatment of Anthrax
A
Causative
-
Without systemic spread
-
All three syndromes
-
Oral monotherapy
- Fluoroquinolone (e.g. ciprofloxacin), or
- Doxycycline
-
Oral monotherapy
- Systemic spread in cutaneous only 5-10%
-
All three syndromes
-
With systemic spread
-
All three syndromes
- Antitoxin therapy
- Raxibacumab, obiltoxaximab, anthrax immunoglobulin
-
Combination of IV ABx
- Pts w/out meningitis
- Ciprofloxacin & linezolid
- Pts w/ meningitis
- Ciprofloxacin & linezolid & meropenem
- Pts w/out meningitis
- Antitoxin therapy
-
All three syndromes
9
Q
Lethality of Anthrax
A
Cutaneous
- < 1% with ABx treatment
- ~ 20% w/out
Inhalation
- ~ 50% with ABx treatment
- > 90% w/out
GI - ~ 40%
10
Q
Vaccine for Anthrax
A
AVA (anthrax vaccine adsorbed)
- Pre-exposure prophylaxis: AVA
- Post-exposure prophylaxis
- AVA along with ABx
11
Q
Overview of Aspergillosis
A
Overview
- Collective term for diseases caused by mould species in the genus Aspergillosis
- Aspergillus spores ubiquitous, but do not usually cause infection in immunocompetent individuals
- RFs
- Immunosuppression
- Underlying pulmonary conditions (TB, COPD)
- Pre-existing bronchopulmonary conditions (asthma, CF)
- May cause allergic bronchopulmonary aspergillosis (ABPA)
- PC asthmatic Sx or sinusitis
- May cause allergic bronchopulmonary aspergillosis (ABPA)
- Elevated IgE levels & eosinophilia > fungal infection
- Dx: Tissue biopsy, HPThology & culture
- Rx
- Voriconazole, or
- Amphotericin B, or
- Caspofungin
- Aspergilloma must be surgically removed
- Immunocompromised pts - prophylactic posaconazole
12
Q
Clinical Features of Aspergillosis
A
Allergic bronchopulmonary aspergillosis (ABPA)
- Due to chronic exposure to Aspergillus
-
Lungs
- Asthmatic Sx (SOB, wheezing)
- Productive cough - brown bronchial mucous casts
-
Sinusitis w/out tissue infiltration
- Chronic rhinosinusitis
- Non-sp Sx - weight loss
-
Lungs
Chronic pulmonary aspergillosis
- Can be asymptomatic (incident finding on CXR)
- Weight loss, fatigue
- Cough, haemoptysis, SOB
- Signs of underlying lung pathology (e.g. digital clubbing in TB)
- Possible clinical manifestation
-
Aspergilloma
- Opportunistic infection of a pre-existing cavitary lesion (e.g. previous TB)
-
Aspergilloma
Invasive aspergillosis
-
Lungs: pulmonary aspergillosis
- Most common form
- Dry cough, in severe cases, haemoptysis, fever, pleuritic ChP
-
Mucous membranes in sinuses
- Aspergillus sinusitis
13
Q
Aetiology of Aspergillosis
A
Pathogen
-
Aspergillus (200 species)
- Aspergillus flavus, fumigatus
Transmission
- Airborne exposure to mould spores
- Aspergillus spores ubiquitous indoors
- May be found in ITUs (CU ventilators)
Risk factors
-
Destructive pulm pathology > Chronic pulm aspergillosis
- Scar tissue or lung cavities (TB)
- COPD, emphysema
-
Severe immunosuppression
- HIV, neutropenia > Invasive aspergillosis
-
Pre-existing bronchopulmonary conditions
- Asthma, CF > ABPA
14
Q
Treatment of Aspergillosis
A
- Voriconazole, or
- AmphotericinB, or
- Caspofungin
15
Q
Overview of Chlamydia infections
A
Overview
- A family of gram-negative, obligate intracellular bacteria
-
Chlamydia trachomatis
- Serotype A-C > affect the eye > trachoma
- Serotype D-K
- GU infection (vaginitis, PID, urethritis)
- Conjunctivitis, infant pneumonia
- Serotype L1-L3 > lymphogranuloma vereneum
-
Chlamydophila pneumoniae
- Respiratory infection
-
Chlamydophila psittaci
- Respiratory infection
- Psittacosis (zoonotic bird infection)
-
Chlamydia trachomatis
- Chlamydial infections
- Diagnosed clinically
- Rx
- Doxycycline, or
- Macrolides (azithromycin)
- In STI infections
- Expedited partner therapy should be started asap
16
Q
Characteristics of Chlamydia
A
Bacteria characteristics
- Gram-negative, but does not gram stain well
- Obligate intracellular > cannot produce its own ATP
- Lack of peptidoglycan in the cell wall (B-lactams ineffective)
- Visible as cytoplasmic inclusion bodies on Giemsa stains
17
Q
Features of Chlamydia
A
18
Q
Infant pneumonia due to Chlamydia Trachomatis
A
- Perinatally during delivery
- Incub period: 4-12 weeks after delivery
- Clinical features: pneumonia
- Stacatto cough, tachypnoea, nasal congestion
- Usually afebrile
- Ass with neonatal conjuctivitis 50%
- Complications - respiratory failure
- Treatment
- Oral erythromycin or azithromycin (macrolides)
19
Q
Chlamydophila psittaci
A
- Psittacosis (‘parrot fever’) latin for parrot
- Airborne > feces > exposure to infected birds
- Incubation 1-3 weeks
- Clinical features
- Acute onset of flu-like Sx, esp fever
- Atypical pneumonia with non-prod cough
- Notifiable
- Treatment
- 1st: doxycycline
- 2nd: macrolides (azithromycin, erithro)
- Choice for kids and preg women
- Alternative: fluoroquinolones (cipro)
20
Q
Overview of Influenza
A
Overview
- Highly contagious
- Typically during the winter months
- Influenza virus A, B, C
- If symptomatic
- Sudden onset high fever
- Headache, myalgia
- Non-prod cough
- Severe malaise
- Dx
- Rapid antigen testing
- In some cases, bacterial superinfection can develop
- Staph. aureus, strep. pneumoniae
- Productive cough, high inflam markers
- Staph. aureus, strep. pneumoniae
- Rx
- Supportive - rehydration, antipyretics
- Antiviral Rx possible for pt at high risk of Cx
- Neuraminidase inhibitors
- Oseltamivir (oral)
- Zanamivir (inh)
- Peramivir (IV)
- If Rx started w/in 48h after Sx onset, can shorten duration and reduce Cx of the disease
- Neuraminidase inhibitors
21
Q
High risk groups for complications of Influenza
A
High-risk groups for complications
- Elderly ≥ 65 yoa
- Children < 5, esp < 2 yoa
- Pregnant women
- Pts with chronic medical conditions
- Asthma
- Heart disease
- DM
- Immunocompromised
- Nursing home residents
22
Q
Cx of Influenza
A
Primary influenza pneumonia
- Haemorrhagic pneumonia with poor prognosis
- May progress to ARDS with respiratory/multiorgan failure
2nd bacterial bronchitis/pneumonia
- After flu Sx improved, pts suddenly become febrile again & develop productive cough with large amounts of purulent sputum (smt bloody)
- Pathogens
- Strep. pneumoniae, but also S. aureus & H. influenzae
- Signs of 2nd infection with S. aureus
- Hyperacute onset of Sx
- Hypoxaemia
- Haemoptysis
- Multiple cavitary lesions on CXR (pneumatoceles)
- Sign of necrotizing bronchopneumonia
- Rx
- Penicillinase-resistant agents should be used
- Aminopenicillins with beta-lactamase inhibitors
- E.g. co-amoxiclav
- Aminopenicillins with beta-lactamase inhibitors
- Penicillinase-resistant agents should be used
23
Q
Overview of Legionellosis
A
Pneumonia caused by Legionella pneumophila
- Gram-negative flagellated rod thriving in aqueous environments
- Whirlpools/hot tubs, swimming pools, showers
- Air-conditioning units
- Ass with nursing homes, hospitals (10% of HAP), hotels, cruise ships etc
- Notable RFs
- Smoking, chronic lung disease
- Advanced age, immunosuppression
-
Legionnaires’ pneumonia (atypical form)
- SOB, cough, fever
- Often in comb. with other Sx
- GI - e.g. diarrhoea, N&V
- Neuro - e.g. confusion
- Notifiable
-
Pontiac fever
- Milder, self-limiting, flu-like illness
- Dx - urine antigen test to confirm L. pneumophilia
- Rx
- Quinolones (e.g. ciprofloxacin), or
- Macrolides (e.g. azithromycin)
24
Q
Legionnaire’s disease
A
- Incubation 2-10 days
-
Clinical features
- Fever, chills, headache
- Pneumonia
- Unilateral lobar pneumonia, or
- Atypical pneumonia (dry cough > can become productive, chills, SOB)
- Diarrhoea, N&V
- Neurological abnormalities - confusion, agitation
- Failure to respond to beta-lactam monotherapy
-
Treatment
- 1st: Quinolones (e.g. cipro) 7-10 days
- 2nd: Macrolides (azithro, erithro) 3 weeks
25
Most common causes of Pleural Effusion
* Cardiac failure
* Pneumonia
* Malignancy
* PE
26
Management of Pleural Effusion
1. Undiagnosed pleural effusion
2. History, examination, CXR, pleural USS
3. Heart failure likely?
1. Yes \> Treatment, monitor
2. No \>
4. Pleural aspiration
1. Protein, LDH, glucose
2. pH
3. M,C & S
4. +/- AFB, Triglycerides, cholesterol, chylomicrons, amylase, haematocrit
5. Cause apparent?
1. Yes \> treat & monitor
2. No \>
6. CT thorax (pleural phase contrast enhancement)
7. Pleural biopsy
1. CT/USS-guided or local anasthetic thoracoscopy/VATS
8. Cause apparent?
1. Yes \> treat and monitor
2. No \>
9. Reconsider PE, TB
1. Aetiology unknown in 10-15% cases
27
**Chlamydophila pneumoniae**
* Transmission via respiratory droplets
* Incub period 3-4 weeks
* Clinical features
* Mild in young adults, severe in elderly
* Can be asymptomatic
* **Atypical pneumonia**
* Fever
* Non-productive cough
* Headache, myalgia
* Can be ass w/ pharyngitis & hoarseness
* Treatment
* 1st: oral **azithromycin**, clarithromycin
* 2nd: oral doxycycline
28
What to do after thoracocentesis (pleural tap)?
1. Note pleural fluid appearance
2. Send sample to **biochemistry**
1. **Glucose, protein, LDH**
3. Send a fresh 20 mL sample in sterile pot to **cytology** (for malignant cells & differential cell count)
4. Send samples in sterile pot to **microbiology** for Gram stain & microscopy, culture
5. For suspected pleural infection \> send pleural fluid in **blood culture bottles**
6. Low threshold for AFB stain & TB culture
7. Process non-purulent, heparinized samples in ABG analyser for **pH**
29
What are the Light's criteria
Pleural effusion is **exudative** if it meets one of the following criteria
* Pleural fluid protein / serum protein ratio \> **0.5**
* Pleural fluid LDH/serum LDH ratio \> **0.6**
* Pleural fluid LDH \> **2/3s** of the upper limit of normal serum LDH
30
Transudative pleural effusions
Mechanism
* Increased hydrostatic pressure, or
* Reduced osmotic pressure (hypoalbuminaemia)
31
Exudative pleural effusion
Mechanism
* Increase in capillary permeability and impaired pleural fluid resorption
32
What is the definition of haemothorax?
If pleural fluid haematocrit \> 50% of peripheral blood haematocrit
33
Pleural fluid characteristics
Bloody
* Trauma, malignancy, PE, pneumonia, pneumothorax etc
Turbid or milky
* Empyema, chylothorax, pseudochylothorax
Viscous
* Mesothelioma
Food particles
* Oesophageal rupture
Bile-stained
* Cholothorax (biliary fistula)
Black
* Aspergillus infection
Brown, 'anchovy sauce'
* Amoebic liver abscess draining into pleural space
Urine odour
* Urinothorax
Putrid odour
* Anaerobic empyema
34
Discuss pleural fluids and pH
* Normal pleural fluid pH ~ **7.6**
* pH \< **7.3** \> suggests **pleural inflammation**
* Often ass w/ a **low pleural glucose** (\<3.3 mmol/L, or fluid/serum glucose ratio \< 0.5)
* MoA - ^ neutrophil phagocytosis & bacterial or tumour cell breakdown \> accumulation of lactate & CO2
35
Causes of low pH & low glucose effusions
* CPPE & empyema
* Rheumatoid pleuritis
* Malignant pleural effusion
* Tuberculous pleural effusion
* Oesophageal rupture
* Lupus pleuritis
36
What is the only transudative effusion that can cause a pH \< 7.3?
Urinothorax
* An abnormally high (alkaline) pH may rarely occur in the setting of *Proteus* pleural infection
37
When should you measure pleural fluid triglyceride & cholesterol?
In turbid or milky effusions or where chylothorax is suspected
38
What is a chylothorax? What does it look like? What are the causes?
Occurs following disruption of the **thoracic duct**
* Pleural fluid will appear turbid, milky, serous, or bloodstained
* Diagnostic:
* Presence of PF chylomicrons, or
* Pleural fluid triglyceride level \> 1.24 mmol/L
* Causes:
* Trauma or following thoracotomy
* Malignancy (esp lymphoma)
* Pulmonary LAM
* TB
39
What is a pseudochylothorax? How is it distinguished from chylothorax?
* Occurs due to cholesterol crystal deposition in chronic effusions
* Most commonly due to
* Rheumatoid pleurisy
* TB
* Cholesterol crystals at microscopy distinguish it from chylothorax
40
What are the common causes of increased pleural fluid amylase?
What is the abnormal level?
* Abnormal if PF amylase \> upper normal limit for serum amylase, or
* PF amylase / serum ratio **\> 1.0**
Common causes of ^ PF amylase
* Pleural malignancy (ass w/ ^ **salivary** amylase)
* Oesophageal rupture (ass w/ ^ **salivary** amylase)
* Pancreatic disease (acute & chronic pancreatitis, pancreatic pseudocyst)
* Ass w/ ^ **pancreatic** amylase
41
Common causes of haemoptysis
1/3 - no cause found (Cryptogenic haemoptysis)
Common causes
* **Bronchial tumour**
* **Bronchiectasis** (common during exacerbation)
* Can cause a massive haemoptysis from dilated & abnormal bronchial artery branches that form around bronchiectatic cavities
* **Active TB**
* **Pneumonia**
* **Pulmonary embolism**
* **Vasculitides/alveolvar haemorrhage syndromes**
* Wegener's, SLE, anti-GBM disease (Goodpasture's)
* **Warfarin** with any of the above causes
Don't forget that haemoptysis can be swollen and present as haematemesis
42
What are the **first-line** investigations for haemoptysis?
* **Bloods**
* FBC, coag, G&S
* If vasculitis suspected \> renal function, urine dip, with microscopy for casts
* Antibodies (ANCA, anti-GBM, ANA)
* **Sputum** - MC&S & AFB
* **CXR**
* **CT chest** (prior to bronchoscopy)
* Can Dx arteriovenous malformations (AVM)
* **Bronchoscopy**
* ****Diagnostic & therapeutic
* Bleeding tumour can be injected with a vasoconstrictor, or catheter inserted for tamponade
* **Trans-bronchial biopsy**
* If vasculitis suspected
43
What are the **second-line** investigations for haemoptysis?
Done if first-line Ix fail to demonstrate a cause
* **CTPA** to exclude PE
* **Bronchial angiogram**
* Diagnostic & therapeutic
* **Bronchial artery embolization**
* Small risk of paraplegia (\<1%) if the _anterior spinal artery_ originates from the bronchial arterial circulation and is inadvertently embolised
* **ENT review** - source of bleed may be the upper airway
* **Echo** - Mod/severe PTH can cause haemoptysis
44
Important history & O/E to elicit in haemoptysis?
* Past Hx of lung disease?
* Document volume of blood and whether old or fresh
* Time course (intermittent, constant)
* For sure from airway and not the nose/mouth/haemetemesis?
* Presence of systemic features
* Associated infections
* Sx consistent with malignancy/vasculitis?
O/E
* May be normal or show signs of
* Bronchiectasis
* Bronchial carcinoma
* Sx of circulatory collapse
45
Cough syncope, why is it important?
LoC following violent coughing, a Valsalva-type manoeuvre
* Impairs venous return to the heart \> bradycardia & vasodilatation
* Important
* Car drivers must cease driving until liability to cough syncope has ceased
* Commercial drivers must have no cough syncope for 5y if they have a chronic resp condition, incl smoking
46
What is Tidal Volume
Volume of inspired or expired air with each breath at rest
* Males: 500 mL
* Females: 350 mL
47
Inspiratory Reserve Volume (IRV)
How is Inspiratory Capacity calculated?
Maximum volume of air that can be **inspired** at the end of a normal tidal inspiration
Inspiratory capacity = TV + IRV
48
Expiratory Reserve Volume (ERV)
Maximum volume of air that can be **expired** at the end of a normal tidal expiration (**750** mL)
49
Residual Volume (RV)
* **1.2 L**
* Volume of air remaining after maximal expiration
* Increases with age
* RV=FRC-ERV
50
Vital Capacity (VC)
Maximum volume of air that can be expired after a maximal inspiration
* **4,500** ml in males and **3,500** ml in females
* Decreases with age
* **VC = inspiratory capacity + ERV**
51
Total Lung Capacity (TLC)
The sum of the **vital capacity** + **residual volume**
52
What is the anatomical dead space?
What is the physiological dead space (VD)?
How is it calculated?
_Anatomical dead space_
The anatomic dead space is the gas volume contained within the conducting airways. The normal value is in the range of 130 to 180 mL and depends on the size and posture of the subject.
_Physiological dead space_
Physiological dead space can be thought of as areas of the lung that are well ventilated but poorly perfused; hence, much of the ventilation to those areas is “wasted.” That is, the well-ventilated areas add little to gas exchange for lack of adequate perfusion.
* VD = tidal volume \* (PaCO2 - PeCO2) / PaCO2
* Where PeCO2 = expired air CO2
53
What is the pathophysiology of bronchiectasis?
1. Initial (usually infectious) insult damages the airways
2. Disordered anatomy \> 2nd bacterial colonization \> dmg the mucociliary escalator
3. This prevents bacterial clearance \> further airway dmg
4. Terminal bronchioles obstructed with secretions \> volume loss
5. Chronic host inflammatory response ensues \> free radical formation and formation of neutrophil elastase \> further inflammation and damage
6. Bronchial revascularization with hypertrophy and tortuosity of the bronchial arteries \> intermittent haemoptyses
54
Imaging signs of bronchiectasis
CXR (all three - thickened airways)
* Ring shadows
* 'Tramlines'
* 'Gloved finger'
HRCT (97% sensitive in detecting bronchiectasis)
* Airway dilatation to the lung periphery
* Bronchial wall thickening
* The airways appearing larger than its accompanying vessel (**signet ring sign**)
55
Signs and treatment of exacerbation of bronchiectasis
* Increase in sputum volume and tenacity
* Sputum discoloration
* Ass w/ chest pain, haemoptysis, wheeze
* CRP not always elevated
* Rx based on the potential pathogens
* Nebulised bronchodilators
* Regular physiotherapy
56
First isolate of *Pseudomonas aeruginosa*
* Initial Rx - **4-6w** of **oral ciprofloxacin** 500-750 mg BD
* Concurrent nebulized **colistin** 1-2 MU BD
* If this fails
* IV ABx, or
* Further **4w** of **oral ciprofloxacin** with nebulized **colistin**, or
* 3 months nebulized colistin 2 MU BD
57
Complications of bronchiectasis
* Infective exacerbation
* Haemoptysis
* Small volume is common
* Massive haemoptysis (tortuous bronchial arteries around damaged lungs) - life-threatening emergency
* Pneumothorax
* Respiratory failure
* Opportunistic mycobacterial colonization
* Allergic Bronchopulmonary Aspergillosis
58
Bronchiectasis and *Aspergillus*
* ABPA
* Excessive immune response to environmental fungus *Aspergillus*
* May be the cause of bronchiectasis (esp upper lobe disease)
* Mucus plugs become impacted in distal airways, causing airway dmg \> dilation
59
Haldane effect
Oxygenation of blood in the lungs displaces carbon dioxide from haemoglobin which increases the removal of carbon dioxide
I.e. O2 displaces CO2 from Hb
60
Systematic approach to ABG
1. Review the patient
2. Analyse the oxygenation
3. Assess the pH
4. Assess for respiratory disturbance
5. Assess for metabolic disturbance
6. Establish if the disturbance is compensatory or mixed
61
Risk factors of Lung Cancer
* Smoking - x factor of 10
* Asbestos (x factor of 5)
* Arsenic
* Radon
* Nickel
* Chromate
* Aromatic hydrocarbon
* Cryptogenic fibrosing alveolitis
Smoking & arsenic - synergistic - both \> exposure 10\*5 times increased risk
62
ARDS
The severe end of a spectrum of acute lung injury due to many different insults
* Manifests as
* Acute & persistent lung inflammation with increased vascular permeability
63
2012 Berlin Definition of ARDS
Requires
* **Resp Sx** within 1 week of known clinical insult
* **B/L opacities** consistent w/ pulmonary oedema (CXR/CT)
* Resp failure must not be fully explained by cardiac failure or fluid overload
* **Oxygenation impairment** - PaO2/FiO2 \< **300** mmHg (40 kPa) despite PEEP ≥ 5 cmH2O
* Mild ARDS - PaO2/FiO2 \> **200** mmHg (27 kPa)
* Moderate - \> **100** mmHg (13 kPa)
* Severe ≤ **100** mmHg (13 kPa)
64
Pathophysiology of ARDS
1. **Inflam dmg to the alveoli**
1. (locally produced pro-inflam mediators or remotely produced and arriving via the pulm artery)
2. **Changes in pulmonary capillary permeability**
3. **Fluid & protein leakage** into the alveolar space
4. **Alveolar surfactant is diluted** with loss of its stabilizing effect
5. **Diffuse alveolar collapse & stiff lungs**
This leads to
1. **Gross impairment of V/Q matching** \> arterial hypoxia & very large A-a gradients
2. **PTH 2nd to hypoxia** (aids V/Q matching)
3. **Reduced compliance** (stiff lungs) due to loss of functioning alveoli
65
Causes of pro-inflammatory mediator release sufficient to cause ARDS
Most common
* **Sepsis/pneumonia**
* **Gastric aspiration** (even if on PPI)
* **Trauma/burns** (sepsis, lung trauma, smoke inhalation, fat emboli etc)
Less common
* **Acute pancreatitis**
* **TRALI** (transfusion-related acute lung injury)
* Caused by any blood product, within a few hours of transfusion, no specific therapy or evid of steroid response
* **Drug-overdose** (TCA, opiates, cocaine, aspirin)
* **Near drowning**
66
The course of ARDS
**Phase 1**
* Early period of diffuse alveolar dmg and hypoxaemia with pulmonary infiltration
**Phase 2**
* Develops after a ~ week as the pulmonary infiltrates resolve
* Histology - ass w/ an increase in type **II** pneumocytes (surfactant producers), myofibroblasts, and early collagen formation
**Phase 3**
* Occurs in some
* A fibrotic stage that leaves the lung with cysts, deranged micro-architecture, and much fibrosis on histology
67
Clinical features of ARDS
* Rapidly worsening dyspnoea (+/- a dry cough) and hypoxaemia
* Requiring escalating amounts of supplemental O2
* 1-2 days after the clinical presentation of the precipitating cause (sepsis, aspiration etc)
* Coarse crackles in the chest
* Intubation & ventilation almost always required
68
DD of ARDS
The CXR or CT shows diffuse alveolar infiltrates and air bronchograms
* Similar in appearance to cardiogenic pulmonary oedema or diffuse pulmonary haemorrhage
1. **LVF** (exclude on echo, or pulm capillary wedge pressure \< 18 mmHg)
2. **Diffuse alveolar haemorrhage**
1. E.g. Goodpasture's, Wegener's, SLE)
2. Clues will include a **drop in Hb**, blood in the airways)
3. **ILD**
4. Idiopathic acute eosinophilic pneumonia
5. Cancer and lymphangitis carcionomatosis
69
Different measures of lung volume using spirometry and their definitions
70
Alveolar Surface Tension & Sur
71
Definition of Sarcoidosis
A chronic, multisystem granulomatous disease characterised by the presence of
1. Noncaseating granulomas, and
2. Chronic interstitial lung disease
72
Definition of Sarcoidosis
A chronic, multisystem granulomatous disease characterised by the presence of
1. Noncaseating granulomas, and
2. Chronic interstitial lung disease
73
Epidemiology of Sarcoidosis
* Most common non-infectious granulomatous disease
* Accounts for 25% of chronic ILD
* Common in blacks & non-smokers
* Peak incidence - 20-39 yoa
74
What is the characteristic histological lesion in Sarcoidosis?
Granuloma composed of macrophages, lymphocytes and epithelioid histiocytes, which fuse to form multinucleate giant cells
75
What are the clinical features of
