Respirology

RUSIRU EKANAYAKA, MACK LEE

rteka1@student.monash.edu, mhlee35@student.monash.edu
 CASE BASED.

Why?
This Presentation
Thinking of medicine in terms of
patients rather than isolated
conditions. Focusing on just
buzzwords and matrix can have
negative effects.

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 What else would you like to know?
◦ On further history-taking
◦ There is also a cough
◦ Symptoms are episodic, worse at night and with
exercise
Case 1
◦ There is a family history of atopic disorder
History
◦ On examination
A 21-year-old man presents with
wheeze and chest tightness. ◦ Widespread, high-pitched, musical wheezes on
expiration
◦ Tripoding and other signs of respiratory distress

What is the most likely problem?

An acute presentation of asthma.

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Asthma – definition and aetiology
“A common chronic disorder of the airways that is complex and characterised by variable and recurring symptoms,
airflow obstruction, bronchial hyper-responsiveness, and an underlying inflammation.”
— Expert Panel 3 of the National Asthma Education and Prevention Program

↑pH and
Airway V/Q
Hypoxemia ↑ventilation ↓PaCO2 muscle ↓ventilation ↑PaCO2/↓pH
obstruction mismatch
fatigue

A summary of pathophysiology
(1) Biphasic reaction with bronchial constriction followed by inflammation, (2) TH2 and IgE-mediated
immunologic reaction characterises atopic asthma, (3) triggers for non-atopic asthma include viral infections
and inhaled pollutants, (4) eosinophils are key inflammatory cells found in almost all subtypes of asthma, (5)
Curschmann spirals and Charcot-Leyden crystals – morphology with severe asthma.

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Triggers and epidemiology
Internal triggers: respiratory infection
(viral or commonly Mycoplasma), cold
air, cigarette smoking, beta-blockers,
GOR/GORD, emotional stress
•1 in 9 Australians have asthma (2.5 million)
External triggers: pollen (worse in
•Ages 0-14: M>F
spring), dust, animal fur, occupational
•Ages >15: F>M
•Rate 2x as common among Indigenous
Australians
•Rate higher in areas with lower SES and in
people living in inner regional areas

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 Investigations in asthma
1. Pulmonary function tests (obstructive) At the bedside:
2. Consider allergy testing 1. Rapid assessment of severity
3. CXR usually not indicated 2. O2 saturation
3. ABGs + peak flows

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Diagnosing and treating asthma

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Initial rapid severity assessment of acute
asthma in adults and adolescents
NB Wheezing may be absent in severe acute asthma (silent chest), pulsus
paradoxus is not a reliable indicator of the severity of acute asthma, life-
threatening acute asthma can occur without cyanosis.

Mild-moderate Severe Life-threatening

• Can walk AND can speak • Increased WOB • Altered conscious level
whole sentences in one breath • Unable to complete sentences in • Exhaustion
• SpO2 >94% one breath • Cyanosis
• SpO2 90-94% • SpO2 <90%
• Poor respiratory effort
• Soft or absent breath sounds

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Preliminary assessment → life-threatening!
BUT you’re responding in the community
000 → advise that the patient is having a ‘severe asthma attack’

4x4x4 asthma first aid plan

1. 4 separate actuations, w/ spacer if
available, one at a time
2. 4 breaths from spacer after each
actuation
3. Wait 4 minutes and give another 4
separate actuations
4. Continue 4x4x4 after calling
ambulance if response still poor

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Acute management of flare-ups in adults
and adolescents in hospital
Preliminary Salbutamol Ipratropium Oxygen
assessment
Mild-moderate pMDI (spacer) Not indicated immediately Not generally required
Severe pMDI (spacer) if Consider starting via pMDI Start if SpO2 <95%
tolerated/intermittent (spacer) if
nebulisation tolerated/intermittent
nebulisation
Life-threatening Continuous nebulisation Intermittent nebulisation Usually required to drive
driven by oxygen nebuliser

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 What else would you like to know?
• On further history taking
• Extensive history of smoking
• Patient reports dyspnoea
Case 2 • No productive cough
History
• On examination
A 55-year-old male with sudden
severe breathlessness and right-
sided pleuritic chest pain.
• Chest hyperinflation
• Reduced breath sounds on the right
• Hyperresonance to percussion on the right

You order a CXR – next slide.

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Case 2
History
A 55-year-old male with sudden
severe breathlessness and right-
sided pleuritic chest pain.

What is the most likely problem?

Secondary spontaneous right pneumothorax in the
setting of bullous emphysema.
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Pneumothorax – the essentials
“Air in the pleural space. If collection of gas constantly enlarging with subsequent compression of mediastinal
structures i.e. one-way valve → tension pneumothorax.”

Types (1) spontaneous primary → tall, Marfan’s, Ehlers-Danlos,

homocystinuria due to ruptured blebs (<2 cm) or bullae (>2 cm);
(2) spontaneous secondary → COPD especially distal acinar emphysema,
PJP, CF, TB; (3) traumatic/iatrogenic

Clinical features (1) pleuritic chest pain, (2) dyspnoea, (3) hyperexpanded
hemithorax, (4) decreased breath sounds, (5) hyperresonance to percussion,
(6) tracheal deviation if tension.

Management (1) O2, (2) analgesia, (3) 14G IV catheter at 2nd ICS mid-
clavicular line or tube thoracostomy at 5th ICS mid-axillary line,
(4) pleurodesis if recurrent.

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Radiographic findings in pneumothorax
CXR (1) visible visceral pleural edge, (2) radiolucency of peripheral space, (3) +/- subcutaneous emphysema
and pneumomediastinum, (4) deep sulcus sign, (5) mediastinal shift.

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Chronic Obstructive Pulmonary Disease
(COPD)
“A common progressive disorder characterised by airway obstruction with little or no reversibility. It includes chronic
bronchitis and emphysema.”

Types of emphysema
Centrilobular → smoking, COPD
involving upper lobes
Panlobular → A1AT deficiency,
COPD involving lower zones
Paraseptal → young adults at risk of
PTX
Irregular → secondary to scarring,
may be most common form despite
being asymptomatic

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Investigations in COPD
FBC → PCV↑

ABG → PaO2 +/- hypercapnia

Obstructive PFTs → FEV1<80%, FEV1/FVC<70%,

poor response to bronchodilators, ↑TLC, ↑RV, ↓DLCO
CXR → hyperinflation (>6 anterior ribs above diaphragm
in mid-clavicular line), flattened hemidiaphragms, large
central pulmonary arteries, ↓peripheral vascular markings,
bullae, stretched vertical heart.

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 Management with COPD-X
1. Confirm diagnosis
1. Persistent airflow limitation post-bronchodilator FEV1/FVC <70% and FEV1<80%
2. FEV>400 mL post bronchodilator → asthma or asthma/COPD overlap
3. Regular assessment of severity

2. Optimise function
1. Non-pharmacological: smoking cessation, regular physical activity, pulmonary rehabilitation
2. Stepwise approach to pharmacotherapy: SABA/SAMA → SABA+SAMA → LAMA → LABA
→ LABA+LAMA → ICS → ICS+LABA → ICS+LABA+LAMA; also option of oral
bronchodilators

3. Prevent deterioration
1. Vaccinations: influenza, pneumococcal
2. Immunomodulatory agents (OM-85 Broncho-Vaxom)
3. Mucolytics
4. Domiciliary oxygen therapy >15 hours/day

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Management with COPD-X
4. Develop a plan of care
3. GP reviews
4. Self-management plan
5. Support for end of life planning
5. Manage exacerbations
3. Controlled O2 delivery (0.5-2 L/min) aiming for a
saturation between 88-92% (reliance on peripherally sensed
hypoxic drive)
4. Non-invasive ventilation for patients with hypercapnia
PaCO2 >45 mmHg and respiratory acidosis blood pH
<7.35

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 What else would you like to know?
• On further history taking
• She has had night sweats
• The weight loss is unintentional
• She was born in India
Case 3 • She has been treated for pneumonia and believes she needs
something stronger
History
• On examination
A 54-year-old woman of South
Asian extraction presents with • The patient is febrile and dyspnoeic
fever, weight loss, and • Amphoric breath sounds
haemoptysis.
• Inspiratory and posttussive crackles
• The sputum mug is ripe with blood-streaked sputum

What is the most likely problem?

Tuberculosis, likely re-activation disease.

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Tuberculosis – definition and aetiology
“Communicable chronic granulomatous disease caused by Mycobacterium tuberculosis. It usually involves the lungs but
may affect any organ or tissue in the body. Typically, the centres of tubercular granulomas undergo caseous necrosis.”

A summary of pathophysiology
(1) Acid-fast bacilli, (2) a Ghon complex is a combination of
parenchymal lesion with nodal involvement and a sequela of primary TB,
(3) Ranke complex = radiologically detectable calcification with
progressive fibrosis of Ghon complex.

Image key
Black arrow = calcified peripheral granuloma
White arrow = calcified hilar lymph node
Black arrow + white arrow = Ranke complex

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Epidemiology and risk factors
Epidemiology (1) 1/3 of the world’s
population is infected with TB, (2)
estimated to kill 2 million people/yr, (3)
cause of death of most people with
HIV.

Risk factors (1) travel to or birth in

endemic regions, (2) being Aboriginal,
(3) crowded living spaces and low SES,
(4) IVDU, (5) personal or occupational
contact.

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Clinical presentation
General features: fever, night sweats,
weight loss.

Pulmonary features include cough, chest

pain, haemoptysis, upper lobe fibrosis.

Pulmonary TB can be primary or

reactivation disease. Primary TB is often
asymptomatic.

Reactivation TB may remain

undiagnosed and potentially infectious
for 2-3 years or longer.

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Extrapulmonary manifestations of TB

Extrapulmonary (1) lymphadenitis, (2) serositis, (3)

osteomyelitis [Pott’s disease], (4) Addison’s disease, (5)
genitourinary including sterile pyuria.

Miliary TB lymphadenitis, hepatosplenomegaly, organ

dysfunction, Addison’s disease, choroidal tubercles in the
eyes.

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Hunting for tuberculosis…
Active TB Latent TB
Sputum MCS: Ziehl-Neelsen stain Mantoux tuberculin skin test
showing AFB within alveolar QuantiFERON TB Gold® test
macrophages
Neutral on gram stain

Chest X-ray findings

(1) consolidation, (2) cavitation, (3) fibrosis, (4) calcification

Histology
The hallmark is the presence of a caseating granuloma.

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Standard short-course therapy for TB
!Isolate with droplet precautions and initiate contact tracing/prevention.

Drug Side effect

Rifampicin Orange bodily fluids
2 + 4 months
Isoniazid Peripheral neuropathy (co-
2 + 4 months administer
pyridoxine/vitamin B6)
Hepatitis
Pyrazinamide (2 months) Gout
Ethambutol (2 months) Optic neuritis

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Algorithm for approaching the patient
with suspected TB

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 What else would you like to know?
• On further history taking
• Short of breath
• She has had a dry cough
Case 4 • Chest pain worse with breathing
History • Just landed from a long-haul flight
A 66-year-old woman presents with • Has had a diagnosis of colorectal cancer
acute dyspnoea.
• On examination
• Tachypnoeic and tachycardic
• Rales with decreased breath sounds

ECG – next slide.

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Case 4
History
A 66-year-old woman presents with
acute dyspnoea.

What is the most likely problem?

Pulmonary embolism.

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PE – definition and aetiology
“Embolic occlusion of the pulmonary arterial system. Almost all large pulmonary artery thrombi are embolic in
origin, usually arising from the deep veins of the lower leg.”

Stasis
A summary of pathophysiology
(1) Saddle embolus → embolus straddling
bifurcation of pulmonary trunk, (2) wedge-
shaped infarcts with bases at pleural surface Virchow’s
triad
and apex pointing toward lung hilus,
(3) coagulative necrosis of lung parenchyma
and haemorrhage Endothelial Hypercoagulability
injury

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Risk factors and clinical assessment for PE
Risk factors
1. Malignancy
2. Immobilisation
3. Haematological – antiphospholipid
syndrome, Factor V Leiden
4. Others – SLE, pregnancy, non-O
blood type, OCP use, etc.

Table – Wells criteria and modified

Wells criteria used in clinical assessment
for pulmonary embolism.

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Clinical presentation
Clinical features
• Unexplained dyspnoea
• Cough or haemoptysis
• Pleuritic chest pain
• Low-grade fever
• Sense of impending doom
• Sudden urge to defecate

ECG → RBB, RAD, S1Q3T3

CXR → usually normal, Hampton hump,

Westermark sign, Fleischner sign, pleural
effusion

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PE – general principles of management

Investigate with CTPA or V/Q scan.

CTPA is the investigation of choice in
moderate/high-risk patients but may not
always be feasible e.g. renal failure,
pregnancy, contrast allergy, mental state or
weight issues interfering with CT logistics.

Initial management involves oxygen,

analgesia, IV unfractionated heparin or
LMW heparin. Consider warfarin loading.

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35
 Key points:
◦ Immunizations up to date
◦ No recent overseas travel
◦ Non-smoker
Case 5 ◦ SaO2 95% RA
History
◦ RR: 22
A 65 year old female presents with a
◦ Looks unwell
productive cough, rust coloured
sputum and fever of 38.3 after a week
◦ Crackles in R lung
of coryzal symptoms.

CXR:

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Pneumonia
Acute inflammation of the lung parenchyma,
including the alveoli, due to a lower respiratory tract
infection. A very common respiratory condition and a
leading cause of death in the elderly.

Community Acquired Pneumonia (CAP):

acquired outside the hospital

Hospital Acquired Pneumonia (HAP): acquired

inside the hospital

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Pneumonia – Risk Factors
More commonly a disease of the very young, old or sick population.

-Impaired immunity: old or young age, HIV, immunocompromise

-Mucociliary impairment: smoking, CF, Kartagener’s Syndrome, bronchiectasis
-Aspiration risk: impaired swallowing, stroke, impaired gag reflex
-Travel: exposure to pathogen
-Particular exposure: see previous slides
-Post influenza/URTI: mostly Strep. Pneumonia/Staph aureus
-Chronic disease: COPD, Heart Failure, alcohol abuse

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Pneumonia – Aetiology
Community Acquired Pneumonia (CAP):
Typical: usually typical presentation with lobar pattern
-Streptococcus pneumonia
-Haemophilus influenza
-Moraxella catarrhalis
-Staphylococcus aureus

Atypical: presentation ‘walking’, not lobar

-Mycoplasma pneumonia
-Legionella
-Viral

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Pneumonia – Aetiology
Hospital Acquired Pneumonia (HAP): usually
due to ventilation and aspiration, higher risk of
multiple drug resistance

-E. coli
-S. aureus & MRSA
-Gastric aspiration: anaerobes
-Klebsiella
-Pseudomonas aeruginosa

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Pneumonia – Pathogen Buzzwords
Presentation Pathogen
Cold agglutinins and haemolytic anaemia, walking pneumonia with flu-like Mycoplasma
symptoms
Working with water cooling tanks, air conditioning, associated diarrhoea Legionella

Red-currant jelly like sputum, alcoholic patient, cavitation in lungs Klebsiella

Rabbits Francsiella

HIV patients with bilateral hilar shadowing Pneumocystis jiroveci (PJP)

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Pneumonia – Pathogen Buzzwords
Presentation Pathogen
Exposure to animals, abattoir Coxiella burnetti, Q fever

Immune compromised, travel history, weight loss TB

Cystic fibrosis patient Pseudomonas aeruginosa

Birds, pigeons, avian Chlamydia psittaci

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Pneumonia – Clinical Presentation
Sx: typical Sx: atypical/walking
-Fever/Rigors - Fever
-Cough - Headache
-Sputum - Myalgia
- Sweating
-SOB
- Dry cough
-Confusion in elderly
- Weight loss
-Haemoptysis
- Fatigue
-Pleuritic chest pain - Loss of appetite

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Pneumonia – Clinical Presentation
O/E:
-Consolidation: dullness to percussion, bronchial
breath sounds, inspiratory crackles, increased vocal
fremitus, diminished chest expansion
-Pleural rub, possible effusion
-Tachypnoeic
-Febrile
-Confused/delirious

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Pneumonia – Investigations
1. Bedsides:
- SaO2, vitals
2. Bloods:
- FBE, UEC, ABG
- Cultures + sputum culture
- Urinary antigens for legionella and pneumococcus if suspected
3. CXR: PA + Lateral, consolidation/opacity in a lobar pattern
usually (which lobe), sometimes broncho and interstitial. Can
assess extent of disease + effusions and cavitations, air
bronchograms.
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 Pneumonia - CXR

RML: occludes the right heart RLL: does not occlude the
RUL: limited by horizontal fissure border, limited by horizontal fissure right heart border,
below above occludes hemi-diaphragm

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Pneumonia - CXR

LUL: occludes the left heart border,

LLL: occludes hemi-diaphragm
can include the lingula

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Pneumonia - Severity
In Australia CORB and SMARTCOP are
more commonly used than CURB-65 to assess
need for IRVS (intensive
respiratory/respiratory support)
CORB: >2
◦ Confusion
◦ Oxygen Sats <90%
◦ RR >30
◦ Blood pressure
SMARTCOP:
https://lifeinthefastlane.com/wp-
content/uploads/2010/07/etg-smartcop.pdf
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Pneumonia – Complications
- Effusions
- Bacteraemia -> Sepsis
- Empyema
- Abscess
- Respiratory Distress

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Pneumonia – Management
1st: DRSABC, fluids, O2, analgesia etc…..

CAP: ABC+D empirical Abx

Mild: amoxycillin or doxycycline (atypical)

Moderate: benzylpenicillin and doxycycline (atypical)
Severe: ceftriaxone and azithromycin or (benzylpenicillin and gentamicin as
alternative)

Follow up 6 weeks CXR to check that disease is cleared.

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Pneumonia – Management
HAP: empirical Abx

Mild: amoxycillin and clavulanate (Augmentin)

Moderate: ceftriaxone
Severe: tazobactam+piperacillin (Tazocin)

Source: Mack Lee

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What's This?
Lung Abscess
◦ Round fluid filled cavity with air-fluid
level, usually due to aspiration
◦ Swinging fever with foul smelling
sputum, clubbing, haemoptysis
◦ Manage with Abx like clindamycin and
ceftriaxone

◦ DDx for cavitating lesion in lung: TB,

cancer

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MFCHA

Best EMQ Book IMHO

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 Key points:
◦ 40 pack years, COPD
◦ No asbestosis exposure in the past
◦ Does not drink alcohol
◦ No recent fever/travel history
Case 6 ◦ Lost 5 kg over 1 month unintentionally
History
A 55 year old male present with
worsening pain in his chest, weight
loss and coughing up frank blood that
has been progressing for 1 month.

CXR:

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Lung Cancer
Malignant carcinoma of the lung, the most common worldwide (not in
Australia, but highest number of deaths) with 1.8 million new cases and 1.2
million deaths in 2012.

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Lung Cancer – Risk Factors
-Smoking
-Radiation therapy
-Environmental:
- Asbestos – mesothelioma
- Fine silica dust
- Radon
- Metals
-Pulmonary Fibrosis
-HIV
-FHx
-Age
-Genetic Source: mediokay from Tumblr.com

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Lung Cancer – Classification
- Adenocarcinoma (most
common)
- Small Cell
- Squamous (highest link to
smoking)
- Large Cell

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Lung Cancer – Adenocarcinoma
Most common (40%)
Peripheral lesions usually
Paraneoplastic syndrome: HPOA (clubbing and
wrist tenderness)
Histology: mucus producing glands and ducts =
adeno

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 Lung Cancer – Small Cell
20%
Central, perihilar lesions. Usually the worst outcomes
due to the fact that when it is diagnosed it is usually
in its latter stages.
Paraneoplastic syndrome: SIADH
(hyponatraemic hypervolemia), Lambert Eaton
Myasthenia Gravis (can precede cancer by >4
years)
Histology: dark and small undifferentiated cells

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 Lung Cancer – Squamous
25%
Central, perihilar lesions that often involves a main
bronchus and can cause obstruction
Paraneoplastic syndrome: hypercalcaemia due to
PTHrP secretion
Histology: keratin pearls in centre of tumour nest

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 Lung Cancer – Large Cell
10%
Poorly differentiated, variants of multiple
cancer cell types
Highly Aggressive and poor prognosis

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Lung Cancer – Clinical Presentation
Constitutional: weight loss, fatigue, night sweats
Cough +/- haemoptysis
Dypsnoea
Wheeze/Stridor – bronchial compression
Chest pain
Hoarse Voice due to recurrent laryngeal nerve entrapment
Pancoast Syndrome: Horner's Syndrome + atrophy of hand muscles + pain
SVC obstruction: Pemberton's Sign = medical emergency
Various paraneoplastic syndromes
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Lung Cancer – O/E
Clubbing = NSCLC
Cachexia
HPOA
Lymphadenopathy
Pleural Effusion
Wheeze
Consolidation
Metastasis: bone tenderness, hepatomegaly, neurological signs, neuropathy

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Lung Cancer – Ix
1. Bloods: calcium, LFTs
2. CXR: nodules and masses
3. Pleural fluid cytology
4. CT: staging and investigation
5. PET: metastasis and locations of tumours. Bone
scan w/ radionucleotide for mets
6. Bronchoscope/CT guided biopsy

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Lung Cancer – Staging

NSCLC = TMN
SCLC has its own staging

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Lung Cancer – Treatment
NSCLC = surgical excision + radio + chemo
SCLC = radio + chemo
Prognosis is poor, usually palliation is required
◦ Analgesia
◦ Pleurodesis for effusion
◦ Radiotherapy for SVC obstruction
◦ Codeine cough suppression
◦ Steroids, bronchodilators

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 What's This
Cannonball Mets
◦ Usually lots of lesions in the lung
(or any other organ) means that
the disease is not primary
(Occam's Razor)
◦ Usually from paired organs such
as: renal and ovarian

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What's This
Mesothelioma:
Almost always due to asbestos
exposure
Take occupational history: miners, brake
pad, insulators, dock workers
Latency period of 30-40 years
Terrible prognosis
Seek legal advice

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70
Which of these cancers is the most
common in smokers?
A. Small Cell
B. Adenocarcinoma
C. Squamous
D. Large Cell
E. Nasal carcinoma

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Which of these cancers is the most
common in smokers?
A. Small Cell
B. Adenocarcinoma – not the most associated with
smoking but most common overall
C. Squamous
D. Large Cell
E. Nasal carcinoma

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 Key points:
◦ Dyspnoeic with SaO2 95%, RR 26, BP 150/90
◦ Left lung field stony dull to percussion
◦ Crackles in the area above the level of dullness
◦ Elevated JVP
Case 7
History
A 62 year old female with a history of
congestive heart failure NYHA Stage
2, 3x CABG, presents with 2 week
history of worsening dyspnoea and CXR:
chest tightness that is increased on
lying down.

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Pleural effusion – sign or disease?
An excess of fluid in the pleural space.

Classified as transudative or exudative.

How?
◦ Protein concentration of transudates
<25 g/L
◦ Protein concentration of exudates
>35 g/L

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 Pleural Effusion - Classification
Commonly encountered terminology:
◦ Haemothorax: blood in pleural space
◦ Hydrothorax: fluid
◦ Empyema: pus in the pleural space
◦ Chylothorax: chyle in pleural space due to
obstruction of thoracic duct
◦ Haemopneumothorax: blood and air in the
pleural space – straight line sign

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Pathophysiology of effusions
Transudative: imbalance in Starling’s forces i.e. increased capillary
hydrostatic pressure, decreased plasma oncotic pressure
◦ Increased venous pressure in cardiac failure, constrictive pericarditis, fluid
overload
◦ Hypoproteinaemia in cirrhosis, nephrotic syndrome, malabsorption
Exudative: increased permeability of pleural capillaries or lymphatic
dysfunction
◦ Infection, inflammation, malignancy
◦ Pneumonia, TB, pulmonary infarction, rheumatoid arthritis, SLE,
bronchogenic carcinoma, malignant metastases, lymphoma, mesothelioma,
lymphangitis carcinomatosis, Meig’s syndrome
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 Transudate v exudate
Transudative effusions are usually bilateral, exudative can be either.
Light’s criteria: (not important to remember exactly)
1. Pleural fluid protein/serum ratio >0.5
2. Pleural fluid LDH/serum LDH ratio >0.6
3. Pleural fluid LDH >2/3 the upper limit of normal serum LDH
Interpreting Light’s criteria:
◦ If at least one is true → exudate
◦ 98% sensitive and 83% specific for identifying exudative pleural
effusions
◦ Criticised for including both (2) and (3) because they are highly
correlated
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Transudate v exudate

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Three-test rule for transudate v exudate
Components of the rule:
◦ Pleural fluid protein >29 g/L
◦ Pleural fluid cholesterol >45 mg/dL
◦ Pleural fluid LDH >60% of upper limit for
serum
Interpretation of the three-test rule:
◦ If any one component true → exudate
◦ Levels below are transudates resulting from an
imbalance of the Starling’s principle of fluid
balance

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Pathophysiology of effusions
Transudative Exudative

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The effusive patient
May be asymptomatic!
May be dyspnoeic.
May be in pleuritic agony!
Signs of pleural effusion:
◦ Decreased expansion
◦ Stony dull percussion note
◦ Diminished breath sounds
◦ Tactile vocal fremitus and vocal resonance are reduced
◦ Tracheal deviation away from effusion
◦ Bronchial breathing above level of effusion, why?

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Investigations and Treatment
1. CXR: blunting of costadiaphragmatic angles can only be
seen with >200ml
2. Ultrasound + Thoracentesis: find border of effusion
and choose 1-2 intercostal spaces below. Infiltrate with
lignocaine and attach 21 gauge needle to syringe and insert it
above the upper border of rib. Take fluid for pathology =
find cause.
Treat cause
Pleurodesis is palliative if there is recurrent effusion that can
not be managed: bleomycin, talc

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http://oldsite.laboklin.com/pages/html/en/VetInfo/aktuell/lab_akt_1108_en.html

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 Pleural Fluid Analysis
Parameter Possible Causes
Protein and LDH Transudate/Exudate
Gram Stain/Culture Empyema
Cytology Malignancy
Glucose <30mg/dL Empyema, rheumatoid
Amylase Pancreatitis
Haematocrit Trauma/Haemothorax
Triglycerides Chylothorax
Lymphocyte Count High TB, sarcoid, lymphoma, cancer

84
 Key points:
◦ Fine bibasilar inspiratory crackles
◦ Clubbing, nil cough/sputum/fever/travel
◦ 15 pack year ex-smoker, no connective tissue disease
◦ Limited exposure to asbestos, birds, dust, hay
Case 8 ◦ No drugs except for perindopril for HTN
History
◦ SaO2: 92%
49 year old man finds that he is
having trouble maintaining his
stamina during his weekly tennis
sessions with his mates from the local
tennis club. Over the next 10 months
he deteriorates till he is short of
breath even upon walking to his car.
CXR:

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Interstitial Lung Disease
•Generic term for conditions which affect the interstitum of the lung, which is the
supportive tissue of the lung which is between the alveoli and capillary
endotheliums
•Characterised by injury and progressive fibrosis and remodelling of the
interstitium, inflammation and hyperplasia of type II pneumocytes

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Interstitial Lung Disease

87
ILD - Aetiology
Category Types
Occupation Asbestosis, silicosis, coal, cotton, berylliosis
Drugs Nitrofurantoin, bleomycin, amiodarone
Infection TB, fungi, viral
Granuloma Sarcoidosis, hypersensitivity pneumonitis
Idiopathic IPF, cryptogenic organizing pneumonia
Systemic Causes RA, SLE, Scleroderma, Sjogren’s, Ankylosing Spondilytis

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ILD - Classification

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Idiopathic Pulmonary Fibrosis (IPF)
•A disease of the ageing
•2-29/10000 in Australia
•A disease process of primary fibrosis
which distinguishes it from other ILD
types
•Irreversible and chronic disease which
damages the alveoli making them unable to
fully expand and carry out their function

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Idiopathic Pulmonary Fibrosis (IPF)
•Unknown aetiology – chronic and irreversible, progressive decline in respiratory
function
•Risk factors:
• Age
• Smoking
• GORD
• Male
• Genetic/FmHx

Complications: respiratory failure, CVD, cor pulmonale, cancer

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 IPF - Features
•Dyspnoea on exertion – progressive and chronic
•Dry cough
•Weight loss
•Fatigue
•Malaise
•Fever
•Arthralgia

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Exam
•Fine bibasilar inspiratory crackles – Velcro
straps
•Clubbing in late disease thought to be due to
increased release of growth factors

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 Ix
•Abnormal Lung Function: restrictive picture with normal
FEV1/FVC but reduced FVC
•DLCO decreased
•Screen for other causes: eg ANA, rheumatoid factor, asbestos
exposure
•SaO2
•Lung biopsy sometimes needed for diagnosis

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 Ix
•CXR – reticular and reticulonodular opacities: lines and dots

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 Ix
•CT – ground glass appearance and honey combing

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 Mx
•There is no way to reverse the fibrosis to the lung, 2-3 year median
survival
•Immunosuppression to stop further inflammation: steroids, azathioprine
•Pirfenidone, nintedanib shown to reduce fibrosis in 12 month trial
•O2
•Definitive treatment is a lung transplantation, 5 year survival is 50%

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 Hypersensitivity Pneumonitis – a 1 page
summary
‘Cell mediated hypersensitivity of alveolar walls and terminal airways induced in a susceptible host by repeated
inhalation of antigens in particular substances. Can be organic or inorganic.’

Causes are varied:

- Farmer’s Lung: Aspergillus
- Bird Fancier’s Lung: protein from bird droppings
- Cheese workers, hot tub workers
- Many others….

Clinical features: acute phase – fever, rigors, dry cough, dyspnoea. Chronic phase – weight loss,
respiratory failure, cor pulmonale

Management (1) antigen testing + CXR, HRCT shows similar pattern to ILD (2) usually a reversible disease
with good prognosis - avoid precipitant (can involve changing work) (3) O2 in acute setting (4)
immunosuppression if worsening

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 Sarcoidosis– a 1 page summary
‘Abnormal collection of inflammatory cells (non-caseating granulomas, Th1 predominant inflammation) that can form
as nodules in multiple organs.’

Diagnosis of exclusion – unknown cause. More common in African-Carribean people.

Features: Lungs: fibrosis leading to dry cough, dyspnoea progressive, chest pain, decreased exercise tolerance.
Skin: erythema nodosum. Arthralgia, fatigue, weight loss, variety of symptoms as can deposit anywhere.

Investigations: CXR – bilateral hilar lymphadenopathy (Garland 123 sign), increased ACE, hypercalcaemia,
nodule biopsy needed for definitive diagnosis

Management (1) analgesia for pain (NSAIDs) (2) glucocorticoids but control dosage, move on the
azathioprine/methotrexate if not responsive (3)treat symptomatically depending on the affected organ

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 Key points:
◦ Coarse crackles on auscultation
◦ Parents complain of pale, difficult to flush stools
◦ Hyperglycaemic
◦ Notice rounded nail beds
Case 9
History
3 year old boy presents with low
weight and height for his age. He was
born at home and did not receive
testing post delivery. He has a chronic CXR:
cough with large amounts of bloody
sputum and recurrent respiratory
infections.

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Cystic Fibrosis
•Autosomal recessive condition (1/2500
Caucasians, 1/25 carriers) due to
mutation (delta F 508 most common
in 75%) of the CF Transmembrane
Regulator gene on chromosome 7
resulting in dysfunctional chloride
channels on the apical membranes of
cells.

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 Cystic Fibrosis
- Multisystem disorder caused by
abnormal ion transport across epithelial
cells
- Impaired ciliary function and retention
of mucopurulent secretions
- Dysregulation of inflammation and
defence against infection
- Pancreatic duct blocked causing
malabsorption and enzyme deficiency
- Abnormal sweat gland function
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Features
Respiratory: productive cough, nasal polyps, haemoptysis, recurrent infections (Pseudomonas, SA,
Haemophilus influenza, Aspergillus fumigatus, Burkholderia), bilateral coarse crackles, bronchiectasis
Pulmonary hypertension
Exocrine pancreatic insufficiency: steatorrhea, diabetes mellitus (decreased insulin), protein and fat
malabsorption, ADEK deficiency
Intestinal dysfunction: distal intestinal obstruction syndrome
Hepatobiliary: fatty liver, choleliathiasis
Low weight/failure to thrive
Sexual: male infertility (not sterility), 20% of women are infertile
Osteoporosis, vasculitis, arthritis, HPOA
Clubbing, Cyanosis
Hyperinflation of the chest due to air trapping

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Ix
Detected in Guthrie heel prick test at birth, immunoreactive trypsinogen (IRT) >99th
percentile by immunoreactive assay,
If positive, gene mutation test for 12 most common CFTR mutations, 2 mutations = diagnostic,
1 = sweat test required
Sweat test: Cl > 80mq/L is diagnostic, twice required, normal 10-40
If positive then CF, if negative then carrier and gene counselling required

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Ix
1. Lung function: obstructive
2. Bloods
3. Cultures – infection
4. CXR shows signs of bronchiectasis: thickened bronchial walls and tram
tracking on CXR
5. CT shows signet ring shadows in bronchietasis

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Mx
Multidisciplinary team required Gastro:
Pancreatic enzyme supplements
Lifestyle: counselling, genetic, chest Vitamin ADEK
physiotherapy, vaccinations, high calorie Salt supplementation
diet, avoid smoking Endo:
Diabetes treatment
Respiratory: Osteoporosis
◦ Antibiotics for infections prophylactically, acute
flucloxacillin for pseudomonas, vaccinations Surgery:
Lung Tx
◦ Mucolytics
Liver Tx
◦ Bronchodilators
40 year median survival.
◦ Pseudomonas treatment: IV ticarcillin + tobramycin
for 2 weeks, long term nebulized tobramycin, oral
ciprofloxacin, re-culture 4 months after for signs of
persistent infection

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 Bronchietasis– a 1 page summary
‘Irreversible dilation of small to medium sized bronchioles.’
Causes: post-infection (TB, pneumonia), neoplastic (cancer), mucociliary (CF, Kartagener’s Syndrome,
Young’s syndrome), RA, SLE, radiation, idiopathic

Features: cough with copious amounts of purulent sputum (>1 cup) mixed with blood, haemoptysis,
clubbing, recurrent infection, wheeze, coarse wheeze

Investigations: CXR – tram tracking and thickened bronchial walls, CT – signet ring sign, blood cultures if
active infection, genetic testing

Management: (1) physiotherapy (2) vaccinations (3) antibiotics

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 Atelectasis– a 1 page summary
‘The loss of lung volume due to collapse of lung tissue resulting in absent gas exchange.’

Causes: commonly occurs post abdominal surgery due to shallow breathing for fear of pain. Other major
causes include obstruction: mucous, foreign body, tumour inside or outside bronchiole wall, surfactant
deficiency in RDS, pneumonia, effusion, TB.

Features: shortness of breath depending on severity of collapse, increased HR and RR, cyanosis if severe.
Post-op fever (thought the evidence is scant), chest pain.

Investigations: CXR can show loss of lung volume and opacification. Linear increased radio-density at the
area of collapse. Mediastinal/hilum shift towards the area of collapse.

Management: (1)physiotherapy – encourage taking deep breaths with help from the chest physio machine.
Mild exercise and mobilization after surgery. (2) CPAP (3) blockages that can not be removed may be suctioned
with bronchoscopy (4) treat underlying cause

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Collapse of the right lower
lobe. The R hemi diaphragm is
elevated by the lobar collapse
and there is increased
expansion of the R upper lobe.
Also slight R mediastinal shift.

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 Obstructive Sleep Apnoea – a 1 page
summary
Unexplained daytime sleepiness + 5 obstructed breathing events per hour of sleep due to relaxing of muscle tone at
back of throat relax during REM sleep which obstructs the airway.

Causes: obesity, shortened lower jaw, hypothyroidism, acromegaly, alcohol

Features: gasping or choking during sleep, pausing during sleep, daytime fatigue, dry mouth on waking,
snoring

Investigations: polysomnography sleep study

Management: (1)lifestyle – weight loss, diet, exercise, sleep on side, sleep hygiene, avoid alchol and driving
commercially. (2)sleeping pills (3)CPAP/BiPAP (4) mandibular advancement technology (5) surgery

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 Acute Bronchitis– a 1 page summary
‘MacFarlane Criteria: (a) an acute illness of <21 days; (b) cough as the predominant symptom; (c) at least 1 other
lower respiratory tract symptom, such as sputum production, wheezing, chest pain; (d) no alternative explanation for the
symptoms’
Causes: usually an inflammation of the bronchi caused by viruses (more common) or bacteria (less common).
Usually similar pathogen to URTI: rhinovirus, coronavirus, adenovirus, influenza, parainfluenza, RSV.

Features: cough, sputum, dyspnoea, haemoptysis. Wheeze on auscultation and increased respiratory rate.
Bronchial breathing.

Investigations: usually a clinical diagnosis, can use CXR to rule out other causes,

Management: none required as this is self-limiting, persuade patient to cease smoking, sometimes can give
NSAIDs for fever. No antibiotics required.

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KCEFG

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LEBFH

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 UpToDate
BMJ Best Practice
OHCM 9th Edition
eTherapeutic Guidelines
Special Thanks Toronto Notes 2015
Radiopaedia (A.Prof Frank Gaillard)
Life in the Fast Lane
All our tutors and lecturers
Parents and colleagues
Rohit Sharma – MBBS V and the best teacher ever
&
MUMUS and associated sponsors.

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