OSCE-Aid Presents:

Respiratory Cases

Harriet Owles

Respiratory Registrar

• Approach to the respiratory

examination

• Presentation

• Examples of main respiratory cases

Approach to the

Respiratory Examination

The examination

Around the bed:

• Sputum pot

• Medications, inhalers, nebulisers

• Walking equipment

• Observations, bedside spirometry,

peak flows.

The examination

Patient from the end of the bed:

• O2

• Cyanosis

• Pattern of breathing:

– Audible wheeze

– Purse lips

– Prolonged expiration

– Accessory muscles

• Cough!

The examination

Hands:

• Peripheral cyanosis

• Clubbing

• Nicotine staining

• Wasting small muscles of hand

• Evidence of systemic disease eg

rheumatoid arthritis, scleroderma

• Flap or tremor

• Heart rate.

The examination

Face and neck:

• Anaemia

• Central cyanosis

• Horners

• Signs of systemic disease

• Cushingoid facies

• Lymphadenopathy

The examination

Chest:

• Inspection

– Scars: mediastinoscopy, thoracoscopy, LN Bx, chest

drains

– Deformity of spine or ribs

• Palpation:

– Trachea

– Expansion

– Vocal resonance

• Percussion

• Auscultation

The examination

For the extra marks….

• Evidence of pulmonary hypertension:

– JVP, parasternal heave, split S2, low sats, peripheral

oedema.

• Any other clues of systemic disease

– Rheumatoid, scleroderma, sarcoidosis, IBD.

• Any obvious complications of therapy

– steroids (purpura, cushingoid facies, buffalo hump)

The examination

Finishing off:

• pulse oximetry +/- ABG,

• PEFR / spirometry

• sputum

Presentation

Presentation

• Present +ve findings

• Come to a likely diagnosis

• What do you think the underlying aetiology

for condition is?

• Do they have any evidence of complications

because of respiratory condition:

– Immediate: oxygen requirements, acutely

dyspnoeic, infection

– Long term: pulmonary hypertension, impact of

therapy eg steroid use

• Any other differentials?

Case 1

Examine Mr Smith a 64 year

old male’s respiratory system.

Case 1

• Purse lipped

breathing with

prolonged expiration

• Inhalers by bed

• 90% on air

• Nicotine staining

• Hyper inflated

• Reduced chest

expansion bilaterally.

• Hyper-resonant

• Quiet breath sounds

especially at the

bases.

Case 1

• Purse lipped

breathing with

prolonged expiration

• Inhalers by bed

• 90% on air

• Nicotine staining

• Hyper inflated

• Reduced chest

expansion bilaterally.

• Hyper-resonant

• Quiet breath sounds

especially at the

bases.

Presenting the positive findings…..

• Today I examined Mr Smith’s respiratory

system.

• From the end of the bed I noted he has purse

lipped breathing with prolonged expiration.

He is not cyanosed but his oxygen levels are

reduced at 90% on air. He has nicotine

staining of his fingers.

• On examination of his chest it is hyperinflated

with symmetrically reduced chest expansion.

There was a resonant percussion note and

reduced breath sounds throughout.

• He has multiple inhalers on by his bedside.

• These finds are consistent with severe

COPD (diagnosis) in a gentleman who

continues to be an active smoker

(aetiology).

Complications…

• He does not have any clinical signs to suggest

acute exacerbation

• However I note that he has significant

purpura of the skin and cushingoid facies

perhaps suggesting recent or concurrent

corticosteroid use.

• There is no clubbing or lymphadenopathy in

this gentleman which is important to note as

this patient is at an increased risk of

malignancy (differential)

COPD: common questions

• What you would expect this patients

spirometry to show?

• How would you manage this patient?

• What are the criteria for long-term

oxygen therapy (LTOT)?

Spirometry in COPD

I would expect this man to have an

obstructive picture on his spirometry…

• FEV1:FVC < 0.7

• FEV1 < 80% predicted

Management of COPD

“Management of a patient with COPD

can be divided into conservative,

medical and surgical options…”

Conservative:

– Education + support groups

– Smoking cessation

– Pulmonary rehabilitation

– Vaccination (influenza and pneumococcal)

Medical Management:

• Bronchodilators and anti-inflammatory

drugs to reduce airway obstruction

→ Stepwise progression up BTS guidelines until symptom

control achieved:

• 1st

line - inhaled SABA

• 2nd

line - if FEV1 >50%: LABA or LAMA

- if FEV1 < 50%: LABA + ICS or LAMA

• 3rd

line - LABA + ICS + LAMA

• 4th

line - trial of home nebulisers consider

adding theophylline if still symptomatic

• Consideration for LTOT

Surgical management:

• Bullectomy

• Lung volume reduction

• Lung transplant

N.B. Also make sure you know how to

manage acute exacerbations of COPD.

Criteria for LTOT

• LTOT: 2-4l 02 for at least 15 hours/day

– Non-smoker

– Pa02 <7.3 on 2 occasions when stable

– Pa02 <8 with any of following:

(1) Pulm hypertension / cor pulmonale

(2) Nocturnal hypoxaemia

(3) Secondary polycythaemia.

Case 2

Examine Mrs Jones a 50 year

old female’s respiratory

system.

Case 2

• Oxygen cylinder

• Slightly tachypnoeic

• Dry cough

• Bilat reduced chest

expansion

• Fine end-inspiratory

crackles which do not

move on coughing

• Occasional squawks

• Evidence of cor

pulmonale

Case 2

• Oxygen cylinder

• Slightly tachypnoeic

• Dry cough

• Bilaterally reduced

chest expansion

• Fine end-inspiratory

crackles which do not

move on coughing

• Occasional squawks

• Evidence of cor

pulmonale

Presenting you positive findings…

• Today I examined Mrs Jones’s respiratory

system…

• She is oxygen dependent and slightly

tachypnoeic. She has a dry cough.

• On examination of her chest there is

bilaterally reduced chest expansion. On

auscultation there are bibasal end

inspiratory crackles with occasional

squawks.

• Her JVP is raised at 5 cm and she has

bilateral pitting oedema of the calves.

• These finds likely to be due to an

underlying diagnosis of pulmonary

fibrosis.

• She has sclerodactyly, calcinosis and

telangectasis making systemic

sclerosis is the most likely aetiology

for this fibrosis.

• It appears to be severe disease as she

has evidence of pulmonary

hypertension and is O2 dependent

(complications).

• A differential diagnosis for fine

bibasal crackles in the context of

hypoxia, and pedal oedema would be

congestive cardiac failure with

pulmonary oedema.

Pulmonary Fibrosis:

Common questions

• What causes of pulmonary fibrosis do

you know?

• How would you investigate this

patient?

• What is the management of pulmonary

fibrosis?

Causes of pulmonary fibrosis

Upper zone fibrosis:

• Radiation

• Infection: TB, ABPA

• Sarcoidosis

• Environmental: silicosis,

pneumoconiosis, berylosis,

EAA

• (Ank Spond and psoriasis)

Lower zone fibrosis:

• Rheumatological: RhA, SLE,

SSc, Sjogrens, polymyositis

• Ideopathic pulmonary

fibrosis

• Drugs: amiodarone,

nitrofuratoin, bleomycin,

methotrexate.

• (Asbestosis)

N.B. this will help to narrow down your differential

diagnosis when examining the patient

Investigation of pulmonary

fibrosisHaving taken a full history from the patient I would like to

then proceed to:

• Assses Oxygenation status: O2 sats +/- ABG (T1RF)

• CXR: reticular-nodular shadowing. Other evidence of

cause eg sarcoid or asbestos.

• HRCT: honeycombing, ground glass.

• Spirometry: restrictive pattern (FEV1/FVC >70%) with

reduced DCLO/KCO + TLC.

Having confirmed that the diagnosis is pulmonary fibrosis

I would go on to…

• Look for a cause: autoimmune screen for rheum

conditions, Ca and serum ACE for sarcoid.

• Assess for pulmonary hypertension: with ECG and

Echo.

Management of pulmonary

fibrosisConservative management:

• Education about disease + advice re support groups

• Avoid further exposure

• Smoking cessation

• Advice re compensation if occupation related exposure

Medical Management:

• Corticosteroids

• Azathioprine / MTX / cyclophosphamide if steroid non-

responder

• LTOT

Surgical management:

• Lung transplant.

Case 3

Examine Mr Allan a 30 year old

male’s respiratory system.

Case 3

• Sputum pot – thick

yellow sputum

• Vitamin supplements

by the bed

• Short in stature

• Chesty cough

• Clubbed

• Widespread coarse

crackles throughout

inspiration and

expiration which

change on ask the

patient to cough.

Case 3

• Sputum pot – thick

yellow sputum

• Vitamin supplements

by the bed

• Short in stature

• Chesty cough

• Clubbed

• Widespread coarse

crackles throughout

inspiration and

expiration which

change on ask the

patient to cough.

XRAY

CT

Presenting your positive findings…

• I examined MR Smiths respiratory

system today…

• He is of short stature. He has a chesty

cough productive of thick yellow

sputum. He has finger clubbing.

• On examination of his chest the

predominant feature is bibasal coarse

crackles which change on coughing.

• These finds are consistent with a

diagnosis of bronchiectasis.

• Cystic fibrosis is the most likely

aetiology given the young age and

pancreatic insufficiency (indicated by

A,D,E,K vitamin supplementation).

• Importantly there is no evidence of

acute infection, nor pulmonary

hypertension as complications of

chronic bronchiectasis.

• Other differentials for a productive

cough, clubbing and coarse crackles

include lung carcinoma, lung abscess,

and ideopathic pulmonary fibrosis.

Bronchiectasis:

Common questions

• What causes of bronchiectasis do you

know?

• How do you manage bronchiectasis?

• What are the common complications

of bronchiectasis?

Causes of bronchiectasis

• Developmental: alpha-1-antitrypsin, Primary ciliary

dyskinesia, Cystic fibrosis

• Immune: primary panhypogammaglobulinaemia,

selected Ig deficiencies, HIV, ABPA, post-transplant.

• Toxic: aspiration

• Mechanical: Cancer, foreign body

• Asscoiated: IBD, Rheumatoid arthritis, Connective

tissue disorders, coeliac disease, vasculitides

• Infections: TB, whooping cough, measles,

bronchopneumonia

• Ideopathic: 40-60%

Management of bronchiectasis

Conservative:

• Education and advice

• Physiotherapy to teach 3x daily

postural drainage.

• Smoking cessation

• Dietician input

Management of bronchiectasis

Medical:

• Antibiotics

• Bronchodilators: if evidence of obstruction on

spirometry

• Mucolytics: carbocysteine

• Vaccinations: yearly influenza, pneumococcal

• In CF replace enzymes of pancreatic

insufficiency (CREON)

Surgical:

• Resection of bronchiectatic segment of lung

• Lung transplantation

Complications of bronchiectasis

• Massive haemoptysis

• Amyloidosis (related to chronic inflammation)

• Pulmonary hypertension

• Pneumonia

• Pleural effusion

• Pneumothorax

Case 4

Examine Mr Allan a 70 year old

male’s respiratory system.

Case 4

• Dry cough

• Nicotine staining

• Clubbed

• Two small scars right

posterior-lateral chest

wall approx 5mm

length.

• Decreased expansion

Right side

• Stony dull percussion

note right lower zone

• Reduced TVF (same area)

• Absent breath sounds

(same area).

Case 4

• Dry cough

• Nicotine staining

• Clubbed

• Two small scars right

posterior-lateral chest

wall approx 5mm

• Decreased expansion

Right side

• Stony dull percussion

note right lower zone

• Reduced TVF (same

area)

• Absent breath sounds

(same area).

Case 4

• Dry cough

• Nicotine staining

• Clubbed

• Two small scars right

posterior-lateral chest

wall approx 5mm

• Decreased expansion

Right side

• Stony dull percussion

note right lower zone

• Reduced TVF (same

area)

• Absent breath sounds

(same area).

Present your positive findings…

• Today I examined Mr Allan’s respiratory

system…

• On examination of his hands he has finger

clubbing and evidence of nicotine staining.

• He has two small scars about 5mm on the

right lateral aspect of his chest.

• There is reduced chest expansion on the

right. Over the right lower zone of the chest

there is a stony dull percussion note, reduced

tactile vocal fremitus and absent breath

sounds.

• These finds are consistent with a

recurrent right sided pleural effusion

with evidence of previous drainages

(diagnosis).

• Currently he doesn’t show any signs of

respiratory compromise secondary to

the effusion (complications).

• Given the fact that it is unilateral it is

more likely to be secondary to an

exudative process (aetiology).

• I would want to exclude malignancy

given that he is cachectic, clubbed and

has evidence of tobacco use.

• Another differential for an exudative

pleural effusion is infection.

Pleural effusions:

Common questions

• How would you classify a pleural

effusion?

• What are the causes of an exudate /

transudate?

• How would you investigate a pleural

effusion.

Classifying pleural effusions:

Exudate or transudate.

• Lights criteria for exudate:

– Pleural fluid protein : serum protein >0.5

– Pleural fluid LDH : serum LDH > 0.6

– Pleural fluid LDH >2/3 upper limit of

normal serum level.

Size: small, moderate or large

Causes of transudate vs exudate

Transudates Exudate

CCF Infective: parapneumonic

/ TB / subphrenic

abscess

Cirrhosis Inflammatory: RA, SLE

Malnutrition /

Malabsorption

Malignancy

Nephrotic syndrome PE

Peritoneal dialysis Pancreatitis (L sided

effusion)

Uraemia

Hypothyroid

Investigations

• Pulse oximetry +/- ABG

• Blood tests: including protein, LDH.

• CXR

• Pleural tap under US guidance.

– Biochemistry: Protein, LDH, Glucose

– MC+S +/- AFBs (if suspect TB)

– Cytology

– pH (if < 7.2 have high suspicion for empyema and drain)

• If cause remains unclear:

– CT chest / abdomen, Echo, TFTs,

autoimmune screen.

Summary

• Main cases:

– COPD

– Pulmonary fibrosis

– Bronchiectasis

– Pleural effusions

• Always try to see if unifying diagnosis

(lots of respiratory cases are due to

systemic disease).

If you are struggling…

• For examples of breath sounds:

– YouTube

– Dr Prodigious videos (on YouTube)

– Littman website

Good luck!