respiratory for paces

Respiratory for PACES

Cases for finals

Monday 8th October 2012

Dr James Milburn

Dr Chris Kyriacou

Outline• Signs to be seen in examination, both expected

and miscellaneous• Common cases we had/are to be expected in the

exam– Hx and Ex

– Ix

– Mx

Respiratory Exam• End of bed inspection• General Exam• Chest

– Inspection– Palpation– Percussion– Auscultation

• Added extras

Inspection (End of bed)

• Observe patient – breathless/comfortable• Look at surroundings –

inhaler/oxygen/nebulisers etc• Use of accessory muscles• Cachexic

General Examination

• Hands

• Face

• Neck

• Legs

• Clubbing– Bronchiectasis, CF, Carcinoma, Fibrosing alveolitis– 4 signs - FACE

• Flucance of nail bed• Angle loss• Curvature of nail• Expansion of terminal phalynx

• Tar staining• Small muscle wasting

– Lung Ca pressure on brachial plexus

• HPOA– Periosteal inflammation in distal ends of long bones– Primary lung Ca, Meso

• Flap/Tremor– CO2 retention– Fine tremor from β2-agonists

• Pulse– Rate and rhythm– Bounding

• Cyanosis

Face• Plethoric

– Secondary polycythaemia, SVC obstruction

• Horner’s (Ptosis, miosis, anhydrosis)– Pancoast’s, (Demyelination, Carotid aneurysm)

• Anaemia • Central cyanosis• Mouth – Halitosis/Thrush

• Lymphadenopathy

• JVP

Inspection - Chest

Inspection Chest

Inspection - Chest

• Shape– Barrel-chested (AP>Lateral)– Excavatum/Carinatum

• Scars• Dilated veins• Ask them to take deep breath

– Reduced expansion– Symetrical

Palpation

• Trachea

• Apex

• Expansion

• Vocal fremitus

Percussion

• Flat – Pleural effusion (thigh)• Dull – Lobar pneumonia (liver)• Resonant• Hyper-resonant – Emphysema/Pneumothorax• Tympany – Large pneumothorax (puffed out cheek)

Auscultation

• Crackles– Nature of crackles

• Fine – Oedema/Fibrosis (velcro)• Coarse – Bronchiectasis

– Timing• Early insp – COPD/Bronchitis• Mid-late – Fibrosis/Oedema

– Clear on coughing? • Yes - ?bronchiectasis• No – Fibrosis/Oedema

Auscultation

• Wheeze– Inspiratory/Expiratory– Fixed monophonic - Bronchial Ca– Polyphonic - Asthma

• Pleural rub• Vocal resonance

Auscultation

• Breath sounds– Vesicular – Insp longer than exp– Bronchial – Exp longer than insp

• Causes of bronchial breath sounds– Consolidation– Collapse– Fibrosis

Back of chest

• Repeat

Added Extras to offer

• Sats• Temp chart• Sputum pot• PEFR• CVS exam

Case 1

• Mrs Jones is 40 yr old women who presents with a chronic cough

• Please take a history

History

• Cough for last 2 years although now worsening– No diurnal variation– No obvious exacerbating factors

• Productive of around ½-1 cupful of foul-smelling green sputum daily

• Occasional flecks of blood mixed in with sputum• Had 3 ‘chest infections’ in the last 6 months• No weight loss

History

• 2 years ago could walk several miles with no SOB

• During exacerbation is <50yards• No fever/night sweats• No chest pain

HistoryPMH,• Laparoscopic cholecystectomy 2007• Whooping cough ~1970

FH,• Nil of note

Drugs and Allergies, • Nil• NKDA

SH,• Legal secretary for last 15yrs no hx of asbestos exposure• Ex-smoker for 5 years in her 20’s• Minimal drinker• No pets• No recent travel

Differentials

• Bronchiectasis– Most likely from pertussis as child– CF unlikely though screen in <40

• Chronic infection

• COPD – very unlikely without FH of α1-antitrypsin• TB – rule out, no foreign travel, no known exposure• Malignancy – rule out, no wt loss, non-smoker etc• Fibrosis – not dry cough, no occupational risk

Examination

• On examination the patient was clubbed and had coarse inspiratory crackles bilaterally R>L

• Not dyspnoeic at rest and no use of accessory muscles.• A/E and expansion equal• No wheeze

Investigations

• Bedside

• Bloods

• Imaging

• Special tests

Bedside

• Sputum

• PEFR

• Sats

• Temperature

Bloods

• FBC – Anaemia (chronic disease/haemoptysis)– Polycythaemia (secondary to hypoxia in more advanced

cases)– Raised WCC if infection– Eosinophilia if ABPA

• Inflammatory markers – ESR/CRP• U&E’s

– Renal dysfunction due to amyloid deposition• Serum immunoglobulins• Genotyping/Sweat test

Imaging

• CXR– Flattened diaphragms

– Tramlines from thickened bronchial walls– Cystic shadows

• CT/HRCT– Signet rings– Bronchial wall thickening

Management

• Conservative

• Medical

• Surgical

Conservative

• Postural drainage• Chest physiotherapy• Pulmonary rehab• Oscillating positive expiratory devices

(Acapella)

Medical

• Check for reversibility with β2-agonists• Saline nebs • Vaccinations

• Little/No role for:– Steroids (unless concurrent asthma/COPD)– Human Dnase– Leukotriene agoinsts– Methylxanthines

Medical• Antibiotics

– Sputum sample before antibiotics– Choose abx depending on previous sensitivities– If previously cultured Pseudomonas need oral cipro or other IV

abx– Consider low dose macrolides if >3 exacerbations/year

• Macrolides have anti-inflammatory effect

Surgical

• Indicated if localised disease or massive haemoptysis

• Lobectomy

• Pneumonectomy

Viva-esque Questions

1. Main organisms responsible for infection in bronchiectasis?

1. H.influezae, S.pneumoniae, Staph aureus, Pseudomonas, anaerobes

2. What are the main causes of bronchiectasis?

1. H.influezae, S.pneumoniae, Staph aureus, Pseudomonas2. Congenital – CF, Kartagener’s, Young’s

Post-infection (childhood) – Measles, pertussis, TB, BronchiolitisPost-infection (adult) – Severe pneumonia, TBAutoimmune – RA, UCObstruction ( localised) – Tumour, Forgien body, lymph nodeIdiopathicImmunocomp – Primary hypogammaglobulinaemiaTraction bronchiectasis – Secondary to fibrosis

3. What are the complications of bronchiectasis?

3. Infection

Respiratory failure

Brain abscess (haematogenous spread of infection)

Amyloidosis (renal failure)

Pneumothorax

4. What is the definition of bronchiectasis?

4. Persistent progressive condition characterised by dilated thick-walled bronchi. Typically >1.5x the diameter of the accompanying arteriole

4. What is the definition of bronchiectasis?

5. What are the different morhpological subtypes of bronchiectasis

Viva-esque questions

5. Cylindrical (uniform calibre and parallel walls)

Varicose (uncommon – bead like appearance)

Cystic (severe form where cyst like bronchi extend to pleural surface)

6. What is Kartagner’s syndrome?

6. Dextrocardia, Bronchiectasis, Chronic sinusitis

Case 2

• Mr Singh has complained of shortness of breath

History

• Worsening over last 3 months• Now exercise tolerance <10 yards• Dry cough and pain on coughing• Sleeps with 3 pillows• No haemoptysis• No weight loss

HistoryPMH,• HTN• DM• Hypercholesterolaemia

Drugs and allergies,• NKDA• Amlodipine• Indapamide• Metformin• Glicazide

History

FH,• Nil of note

SH,• Ex-smoker (20 pack years)• Around 8 cans strong lager a day• No travel/pets• Lives with wife and 2 children

Examination

• Appears dyspnoeic at rest• Reduced chest expansion• B/L lower zone

– Stony dull to percussion– Absent breath sounds– Reduced vocal resonance

• No obvious signs of wt loss• No lymphadenopathy• No tracheal deviation

Differentials

• Pleural effusion– Secondary to HF– Secondary to cirrhosis– Malignancy

• PE

• Fibrosis

Investigations

Bedside

• PEFR

• Sats

Bloods

• FBC• BNP• U+E• LFTs • CRP• LDH• BNP• Thyroid Function Tests

Imaging

• CXR

• Echo

• USS – for guiding drainage

• CT (with contrast)/CTPA if ?PE

Imaging

Imaging• CXR

– Blunting of costophrenic angles– If larger then opacity with concave upper margin –

Meniscus sign– Even bigger...complete white out +/- mediastinal shift– Elevated hemidiaphragm if subpulmonic effusion

What is this....

Pleural fluid analysis

• Transudate <25g/L protein• Exudate >35g/L• 25-35g/L

– Exudative if:• Ratio of pleural fluid to serum protein >0.5

• Ratio of pleural fluid to serum LDH >0.6

• Pleural fluid LDH > 2 thirds of the upper limits of normal serum value

Pleural fluid analysis

• Glucose <3.3mmol/L– Malig/Ra/SLE/TB• pH <7.2 – Malig/Ra/SLE/TB• Increased LDH – Malig/Ra/SLE/TB• Increased amylase – pancreatitis/Carcinoma/Bacterial

pneumonia/Oesophageal rupture

Management

• Conservative

• Medical

• Surgical

Management

• Conservative

Management

• Medical– BAD ALS (for management of heart failure)

• Β-blockers• ACEi• Digoxin• ARBs• Loop diuretics• Spirinolactone

– Pleurodesis – if malignant

Management

• Surgical– Drainage

• Re-inflation oedema

– Pleurodesis

Intercostal Space

IntercostalNerves and Vessels

Intercostal Muscles

Diaphragm

Fluid (or air) free in the pleural cavity

1. Complications of chest tube drainage

1. Organ damage

Lymphatic drainage chylothorax

Long thoracic nerve of bell

Rarely arrythmias

2. What are the common causes of a exudative effusion

2. PRISM

Infection

Malignancy

3. What are the common causes of transudative effusions

3. ‘The failures’Cardiac failureNephrotic syndromeCirrhosisFailure to eat – Malabsorption

4. How big does an effusion have to be before it can be seen on CXR

4. 175-200mls blunting of C-P angle

Case 3

• Mrs Smith is a 30 year old female who has come in with a long standing cough

History

• Cough for last 6 months, remained relatively constant

• Unproductive of any sputum or blood

• She says she has a constant ‘tightness of the chest’

• Begun to notice some weight loss

History

• Since the cough began, she has felt more lethargic with polyarthralgia

• Has recently begun to feel breathless, even at rest

• Chest pain noted – central, constant, throbbing, relieved by paracetamol

• Noticed that her eyes feel very itchy and dry

HistoryPMH,• Recurrent conjunctivitis – 2011-12

FH,• Nil of note

Drugs and Allergies, • Nil• NKDA

SH,• Minimal drinker and non smoker• No pets, No recent travel• Work - waitress

Differentials

• Sarcoidosis– Young, female– Past history of non-pulmonary manifestation of sarcoid– Cause of apical pulmonary fibrosis

• Malignancy – rule out as weight loss noted, but non smoker, young

• Extrinsic allergic alveolitis – no occupational exposure• TB – another cause of pulmonary fibrosis – but no foreign

travel

Examination

• Lupus pernio– Dusky– Purple– Face, Fingers, Feet

• Inspection– Plaques noted on skin

• Percussion, Palpation – N

• Auscultation– End inspiratory– Fine crackles– APICAL

• Erythema nodosum– Panniculitis

1. What is sarcoidosis?

• 1. A Multisystem, granulomatous disease– Of unknown cause– Scattered collections of granulomas

• Mixed inflammatory cells• Non-caseating, epithelioid

• 2. What % of patients with sarcoidosis have pulmonary involvement?

• 2. 90%– Bilateral hilar lymphadenopathy– Pulmonary infiltrates– Fibrosis

• 3. What are the causes of APICAL pulmonary fibrosis?

Causes of apical pulmonary fibrosis

• B – Borelliosis• R – Radiation• E – Extrinsic allergic alveolitis• A – Ankylosing spondylitis• S – Sarcoid• T – Tuberculosis

Case 4

• Mrs Jenkins is a 65 year old female who has noticed she gets breathless after walking 50 yards

History

• Her breathlessness was first noted 6 months ago, which began after walking 500 yards

• Over the last 2 months this has reduced to 50 yards

• Chronic cough for about 2 years– Productive of white sputum

• Always has pain in both her hands, but she puts it down to ‘everyday wear and tear’. Has not sought medical attention

HistoryPMH,• Hypertension• Hypercholesterolaemia

FH,• Mother ‘suffered from arthritis’

Drugs and Allergies, • Amlodipine• Simvastatin• NKDA

SH,• Minimal drinker and non smoker• Has 2 cats• No recent travel• Work – retired lawyer

Differentials

• Rheumatoid arthritis– Older female– Bilateral long standing small joint arthralgia– Cause of basal pulmonary fibrosis

• Malignancy – rule out as no weight loss noted, non smoker• Drug induced – worsening SOB not usually associated with

CCB and Statins• Scleroderma/CREST – no other extra-pulmonary signs noted• Asthma – highly unlikely for age, no diurnal variation

Examination

• PIP and MCP affected• Elbow nodules

• Auscultation– End inspiratory– Fine crackles– BASAL

• 1. What are the pulmonary complications of rheumatoid arthtitis?

Pulmonary complications of RA

• Pleural effusion• Nodular lung disease• PULMONARY FIBROSIS• Pulmonary vasculitis• Alveolar haemorrhage• Obstructive pulmonary disease• Infection

• 2. What are the BASAL causes of pulmonary fibrosis?

Causes of basal Pulmonary Fibrosis

• D – Drugs– ABC

• A – Asbestosis

• R – Rheumatoid arthritis

• S – Scleroderma/Systemic sclerosis

• I – Idiopathic pulmonary fibrosis

• 3. What three findings constitute Felty’s syndrome?

PLUS Neutropenia

PLUS Rheumatoid arthritis

Investigating Pulmonary fibrosis

Bedside

• Sputum– ?TB – AFB

• Sats• Temperature• Resp rate

Bloods

Imaging

Investigating?

Special tests

• FEV1?

• FVC?

• FEV1/FVC ratio?

• Restrictive or obstructive?

• Why?

Lung function

• FEV1 Reduced• FVC Reduced• FEV1/FVC ratio same or increased• Restrictive• Why? Decreased lung compliance• Other causes: Obesity, pregnancy, air trapping in COPD (mixed

picture), paralysis/muscle weakness

Management

• Conservative

• Medical

• Surgical

Conservative

• Oxygen support

• Pulmonary rehab

Medical

• Corticosteroids– Low dose prednisolone

• Months in duration• N-Acetylcisteine• Sildenafil• Pirfenidone

Surgical

• Lung transplant– Dependant on

• Severity of pulmonary fibrosis• Patient health• Potential improvement

Case 5

• Mr Patel is a 75 year old male with long term shortness of breath

• Take a history

History• SOB began 15 years ago, and has been worsening gradually

• Now SOB at rest, although previously only on exertion

• Associated chesty cough– Productive of ++ sputum– With associated wheeze

• No weight loss

HistoryPMH,• Nil relevant

FH,• Nil of note

Drugs and Allergies, • Salbutamol• Seretide (salmeterol + fluticasone)• NKDA

SH,• Started smoking at 25• Continues to smoke 20 a day• Drinker in the past, now quit

Differentials

• COPD– Progressive, irreversible airway obstruction

• Cough, SOB, Wheeze• Long term smoker

• Pneumonia – unlikely, as no acute pathology• Asthma – unlikely due to age and ++ sputum

Examination

• Inspection– Barrel chest– Use of accessory muscles– Raised RR

• Palpation– Reduced expansion

• Percussion– Hyper-resonance

• Auscultation– Quiet breath sounds

• 1. The term COPD constitutes chronic bronchitis and emphysema. How would you recognise each COPD subtype clinically?

Chronic Bronchitis vs Emphysema

• Obesity• Frequent, productive

cough• Accessory muscle use• Rhonchi• Wheezing• Cor pulmonale signs

– Oedema– Cyanosis

• Thin, barrel chest• Little/no cough• PURSED LIP breathing

and accessory muscle use

• TRIPOD sitting position• Hyper-resonance• Wheezing• Quiet HS

Investigations

Bedside

• Sputum– Mucoid– Macrophages typically

• Sats• Temperature• Resp rate

Bloods

• FBC– Raised PCV

• U+E– Na 147

• a1AT• BNP?

• pH 7.40• PO2 8.3• CO2 5.2• BE +1• HCO3 23.4

Investigations?

Lung function

• FEV1?• FVC?• FEV1/FVC ratio?• Restrictive or obstructive?• Why?

Lung function

• FEV1 low• FVC normal• FEV1/FVC ratio reduced, LESS than 0.7• Obstructive• Why? Decreased expiratory flow• Other causes? Asthma

Investigations

Management – Chronic COPD

Conservative

• Smoking cessation– Education– NRT– Varenicline– Bupropion

• Physiotherapy

Medical• Initial

– SABA (Salbutamol) or SAMA (Ipratropium) prn

• If SOB continues or 2+ exacerbations– FEV1 >50% (Mild COPD)

• Add LABA (Salmeterol) OR LAMA (Tiotropium)– If LAMA, STOP SAMA

– FEV1 <50% (Moderate-Severe COPD)• Add LABA/Steroid combo (Seretide – salmeterol + Flixotide; Symbicort – formeterol + beclomethasone)

• If exacerbations continue– Maximise inhaled therapy with LABA/steroid combo + LAMA + SABA

Medical

• PO theophylline

• PO Carbocisteine

• ? Oral steroid trial

• ? Alpha tocopherol ? Beta carotene

• 2. When should long term oxygen therapy be considered in COPD?

Long term oxygen therapy

• PaO2 <7.3• PaO2 7.3-8.0 AND

– Secondary polycythaemia– Nocturnal hypoxaemia – sats <90%– Peripheral oedema– Pulmonary hypertension

• Supplemental oxygen for at least 15hours per day

• Greater benefits if 20 hours per day

• Reduces hospital admissions and frequency of exacerbations

Surgical

• Bullectomy

• LVRS

• Lung transplantation

Acute exacerbations of COPD

Investigations• Sputum

– Purulent– Neutrophils

• 3. What organisms commonly can cause an acute exacerbation of COPD?

• S. pneumoniae• H. influenzae• M. catarrhalis• P. aeruginosa

Investigations• Bloods

– FBC– U+E - ? Effect of theophylline– CRP

• ABG– pH 7.30– PO2 7– CO2 7.2– BE -10– HCO3 12

Treatment - Exacerbations• Oxygen – sats 88-92% - why not higher?• Antibiotics

– Dependant on organism

• Nebulised bronchodilators• Oral Prednisolone, to continue as part of rescue package• IV aminophylline• NIV?

Non invasive ventilation

• Persistent hypercapnic ventilatory failure– T2RF

• No response to medical therapy

• BIPAP can then be used

Case 6

• Mr Baldwin is a 15 year old boy whose mother is worried about a longstanding cough

History

• Cough has lasted around 1 year, worse in the evenings and in the mornings

• Mr Baldwin has mentioned he feels a ‘band’ around his chest when he needs to cough, which is dry and hacking

• When this happens, it leaves him very breathless and wheezy

History

• Also known to have hayfever and eczema, something that his father also suffers from

Differentials

• Asthma– Cardinal features - Wheeze, SOB, Cough– Usually diurnal reversible and variable airflow obstruction– Associated atopy and family history

• Aspergillosis – unlikely as no trigger identified, not diurnal

Examination

• Inspection– Raised RR

• Palpation– Hyperinflated chest

• Percussion– Hyper-resonance

• Auscultation– Expiratory polyphonic wheeze bilaterally

Investigations

Bedside

• PEFR

• Diary of symptoms/Peak flow

Bloods

• Serum precipitins

• Hyperinflation

Imaging

Special tests

• Spirometry – obstructive picture– Usually >15% improvement in FEV1 following

SABA or steroid trial

• Skin prick testing

Management of chronic asthma

• 1. What are the aims of asthma treatment, and what guidelines are they based on?

• 1. British thoracic society guidelines; no daytime symptoms, no exacerbations, no rescue medications, lung function >80% predicted

Conservative

• Removal of any allergens

• Patient education

Medical• Step 1

– Inhaled SABA prn

• Step 2– Add inhaled steroid 200-800micrograms/day

• Step 3– Add inhaled LABA +/- increase inhaled steroid up to 800micrograms/day

• Step 4– Increase inhaled steroid up to 2000micrograms/day +/- leuotriene receptor antagonist, beta agonist PO, MR

Theophylline

• Step 5– Add long term oral prednisolone

Acute exacerbation of asthma

• Moderate– PEFR 50-75%

• Severe– PEFR 33-50%

• Life threatening– PEFR <33%

Investigating

• Bedside– PEFR– Sputum

• Bloods– FBC, UE, CRP, cultures– ABG, especially in life threatening

Management of acute asthma• Oxygen• Nebulised salbutamol and ipratropium• Prednisolone 50mg PO OD/Hydrocortisone 100mg IV QDS• Call a senior!• IV Magnesium 1.2-2g infusion• IV Salbutamol or IV aminophylline• If numbers not improving ITU!

Summary

• Signs – common and miscellaneous• Cases

– Bronchiectasis

– Pleural Effusion

– Pulmonary fibrosis

– COPD

– Asthma

respiratory for paces

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