COPD: chronic obstructive pulmonary disease
Chronic lung disease with obstructive spirometry pattern
Typically caused by smoking, rarely alpha-tripsin deficiency
Acute Management: steroids, antibiotics, nebulisers and NIV (if required)
Chronic management
LABA/ LAMA
LABA / LAMA / ICS
Common cause for admission to hospital, c.10% admissions
History
Symptoms: shortness of breath, reduced exercise tolerance, fatigue, cough +/- productive, fevers
Timescale: 1-5d, progressive
Background: known COPD with multiple exacerabations previously
Examination & observations
Tachypnoeic +/- hypoxia
Polyponic wheeze, coarse crackles if consolidation
Frail
Investigations
Standard Ix: CXR, ECG, bloods gas FBC, EUC, CRP, LFTs, VBG
CXR: can be commonly normal in a viral excerbation, can show consolidation/ pneumothorax or differential of heart failure
Blood gas: ABG usually not required, VBG useful to look at CO2 and bicarb
If severely acidotic from hypercapnia consider NIV
Raised bicarbonate suggests chronic C02 retainer, hence aim sats 88-92%
ECG: sinus tachycardia with right axis deviation/ RBBB
Pulmonary function tests: obstructive pattern
Diagnostic criteria: clinical
Differentials: PE, CAP, CHF / core pulmonale; IPF, asthma
Classification
Aetiology: primary, secondary (alpha-trypsin 1 deficiency)
Severity: FEV1
Prednisolone 50mg OD 5 days
If bacterial infection suspected or unwell: amoxicillin/ benzyl penicillin & doxycycline / clarithromycin
Aim sats 88-92% if chronic CO2 retainer
Nasal prongs, nasal high flow or NIV
Optimising ward base medical management
Oxygen
88-92% sats if chronic C02 retainer
Nasal prongs -> venturi -> Non rebreathe
NIV for T2RF, very rarely intubated
Steroids:
50mg prednisolone 5d PO
IV Hydrocortisone 200mg stat + 100mg QID if nil by mouth
Antibiotics
If signs of consolidation on chest XR or unwell
If pneumonia, antigens: streph, legionella, mycoplasma
Inhalers
Salbutamol burst 2.5mg x3 every 20 mins then stretch to 3-4hrly
Ipratropium 500mcg stat + QID
Saline nebulisers if struggling to bring up sputum
Continue home inhalers
Disposition:
Discharge to community if mild work of breathing
Admit to medical (respiratory) ward for observation/ oxygen
HDU admission for NIV (new T2RF or acidosis)
Housekeeping
Escalation status : majority with severe COPD would be DNR but for NIV
Morphine 2mg QID prn for symptomatic relief
VTE prophylaxis as normal
Some believe in Magnesium! (MgSO4 10mmol)
Differentials
COPD ward management not optimised (common)
Requires escalation of care to HDU for NIV
Differential: Pulmonary Embolus , Congestive Heart Failure (CHF) , infection not covered
End of life scenario
Investigations
VBG: ?T2RF/ acidosis, > ABG
CTPA
ECG/ troponin if cardiac cause suspected
Baseline bloods: FBC, EUC, LFTs +- CRP/ PCT
Management
BiPAP- if tachypnoea, tiring, acidotic
Escalate antibiotics to Tazocin
Furosemide if APO suspected; enoxaparin if PE suspected
Discussions
Call HDU/ ICU ? biPAP
Escalation status update
Inform family
Senior registrar/ consultant
HDU Criteria
MCQ answer: NIV for T2RF
Real life answer: RR/ work of breathing, whether they look comfortable without NIV
Off oxygen for 24hrs (i.e. overnight)
Safe to function at home, depending upon care receiving
Expected discharge 2-5 days
Pulmonary rehab, smoking cessation, inhaler technique, pneumococcal vaccinations
Respiratory follow up
Target Sats
The aim is to match the oxygen saturations between when they are well vs unwell. For example, most individuals saturate 98-100% whereas individuals with lung disease live with reduce saturations. As the lung disease progresses the saturations drop further to at worst 88% (rarely 86-88%). 88-92% is commonly the COPD target range.
100% Normal saturations
94-98% Sats aim in individuals who aren't C02 retainers
> 92% Commonly accepted threshold in generally very unwell patients, often used in ICU
88-92% Target sats in COPD
< 85% Not compatible with life
Why do COPD patients require a lower target range?
Our respiratory rate is dictated from CO2 levels rather than hypoxia. In COPD patients, their lungs are sub-optimal therefore poor at elimating CO2. Therefore severe COPD patients will live with degree of CO2 retention and hypoxia (around 90% sats). These patients' breathing is stimulated by hypoxia and they have 'turned down' their sensitivity to CO2, through exposure. If we give these patients oxygen during an acute exacerbation, their breathing will slow and they will become hypercapnic. Hypercapnia causes drowsiness, called narcosis.
Which COPD patients are target 94-98% and which are 88-92%?
COPD patients who are 'chronic CO2 retainers' require lower sats. In short if their usualy sats are 98%, this should be the aim during an acute illness. Similarly if their usual sats are 90%, this should be used instead. Old venous blood gasses can be useful to see if their CO2 is normally raised, suggesting they are a CO2 retainer. Other signs include a raised bicarbonate. This compensatory mechanism takes time to occur, therefore if raised in the acute setting suggests chronic CO2 retention.
Clinical diagnosis, key factors:
Reduced exercise tolerance
Smoking history
CXR: hyperinflation, CT-Thorax: emphysematous changes
Spirometry: obstructive picture
Pulmonary rehab, smoking cessation, vaccines (pneumococcal & influenza)
LABA/ LAMA or LABA/ ICS (high dose)
Add ICS
Add Roflumilast (PDE-4)
LTOT: Pa02 < 55
EoL/ palliative care input: morphine
Indications for Roflumilast
FEV1 < 50% after bronchodilator
Exacerbations x2 in last year, despite triple therapy
Associations
Alpha Trypsin 1 Deficiency: consider in COPD presentation if under 50 & non smoker
Asthma: significant number of COPD presentations meet the criteria of reversibility on spirometry (FEV1 > 15% with bronchodilator), therefore ICS is an important first step.
Acute Management
Benzodiazepines & morphine in COPD
There is little evidence that benzodiazepines relieve the symptom of shortness of breath in COPD [1]. I was surprised because I've seen many COPD patients prescribed both morphine & lorazepam. There is evidence morphine relieves breathlessness, therefore I will only prescribe this now [2].
Magnesium in COPD
Seen variance in practice and sometimes given- unlikely to cause harm but lack of solid evidence it is helpful.
Long Term Management
Eosinophils
Raised eosinophils can suggest steroid responsiveness, here NICE recommends LABA/ ICS as first line, then triple therapy. ICS may increase the risk of pneumonia.
LTOT Indications
Resting PO2 < 7.3kPA or < 55 mmHg
If signs of pulmonary HTN: PO2 < 8kPA or < 60mmHg
ICS
Inhaled corticosteroids do not affect disease progression but reduce exacerbations, whilst increasing the risk of pneumonia. If there is evidence of reversibility (i.e. asthma), can start with an ICS / LABA rather than LABA/ LAMA.
Smallwood N, Le B, Currow D, Irving L, Philip J. Management of refractory breathlessness with morphine in patients with chronic obstructive pulmonary disease. Intern Med J. 2015 Sep;45(9):898-904. doi: 10.1111/imj.12857. PMID: 26332621.
Ni H, Aye SZ, Naing C. Magnesium sulfate for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2022 May 26;5(5):CD013506. doi: 10.1002/14651858.CD013506.pub2. PMID: 35616126; PMCID: PMC9134202.
Written in 2025