Chronic Obstructive Pulmonary Disease (COPD) is a slowly progressive disease of fixed airflow obstruction – characterized by minimal to no reversibility with bronchodilators. COPD is most commonly caused by chronic smoking, however other causes – particularly in younger patients – include α1-antitrypsin deficiency and pollution/biomass exposure.
COPD is composed of two distinct disease processes:
a) Chronic Bronchitis – Cough with mucous production >3mo per year x 2 years
b) Emphysema – Abnormal permanent enlargement of distal airways (distal to terminal bronchioles)
Very Brief COPD Pathophysiology
COPD is characterized by an abnormal response of the lung to injury. Specifically, macrophages and epithelial cells in the bronchioles are activated by cigarette smoke and other irritants, triggering the release of neutrophil chemotactic factors (Particularly IL-8 and Leukotriene B4). Neutrophils/macrophages then release proteases that break down connective airway tissue and stimulate the hypersecretion of bronchial mucus. COPD ultimately tips the normal protease-antiprotease balance in favor of proteolysis. Understanding the protease pathophysiology of COPD explains the effect of various disease processes on developing the disease – Smoking increases proteases, leading to the break down of connective tissue while α1AT deficiency (Review Article) leads to decreased anti-proteases, making these individuals prone to develop COPD and much more susceptible to the effects of smoking.
It is important to note that the chronic inflammatory process is markedly different to asthma – with different inflammatory mediators and therefore vastly differing treatments.
- Symptoms of COPD include dyspnea, chronic cough and sputum production. The presence of a post-bronchodilator FEV1/FVC <0.70 confirms the prescence of persistent airflow limitation and therefore, COPD.
- Ddx: Asthma, CHF, Bronchiectasis, TB, Obliterative bronchiolitis (Young, Post-transplant), Diffuse Panbronchiolitis (Asian Non-Smokers w/ Sinusitis)
Complications associated with COPD
- Acute Exacerbation, Infection, Pneumothorax
- Respiratory Failure, Cor Pulmonale, Ca Lung, Secondary Polycythemia (increased CO)
- Air travel risk (particularly if FEV1 <50% or PaO2 <50mmHg (<6.7kPa)
History Taking – Key Questions
While history taking typically focuses well on the presenting complaint; (Such as SOB,Cough, Weight loss, Haemoptysis, Exercise Tolerance etc.) key questions which (a) give great insight into the severity of the patients exacerbation of COPD (AECOPD) and (b) aid subsequent risk stratification may often be missed. The following four questions should be asked in all patients with COPD presenting with dyspnoea/new productive cough. These 4 questions may help in nearly all chronically managed conditions presenting with a deterioration from baseline – not just COPD.
- When was your COPD first diagnosed?
- How has it progressed?
- What is your control like?(Exacerbations/Antibiotics per year – recent multiple courses of ABX may indicate resistant strain)
- What is the best/worst your COPD has been? (Previous Hospitalisation/Ever in ICU?)
- History should include a modified MRC dyspnoea score (0-4) which assesses the patients dyspnea level on various levels of exertion – used for GOLD staging:
- Vigorous exercise (0)
- Hurrying up stairs (1)
- Walking: Slows down on the flat (2)
- Walking: Stops
- Cant leave home/SOB on dressing oneself (4)
- A crude interpretation of the BODE index may be performed at the bedside (by estimating the patients 6 minute walk distance)
- Assess requirement for antibiotics –
- 1. Increased Dyspnoea from baseline
- 2. Increased Sputum volume from baseline
- 3. Purulent Sputum (Seqeulae of leukocyte peroxidase = bacteria)
- Any 2 of the above 3 factors (or new CXR changes) means that antibiotic therapy is likely appropriate.
- Obvious breathlessness, pursed lips (Pursing ones lips increases intrinsic PEEP)
- Warm palms with a bounding radial pulse (Carbon dioxide retention)
- Clubbing – not a COPD association –> think Lung Carcinoma
- Lips + Tongue (Central Cyanosis)
- Assessment of the neck for use of accessory muscles of respiration & raised JVP
- Inspiratory Descent of the trachea – Flattened diaphragm pulls on pericardial sac if there is emphysema, leading to downward pull of the trachea on inspiration
- Hoovers Sign – Emphysema results in a flattened diaphragm which contracts inwards instead of downwards, thereby paradoxically pulling the inferior ribs inwards with its movement (instead of outwards during normal respiration)
- Dahls Sign – Symmetric, slanting regions of hyperpigmentation the thighs – from patients with COPD resting in the tripod position (elbows on thighs)
- Hyper-resonance during percussion and obliteration of the normal cardiac and liver dullness due to air trapping (liver may be palpable due to airway displacement)
- Auscultation – aside from the typical wheeze and crackles, quick vital capacity assessment may aid in stratifying a patient in terms of severity. Technique: Place the stethoscope over the patients trachea and ask them to ‘take a big breath and then blow all the air out quickly’. Normal adults can empty their vital capacity in ~3 to 4 seconds; prolongation > 6 seconds indicates airflow obstruction – a potential indicator of exacerbation severity.
1. Bloods: CBC, Urea+Electrolytes, LFT’s, CRP, Arterial Blood Gas (nB*) +/- Troponin & BNP if background of IHD
2. Imaging: Chest X-Ray- (Link to Radiology features)
3. Respiratory: Respiratory Therapist Consult + Spirometry (Note: Spirometry is often not useful during an acute exacerbation due to patient difficulty)
4. Other Tests: ECG (P.Pulmonale/RAH/RVH/RAD/A.Fib – responsive to ABX), Sputum Culture, Urine (Legionella) Physiotherapy Consult,
5. GOLD Guideline: Stratification (Link)
The GOLD guideline aids in the stratification of patients with COPD into various treatment catogories and also helps to target those individuals who are high risk for repeat hospital admissions. Its may be used in both the ambulatory setting and the initial inpatient workup of a patient with COPD.
Much literature exists on treatments depending on GOLD stages. However, to put it very crudely – The mainstay treatments of GOLD stages A and B (bottom row) are SABA, LABA & LAMA’s. GOLD stages C and D (top row) typically then require steroids.
- Cigarette Smoking
- Other drugs
- DVT/Diet/Discharge Advice
“ASBO-COPD” is an easy to remember mnemonic to hit all the major points when dealing with an inpatient admission of COPD. (For North American readers – an “ASBO” is a UK/Ireland term which stands for Anti-Social Behavior Order!)
Assess patients need for antibiotic therapy – described above (Increased Sputum or Dyspnea, New purulent sputum, CXR changes)
Organisms: H.Influenzae & S. Pneumoniae accounted for 43% and 25% of exacerbations of COPD respectively in one study. Moraxella is also commonly isolated. Less commonly -Chlamydia & Pseudomonas Aeruginosa are isolated.
- Local antibiotic guidelines will direct treatment*
- Co-Amoxiclav TDS 1.2gram IV – is a basic 1st line empiric
- Doxycycline 100mg BD or Clarithromycin 500mg BD (if Penicillin allergic)
- Piparcillin-Tazobactam for severe exacerbations/poorly responsive/multiple courses of antibiotics in the community
- If a patient is maintained on Azithromycin prophyactically you may discontinue it during the patients inpatient admission and restart upon discharge/finishing course of ABX
- Focus antibiotic choice as sputum cultures become available
- Hydrocortisone 100-200mg IV TDS x 24 hours followed by oral switch – pending severity at initial presentation and/or clinical response on Day 2
- PO Prednisolone (40mg once daily PO x 5 days without taper) – REDUCE trial = 5 days of steroids is non-inferior to 14 days. Tapering steroids typically unnecessary for such a short duration of therapy.
- Steroids are proven beneficial in COPD in those patients w/ FEV1 < 60% predicted
Various bronchodilator options/combinations exist – inhalation therapy is BEST when using bronchodilators
- Salbutamol + Ipratropium q4h
- Driven with oxygen
- Note: Indecaterol is the #1 LABA in COPD
- Sit patient upright
- Respiratory Physiotherapy (To aid drainage of secretions/improve resp muscle strength)
- 24% O2 via Venturi Mask + Titration Venturi O2% up to an SpO2% of 88-92% initially
- Once ABG available –> aim for PaO2 >60 mmHg (>8kPa)
Note: Beware of hypoxic drive + lung shunting when giving oxygen – although clinically it is often more important to give oxygen rather than worry about cessation of hypoxic drive.
(C) Cigarettes – Quit
- Stopping smoking is crucial – plain and simple. Many hospitals have smoking cessation staff. Consider nicotine replacement on discharge. Studies suggest that cessation of smoking has some reversibility potential in COPD – not only slowed progression.
- Multiple studies have shown that the best method to communicate spirometry results/severity to patients with COPD are through the use of lung age and graphic displays. (aka. Fletcher and Peto diagrams). Evidence based medicine – Use these to convince your patient to give up smoking and enjoy extra years of disability free life.
(O) Other Meds & Oxygen Part 2
- Promethazine or Dihydrocodeine may decrease the sensation of breathlessness
- Penumococcal Vaccine
- Oxygen – Assess patients need for long term oxygen therapy (LTOT)
(P) Positive Pressure Ventilation
Positive pressure ventilation may be commenced early on over the course of the admission. Use BiPAP when you have hypercapnia and use hi-flow O2 in cases of pure hypoxic respiratory failure. CPAP may be used in some cases of Type 1 Respiratory failure
- Type 1 Respiratory Failure = High Flow O2 or CPAP (CPAP less commonly)
- Type 2 Respiratory Failure = BiPAP
Positive end-expiratory pressure (PEEP) is the number for CPAP or the bottom number in a BiPAP setting. Increasing PEEP using either method of ventilation can open up airways and recruit more alveoli – therefore increasing your oxygenation. Increasing FiO2 is more straight forward- though as mentioned earlier, be wary of increasing FiO2 rapidly in the COPD patient, as increasing FiO2 can worsen oxygenation due to hypoxic drive + V/Q mismatch (you put oxygen in parts of the lung that are poorly functioning so it doesn’t work well)
BiPAP is the key in Co2 retention (Type 2 Respiratory Failure) because the difference between the top and bottom number are what determines how much Co2 you are “pumping out”. You can also increase the respiratory rate using BiPAP.
- Consider BiPAP if pH <7.35 or RR>30 (not a hard/fast rule)
- Consider ventilation if pH <7.25 (Note: Admission pH is predictive of survival)
- Nocturnal CPAP may be beneficial in many of these patients – particularly if PMHx of Obesity Hypoventilation Syndrome or Obstructive Sleep Apnea
(D) DVT Prophylaxis + Diet + Discharge Advice
- DVT/P.E ruin everyones day!
- Remember to consider interaction with Clarithromycin and Warfarin in the respiratory patient (Increased INR)
- Diet: Undernutrition is associated with reduced muscle function and increased mortality rate. A high dietary intake of n-3 fatty acids may protect smokers against COPD.
- Discharge Advice: Table 1 (below)
Useful Link: Formulation + Typical Doses for COPD Medications
Future COPD Targets
Many new treatments for COPD exist and are currently in development: 5-lipoxygenasee inhibitors, IL-8 antagonists, LTB4 inhibitors, protease inhibitors and phosphodiesterase-4 inhibitors amongst others. However, it is important to note that the 3 well studied factors which decrease mortality in COPD are very basic – smoking cessation (#1), pneumococcal/influenza vaccines and long term oxygen therapy (>15hrs/day).
The next time a patient presents with an exacerbation of COPD think ASBO-COPD !
(Last Updated: October 2016)