COPD

Key facts:

Authors: Gideon Diamond, Ruth de Souza and Ricky Jones
Top Tip: Think about NIV early, if hypercapnic and acidotic

Key Differential Diagnoses

• Asthma (reversible bronchospasm)
• Acute heart failure (± MI)
• Acute exacerbation of other chronic lung disease
• Pulmonary embolus, pneumonia, pneumothorax
  Note: can have combination of above

Key Investigations

• ABG (and repeat; regularly if necessary)
• CXR, ECG
• FBC, CRP, U+E, LFT, Bone, Glucose
• BC (if septic), Sputum culture

Key Treatment

• NEB SALBUTAMOL 5.0 mg qds (or continuously until improvement noted)
• NEB IPATROPIUM BROMIDE 500 mcg qds
• PO PREDNISOLONE 30 mg od or IV HYDROCORTISONE 100 mg qds
• OXYGEN (to maintain target saturation 88-92%)
  ± PO AMOXYCILLIN 500 mg tds
  ± IV/PO FUROSEMIDE 40-80 mg, if LVF possibility 

Key Management Decisions

• NIV (CO2 > 6.0 kPa + pH < 7.35)
• Ventilation
• Limitations of care (ward, ITU etc) and DNR

Background

COPD is the second most common reason for emergency admission

Introduction

• Chronic obstructive pulmonary disease (COPD) is characterised by airflow obstruction. This obstruction is only partially reversible and usually progresses slowly with time
• The airflow obstruction is caused by a combination of airway and parenchymal damage (chronic bronchitis and emphysema)
• The damage is the result of chronic inflammation predominantly caused by smoking
• Even though smoking is the main risk factor, only 15% smokers get COPD (ie genetic/other factors also important). It is rare in non-white people. Thus it is a disease of the white working class, that smoke
• α1-Antitrypsin deficiency and various occupational agents are less common causes in nonsmokers
• The three main symptoms are cough, sputum and shortness of breath. Common signs include a hyperinflated chest, wheeze and decreased breath sounds (particularly over bullae)
• Complications include exacerbations, polycythaemia, pneumothorax, weight loss and cor pulmonale
• Exacerbations are common. The cause can be infective (50-70%), due to pollution (10%) or unknown (up to 30%). The majority of infective cases are viral but common bacterial pathogens include Streptococcus pneumonia, Haemophilus influenza and Moraxella catarrhalis (Sapey 2006)
• 35% of patients are re-admitted after discharge; and 14% die within 3 months (NICE 2010)
• Make sure you have read the recent (Oct 08) BTS guideline for emergency oxygen therapy: [Ref]
• Recent advances in COPD therapy, including NIV, have made care a lot more effective

Definitions

• Acute exacerbation of COPD
  • “A sustained worsening of the patient’s symptoms from their usual stable state which is beyond normal day-to-day variations, and is acute in onset.
  • Commonly reported symptoms are worsening breathlessness, cough, increased sputum production and change in sputum colour.
  • The change in these symptoms often necessitates a change in medication.” (NICE 2010)
• Chronic bronchitis (also called chronic mucous hypersecretion syndrome) is defined as a daily productive cough for at least 3 months, in 2 successive years.
  [Ref]

Epidemiology

• COPD is common. Approximately 900,000 people are diagnosed with COPD in the UK although it is estimated that up to 2 million people are undiagnosed (NICE 2010). 210 million are affected worldwide (WHO 2011)
• Mainly affects people over the age of 35. It accounts for more time off work than any other illness
• Prevalence increases with age (Bednarek 2008, NICE 2010)
• 5th most common cause of death in UK (about 30,000 pa), 4th in the world (by 2020, it is projected to be the third behind IHD and CVD) (NICE 2010)
• Frequency and severity of exacerbations are associated with worse outcomes (Donaldson 2002)
• Incidence and prevalence both increasing. Unclear why. May be to do with increased smoking in women, and better prognosis of IHD in recent years, and an ageing population (NICE 2010)
• The use of antibiotics reduces treatment failures, mortality, readmission rates and time-to-next exacerbation - especially in frequent exacerbators

Risk factors

• Smoking: cigarette smoking is the primary risk factor in most countries, although only about 15% of smokers develop clinically apparent COPD; an exposure history of 40 or more pack-years is especially predictive
• Smoke from burning biomass fuels (coal, wood, charcoal) for indoor cooking and heating is an important contributing factor in developing countries, especially in women (cooking in confined areas). Biomass fuel has an exposed pop of 3 billion, compared to 1 billion for tobacco; [Ref]
• Genetic (85% smokers don't get COPD)
• Caucasian (rethink the diagnosis if patient is Black or Asian)
• Low SE class     

Symptoms

• Increased SOB [Ref]
• Increased Cough
• Increased Sputum ±  purulence       

Key questions

• Continued smoking? No of pack years. Note: consider other diagnosis if no significant smoking history
• O2 therapy at home?
• Previous admissions?/in ITU?    Precipitating factors, eg recent cold
• Do they climb stairs/exercise tolerance, activities of daily living, patient assessed QoL?

Note: the last three questions in bold aid severity assessment and decide levels of care eg ward/HDU/ITU/NIV/DNA

Signs

• Inspection - confusion, distressed, central cyanosis, use of accessory muscles, tracheal tug, barrel chest, purse-lip breathing, tachypnoea
• Palpation - trachea (exclude tension pneumothorax),
• Percussion - may be hyper-resonant over bullae or consider pneumothorax. Localised dullness - ?pneumonia
• Auscultation - symmetrical wheeze, decreased breath sounds
• Assess for severe sepsis or SIRS
• Consider pneumonia if localised signs → Assess wfor CURB 65
• Consider LHF if bibasal crackles. Though patients with COPD often have crackles
• Consider RHF/cor pulmonale if elevated JVP, tender RUQ (hepatic congestion) and peripheral oedema
  Note: it may be difficult to distinguish COPD exacerbation/pneumonia/acute heart failure. Smoking is a common rosk factor. The patient may have a combination. If in doubt, treat them all
  Note: COPD is not a cause of clubbing; if present consider malignancy or interstitial lung disease

Investigation

COPD, Asthma and Acute Heart Failure surprisingly difficult to distinguish, clinically and on Ix. The patient can have all three. If in doubt, treat the lot

Blood

• ABG
  Note: if you are going to do one blood test, do this one. It gives management affecting information, eg PaO2, PaCO2, lacytate and pH
• FBC (secondary polycythaemia, WCC), CRP
• U+E, LFT, Bone (calcium?), Glucose
• Theophylline level on admission if the patient is on theophylline
• BC if pyrexial 

Other

• Sputum microscopy and culture, if purulent
• ECG (to help exclude other diagnoses)
• CXR to exclude pulmonary oedema (often difficult as COPD causes upper lobe diversion), pneumothorax, bullae and pneumonia; can have combination
  Note: do not put chest drain into a bulla, thinking it’s a pneumothorax; if unsure, do CT

Key Investigations

• ABG
• CXR

 COPD - large lungs, flat diaphragms, 'narrow' heart

Differential diagnoses

• Asthma (reversible bronchospasm)
• Acute heart failure (± MI)
• Acute exacerbation of other chronic lung disease (bronchiectasis,pulmonary fibrosis)
• Pulmonary embolus, pneumonia, pneumothorax
• Lung cancer (can have both)
• Pleural effusion
• Recurrent aspiration
  Note: can have combination of above

Treatment

Tirate O2. Consider NIV early. You can ventilate COPD patients

Treatment (first line)

Procedures

• Sit at 45o
• Prescribe controlled OXYGEN therapy; if initial ABG reveals hypercapnoea, or patient is a known CO2 retainer, maintain SpO2 between 88 and 92% and use air driven nebuliser with appropriate nasal cannulae; otherwise maintain SpO2 95 to 97%. If drowsiness develops or deterioration occurs repeat ABG immediately 
• IV line (correct fluid and electrolyte imbalances)

Drugs

• Air driven NEB* SALBUTAMOL 5.0 mg qds (or continuously until improvement noted)
• ± Air driven NEB IPATROPIUM BROMIDE 500 mcg qds
  Note: can give OXYGEN via nasal cannula, whilst giving nebulisers to maintain saturation target
  Note: hand-held inhalers (when used with spacer devices and a good inhaler technique) and nebulisers are equally effective in achieving bronchodilation in COPD exacerbations. However, for convenience nebulisers are often used in hospitals. Switch to hand held inhalers when condition is stable (NICE 2010)
  Note: there is no evidence that using a combination of bronchodilators are more effective than using a single agent (McCrory 2002, Rodriguez-Roisin 2006, Patel 2009)
• PO PREDNISOLONE 30 mg od (7-14d, then stop)
1. If the oral route is compromised give IV hydrocortisone 100-200mg qds
2. There is good evidence for this intervention. Steroids reduce treatment failure: [Ref] . There is no good evidence for the superiority of IV over oral steroids: [Ref]
3. Stop steroids as per BNF guidelines (http://www.medicinescomplete.com/mc/bnf/current/PHP4341-withdrawal-of-corticosteroids.htm)
• ±  PO ANTIBIOTICS if purulent sputum. If sputum not purulent only give antibiotics if clinical signs of pneumonia or consolidation on CXR (NICE 2010). Refer to local guidelines for antibiotic choice
1. One commonly used antibiotic is PO AMOXYCILLIN 500 mg tds (Penicillin Allergy: PO DOXYCYCLINE 200 mg od)
2. Do NOT repeat any failed outpatient treatment. Give antibiotics if purulent sputum, significantly raised inflammatory markers (ie don't treat a mildly raised CRP), pyrexial, or pneumonia on CXR. Non-infective exacerbations occur
3. Antibiotics reduce treatment failure and mortality in COPD exacerbations: [Ref] ; and, [Ref]
• Check previous sputum results for resistant organisms as bronchiectasis may be an additional pathology
• ± IV/PO FUROSEMIDE 40-80 mg od (if pulmonary oedema; can have both)
• ± Inhaler: FLUTICASONE/SALMETEROL 1 puff bd (3 different strengths)
  Note: if severely ill, pneumonic consolidation or requiring NIV, use intravenous route for medications. Check previous sputum results for resistant organisms as bronchiectasis may be an additional pathology

Controversy: High-flow oxygen in COPD exacerbation

• Even though it is common belief that high flow oxygen is 'bad' in the initial management of a COPD exacrebation, there is not much evidence for this: [Ref]
• It is probably safest to say that, for patients who might be CO2 retainers (therefore running on hypoxic drive), if high flow oxygen is used initially, it is done with caution. Conversely, it may also be dangerous not to give high flow to someone who has life-threatening hypoxia, as you are frightened of making them worse. Ie, the priority is getting oxygen to the brain. If they are one of the few patients that becomes apnoeic, then we ventilate them.
• This is part of the reason why most ambulance crews in the UK only carry high flow oxygen masks (non-rebreathe bags)
• In other words, by the time the patient has arrived in the ED, any problems induced by high-flow oxygen can be reversed
• There is much debate surrounding oxygen prescription in patients with COPD. However, there is an agreed consensus in the guidance from NICE (NICE 2010), the NHS Evidence 2012 update (NHS Evidence 2012) and the British Thoracic Society on Oxygen therapy (BTS 2008): O2 should be given to keep the SaO2 within an individualised target range

In general

• All patients should have an initial ABG taken on admission to hospital and inspired oxygen concentration noted
• Aim at a pre-specified saturation range (e.g. from an oxygen alert card)
• If no pre-specified range is available aim for target saturations of 88-92% and re-evaluate later based on blood gas results. Oxygen can be given at 2L via nasal prongs with concurrent bronchodilator treatment administered by air driven nebulisers
• If following ABG measurements, the pH and PaCO2 are normal, aim for an oxygen saturation of 94-98% unless there is a history of previous hypercapnic respiratory failure requiring ventilation
• If the PaCO2 is raised but the pH normal the patient is probably a CO2 retainer. Maintain target of 88-92%
• Recheck blood gases regularly after 30-60 minutes (or if there is a clinical deterioration) even if the initial PaCO2 is normal and adjust oxygen accordingly
• If the patient is hypercapnic (PaCO2 >6) and acidotic (pH<7.35) consider NIV especially if the acidosis has persisted for 30 minutes despite appropriate therapy
• Note: BTS guidance suggests than in critical/peri-arrest situations, patients with COPD should have the same initial target sats at 94-98% pending ABG analysis where oxygen therapy should then be tailored
• Note: in patients without known COPD above 50 years old, who are smokers and have a history of chronic breathlessness on minor exertion, consider COPD and aim for initial sats of 88-92%

Key management decisions

• NIV/Not
• Ventilation/not

Stop

• Beta-blockers, if may have precipitated attack

Treatment (second line): if inadequate response to bronchodilators

Drugs

IV AMINOPHYLLINE BOLUS (NOT IF ON ORAL MAINTENANCE THEOPHYLLINE: GIVE INFUSION ONLY) 
5 mg/kg over 20 to 30 mins (not > 25 mg/min) and then maintenance infusion of 0.5mg/kg/hr (0.3 mg/kg/hr, in elderly or those with cardiac failure). Levels should be performed at 12 to 24hrs and infusion rate adjusted. Aim for 10-20mg/litre (55-110 µmol/l). Cardiac monitoring should be arranged

Other

• NIV (If persistent PaCO2 >6.0 kPa and pH < 7.35), especially if patients are known to be slow to wean from invasive ventilation
• Should be delivered in a dedicated setting by trained and experienced staff (NICE 2010)
• IV DOXAPRAM 1.5-4.0 mg/min (If NIV unavailable)
• Ventilation (arrange with ITU) (should be discussed with patient and family)

Prescribing issues

• OXYGEN is a drug and can make the patient worse. It shoud be written  up

Admit?

• Usually, though mild attacks can be managed as an OP
• Always, if significantly worse SOB than normal, has already been on adequate outpatient treatment or drowsy/confused

Bed plan

• Respiratory
• ± ITU if appropriate (if can walk further than garden gate or equivalent)

Referrals

Medical

• Respiratory
• ± ITU

Other

• COPD nurse

The Rest

Maxim

• "COPD is common, and getting more common"

Complications

• Polycythaemia (due to chronic hypoxaemia)
• Pneumothorax (burst bulla)
• Cor pulmonale (chronic hypoxemia→pulmonary artery vasoconstriction→pulmonary hypertension→right heart failure)

Prognosis

• 35% get re-admitted
• 8% die in-hospital (25% in ITU) 
• 14% die within 3 months of discharge from hospital
• 25% die within 1 yrs, 50% die within 3 years
• Poor prognostic indicators: poor performance status; respiratory or metabolic acidosis; an increasing frequency of severe exacerbations
  Note: most patients will however leave hospital: beware of inappropriate nihilism

2° Prevention + Health Promotion

• Patient education
• Smoking cessation (yes, there is a point)
• Vaccination
• Pulmonary rehabilitation programme
• Home or ambulatory oxygen
• Referral to Respiratory MDT (NICE 2010):
1. Physiotherapy - educate people with excess sputum about positive expiratory pressure marks and active breathing cycle techniques
2. Dietician - Control BMI, whether high, low or changing
3. Occupational Therapy - for help with daily activities
4. Social Services - for help at home
• Palliative care teams - for patients with end stage COPD, their carers and families

Don't forget

• If deteriorates after oxygen, you may need lower dose 
• You can very definitely ventilate COPD patients
• Surgery, for bullous disease in selected cases
• Do not put a chest drain into a bulla
• Exacerbations or slow deterioration may be precipitated by lung carcinoma; so consider it - and do not ignore haemoptysis
• It is rare in Black or Asian people, or non-smokers

Red flags

• Cannot speak
• Drowsy/confused 
• Poor performance status
• Respiratory or metabolic acidosis

References