COPD

Key Differential Diagnoses

Asthma
Acute heart failure (± MI)
Acute exacerbation of other chronic lung disease
Pulmonary embolus 
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
IV HYDROCORTISONE 100 mg qds or PO PREDNISOLONE 30 mg od
OXYGEN (to maintain target saturation as described below)
  ±  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

• COPD is a common progressive disorder of airway obstruction with partial or no reversibility. The second component is peripheral tissue destruction (Emphysema). It is caused by an inflammatory response to inhaled toxins, often cigarette smoke
• Smoking is the main risk factor, though 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
• Symptoms are productive cough and SOB that develop over years; common signs include decreased breath sounds, prolonged expiratory phase of respiration, and wheezing. Severe cases may be complicated by weight loss, pneumothorax, right heart failure, and respiratory failure
• Infective and non-infective exacerbations are common. If infective, most community-acquired infections are due to Streptococcus pneumoniae and Haemophilus influenzae - and less commonly Moraxella catarrhalis. Recent advances in COPD therapy, including NIV, have made care a lot more effective
• 35% of patients are re-admitted after discharge; and 15% die within 3 months. Make sure you have read the recent (Oct 08) BTS guideline for emergency oxygen therapy: [Ref]

Definitions

Acute excerbation of COPD = 'Sustained worsening of a COPD's patients' condition, from the stable state and beyond normal day-to-day variations, acute in onset and necessitating a change in regular medication'. 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 1 million people have COPD in the UK, 210 million worldwide
• Mainly affects people over the age of 40. It accounts for more time off work than any other illness
• 5th most common cause of death in UK (about 30,000 pa), 4th in the world (by 2030, it is projected to be the third behind IHD and CVD)
• Incidence and prevalence both increasing. Unclear why. May be to do with increased smoking in women, and better prognosis of IHD in recent years
• 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

SOB [Ref]
Cough (productive)          

Key questions

"Have you ever smoked?"
Note: consider other diagnosis if no significant smoking history
Questions about severity: baseline exercise tolerance; patient assessed QoL and LTOT use (affects ITU discussion)
"When was your last admission for COPD?; how many admissions in the last year?; have you ever been on ITU?"

Signs

Distressed, postural splinting of diaphragm
Central cyanosis, use of accessory muscles, tracheal tug, barrel chest, purse-lip breathing
Symmetrical wheeze; if asymmetrical consider focal pathology
Of heart failure; mild pedal oedema is common, COPD patients often have sparse basal crackles thus differentiating it from LVF can be difficult; if in  doubt, treat both
Confusion
Note: COPD is not a cause of clubbing; if present consider malignancy or interstitial lung disease

Other

ECG (to help exclude other diagnoses)
CXR to exclude pulmonary oedema (often difficult as COPD causes upper lobe diversion, consider requesting nTBNP), pneumothorax, bullae and pneumonia; can have combination
Note: do not put chest drain into a bulla, thinking its a pneumothorax; if unsure, do CT

Key
investigations

ABG
CXR

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

Differential
diagnoses

Asthma (reversible airflow obstruction)
Acute heart failiure ± MI (can have both; smoking risk factor for both)
Acute exacerbation of other chronic lung disease (bronchiectasis, fibrosis)
Pulmonary embolus (can have both)

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
NEB SALBUTAMOL 5.0 mg qds (or continuously until improvement noted)
NEB IPATROPIUM BROMIDE 500 mcg qds
Note: can give OXYGEN via nasal cannulae, whilst giving nebulisers, if very unwell
IV HYDROCORTISONE 100 mg qds or PO PREDNISOLONE 30 mg od (7-14d, then stop); 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]
±  PO AMOXYCILLIN 500 mg tds (Penicillin Allergy: PO DOXYCYCLINE 200 mg od)
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
Antibiotics reduce treatment failure and mortality in COPD exacerbations: [Ref] ; and, [Ref]
± IV/PO FUROSEMIDE 40-80 mg od (if have/may have 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. Check previous sputum results for resistant organisms as bronchiectasis may be an additional pathology

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 

Key management decisions

NIV/Not
Ventilation/not

Stop

Beta-blockers, if may have precipitated attack

Treatment
(second line)

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
IV DOXAPRAM 1.5-4.0 mg/min (less often used, since advnet of NIV)
NIV (if CO2 >6.0 kPa and pH < 7.35); NIV reduces in-hospital mortality, and need for ventilation

[Ref]

Ventilation (should be discussed with patient and family)

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

Prognosis

• 35% get re-admitted
• 10% die in-hospital (25% in ITU)
• 15% die within 3 months of discharge from hospital
• 25% die within 3 yrs, 50% die within 10 years of first diagnosis
• Poor prognostic indicators: poor performance status, respiratory or metabolic acidosis, and the presence of leg oedema
Note: most patients will however leave hospital: beware of inappropriate nihilism

2° Prevention + Health Promotion

• Smoking cessation (yes, there is point)
• Vaccination
• Pulmonary rehabilitation programme
• Home or ambulatory oxygen
• Trial of mucolytics in those with chronic bronchitis

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