Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation due to impedance to expiratory airflow, mucosal edema, infection, bronchospasm and bronchoconstriction due to decreased lung elasticity.
Smoking is the main cause, but others are chronic asthma, α-1 antitrypsin deficiency and chronic infection (eg bronchiectasis).
Exertional dyspnoea, cough, and sputum are usual complaints.
• Present treatment including inhalers, steroids, antibiotics, theophyllines, nebulizers, opiate analgesia, and home O 2 treatment.
• Past history: inquire about previous admissions and co-morbidity.
• Exercise tolerance: how far can they walk on the flat without stopping? How many stairs can they climb? Do they get out of the house?
• Recent history: ask about wheeze and dyspnoea, sputum volume and color. Chest injuries, abdominal problems and other infections may cause respiratory decompensation.
• Read the hospital notes: have there been prior ICU assessments? Has the respiratory consultant advised whether ICU would be appropriate?
- Examine for dyspnoea, tachypnoea, accessory muscle use, and lip-pursing.
- Look for hyperinflation (‘barrel chest’) and listen for wheeze or coarse crackles (large airway secretions).
- Cyanosis, plethora (due to secondary polycythaemia) and right heart failure (cor pulmonale) suggest advanced disease.
- Look for evidence of hypercarbia: tremor, bounding pulses, peripheral vasodilatation, drowsiness, or confusion.
- Check for evidence of other causes of acute dyspnoea, particularly: asthma, pulmonary edema, pneumothorax , Pulmonary embolism. Remember that these conditions may co-exist with COPD.
• SpO 2 , respiratory rate, pulse rate, BP, Temperature , and peak flow (if possible).
• Chest X ray (look for pneumothorax, hyperinflation, bullae, and pneumonia).
• ABG (or capillary blood gas), documenting the FiO 2 . Use pCO 2 to guide O 2 therapy.
• CBC, U&E, glucose, theophylline levels and, if pneumonia is suspected and/or pyrexial, blood cultures, CRP, and pneumococcal antigen.
• Send sputum for microscopy and culture if purulent.
- Give O 2 — remember that hypercapnoea with O 2 is multifactorial. The aim is to maintain SpO 2 88–92 % without precipitating respiratory acidosis or worsening hypercapnoea .
- If the patient is known to have COPD and is drowsy or has a documented history of previous hypercapnoeic respiratory failure, give FiO 2 of 28 % via a Venturi mask and obtain ABG. Titrate up the FiO 2 with serial ABG sampling until the minimum FiO 2 that achieves SpO 2 88–92 % .
- Reduce inhaled oxygen concentration if SpO 2 > 92 % .
Give bronchodilators and steroids
• Give nebulized salbutamol 5mg or terbutaline 5–10 mg.
• Consider adding nebulized ipratropium 0.5mg.
• Use O 2 driven nebulizers unless the patient has hypercapnoeic, acidotic COPD, in which case use nebulizers driven by compressed air, supplemented by O 2 via nasal prongs at 1–4 L/min.
• Give steroids (eg prednisolone 30 mg PO stat or IV hydrocortisone 100 mg).
Other drug treatments
• Give antibiotics (eg amoxicillin, tetracycline, or clarithromycin) if the patient reports increased purulent sputum, or there is clinical evidence of pneumonia and/or consolidation on chest X ray.
• Consider IV aminophylline or salbutamol if there is an inadequate response to nebulized bronchodilators.
• Consider naloxone if the patient is taking an opioid analgesic that may cause respiratory depression.