This guide provides an overview of the recognition and immediate management of COPD using the ABCDE approach. The ABCDE approach is a tool used to perform a systematic assessment of a critically unwell patient. It involves working through the following steps:
Each stage of the ABCDE approach involves clinical assessment, investigations and interventions. Problems are addressed as they are identified and the patient is re-assessed regularly to monitor their response to treatment. This guide is intended to assist students in preparing for emergency simulation sessions as part of their training and not to be used for patient care.
COPD is a respiratory disease characterised by airflow obstruction that is not fully reversible. Airflow obstruction occurs secondary to structural damage to the airways and parenchyma as a result of chronic inflammation. COPD is most commonly caused by chronic exposure to tobacco smoke, however, occupational exposure and genetic abnormalities may be contributory factors.
An exacerbation of COPD is defined as a sustained deterioration in a patient's respiratory symptoms beyond their normal day-to-day variability. This worsening of respiratory symptoms occurs acutely and normally requires additional medical therapy.
The most common trigger for an exacerbation of COPD is respiratory tract infection. In the community, Streptococcus pneumoniae and Haemophilus influenzae are the most common bacterial culprits. Viral causes include rhinoviruses, influenza and respiratory syncytial virus (RSV). Pollutants can also trigger an exacerbation.
Typical symptoms of COPD include:
Typical clinical signs of COPD include:
General tips for using an ABCDE approach in an emergency setting include:
Acute scenarios typically start with a brief handover from a nurse that includes the patient's name, age, background and the reason for the review.
You may be asked to review a patient with COPD due to shortness of breath and/or wheeze.
Introduce yourself to whoever has requested a review of the patient and listen carefully to their handover.
Introduce yourself to the patient including your name and role.
Ask how the patient is feeling as this may provide some useful information about their current symptoms.
An inability to speak in full sentences indicates significant shortness of breath.
Make sure the patient's notes, observation chart and prescription chart are easily accessible.
Ask for another clinical member of staff to assist you if possible.
If the patient is unconscious or unresponsive, start the basic life support (BLS) algorithm as per resuscitation guidelines.
Yes: if the patient can talk, their airway is patent and the assessment of breathing can proceed.
Airway compromise can feature few signs, including cyanosis, see-saw breathing, use of accessory muscles, diminished breath sounds and added sounds. To assess airway compromise, open the mouth and inspect for anything obstructing the airway such as secretions or a foreign object.
Causes of airway compromise can include:
When assessing airway compromise, seek immediate expert support from an anaesthetist and the emergency medical team. While awaiting assistance, some basic airway manoeuvres can help maintain the airway.
To open the patient's airway, use a head-tilt chin-lift manoeuvre:
If the patient is suspected to have suffered significant trauma with potential spinal involvement, perform a jaw-thrust rather than a head-tilt chin-lift manoeuvre:
Airway adjuncts are often helpful and in some cases essential to maintain a patient's airway. To insert an oropharyngeal airway:
A nasopharyngeal airway is a soft plastic tube with a beveled end and a flange at the other. NPAs are usually better accepted by patients who are partly or fully conscious than oropharyngeal airways. It is not recommended to use an NPA if a patient may have sustained a skull base fracture, as entering the cranial vault with the NPA can be life-threatening.
Instructions for inserting a nasopharyngeal airway:
If the patient exhibits signs of anaphylaxis (e.g. angioedema, rash), administer the appropriate treatment.
If the patient loses consciousness and has no signs of life, issue a crash call and commence CPR.
Remember to re-assess the patient after any intervention.
Evaluate the patient’s respiratory rate:
Check the patient’s oxygen saturation (SpO2):
Inspect the patient from the end of the bed:
Check the position of the patient’s trachea to identify deviation which may be a result of a tension pneumothorax.
Locate the apex beat, which is typically located in the 5th intercostal space in the midclavicular line. A displaced apex beat can be caused by a large pleural effusion, tension pneumothorax or right ventricular hypertrophy.
Assess chest expansion which may be restricted in the case of consolidation and pleural effusion.
Listen to both lungs:
Wheeze is a common finding in people with chronic obstructive pulmonary disease (COPD) and typically worsens during exacerbations. To properly assess the patient, medical practitioners should perform percussion on the chest to identify areas of dullness which may be associated with consolidation, lobar collapse, or pleural effusion.
If indicated (e.g. low oxygen saturation), an arterial blood gas (ABG) should be taken to quantify the degree of hypoxia. A normal PaO2 on room air should be greater than 10 kPa (75 – 100 mmHg). If the patient is receiving supplemental oxygen, then the PaO2 should be roughly 10 kPa less than the inspired oxygen concentration (FiO2).
The CO2 binds with H2O and forms carbonic acid, so if a patient is retaining CO2, their pH will decrease. A low pH with a raised PaCO2 indicates the patient is failing to ventilate effectively and may require non-invasive ventilation.
Some patients with severe COPD will have chronically raised CO2, which can complicate ABG interpretation when they are acutely unwell. In this setting, the bicarbonate (HCO3-) rises to ‘mop up’ the acidic effect of carbonic acid and normalise the pH. It takes several days for this metabolic compensation to occur, so a raised HCO3- in the acute context suggests the patient has some degree of chronic hypercapnia with metabolic compensation.
A raised lactate indicates anaerobic metabolism secondary to reduced end-organ perfusion. Sepsis is a common cause of a raised lactate.
A patient presenting with an acute exacerbation of COPD will likely require serial ABGs to monitor their response to oxygen therapy. After any change in inspired oxygen concentrations, consider repeating an ABG.
A chest X-ray may be useful in ruling out other respiratory diagnoses if the patient is primarily short of breath (e.g. pneumothorax, pneumonia, pulmonary oedema). Chest X-ray should not delay the emergency management of an acute exacerbation of COPD.
A sputum sample should be taken to the microbiology lab for culture and sensitivity, as this information can be useful later to understand the causative organism and its antibiotic sensitivities.
Oxygen should be administered to all critically unwell patients during the initial assessment. If the patient has COPD and a history of CO2 retention, a venturi mask should be used and the oxygen titrated appropriately. If the patient is conscious, have them sit upright, as this can also help with oxygenation.
A high-dose inhaled beta-2 agonist (e.g. salbutamol 5mg) should be administered as a first-line treatment in the management of an acute exacerbation of COPD. Prescribe the salbutamol on the STAT section of the drug chart. If the patient is hypercapnic or acidotic, the nebuliser should be driven by compressed air rather than oxygen (to avoid worsening hypercapnia).
Check the patient’s respiratory rate which is typically increased in acute exacerbations of COPD.
Check the patient’s SpO2 which is typically reduced in COPD exacerbations, unless they are hypoxic due to a concomitant pulmonary pathology.
If the patient is hypoxic, connect pulse oximetry.
Auscultate the chest to assess breath sounds which may be reduced bilaterally in COPD.
Observe the patient for accessory muscle use which may indicate severe respiratory distress.
Look for use of accessory muscles which may suggest severe respiratory distress.
Initiate treatment of an acute exacerbation of COPD with:
Give repeat doses of salbutamol at 15-30 minute intervals or give continuous nebulised salbutamol at 5-10 mg/hour if there is an inadequate response to initial treatment.
If the patient does not respond adequately to nebulised salbutamol, administer ipratropium bromide 500 micrograms. This can be given with salbutamol in the same nebuliser.
All patients with an acute exacerbation of COPD should receive oral corticosteroids to reduce airway inflammation. NICE recommends oral prednisolone 30 mg once a day for 5 days.
If the above interventions fail to improve breathing, escalate the patient’s care to senior medical staff to consider further management options including non-invasive ventilation (NIV) for persistent hypercapnic respiratory failure, respiratory stimulants and intravenous theophylline.
If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.
Make sure to re-assess the patient after any intervention. If the patient’s clinical condition has not improved (e.g. the patient is still hypoxic and/or dyspnoeic despite treatment, or even worse they are becoming drowsy and fatigued) then escalate to a senior for urgent review.
Patients with an acute exacerbation of COPD may be tachycardic, particularly if beta-agonists have been administered. A bounding pulse may be noted secondary to CO2 retention.
Hypotension may be present in the context of sepsis.
Capillary refill time may be prolonged in the context of sepsis.
Inspect for a raised JVP which may be associated with cor pulmonale.
Palpate the patient’s chest to feel for a ventricular heave or displaced cardiac apex both of which are associated with cor pulmonale.
Auscultate the patient’s praecordium to assess heart sounds. A gallop rhythm is a feature of congestive heart failure (e.g. secondary to cor pulmonale).
Calculate the patient’s fluid balance. Calculate the patient’s current fluid balance using their fluid balance chart (e.g. oral fluids, intravenous fluids, urine output, drain output, stool output, vomiting) to inform resuscitation efforts. Reduced urine output (oliguria) is typically defined as less than 0.5ml/kg/hour in an adult.
Insert at least one wide-bore intravenous cannula (14G or 16G) and take blood tests as discussed below.
Collect blood tests after cannulating the patient including: FBC to rule out anaemia and to look for a raised white cell count which may suggest underlying infection, and U&Es to assess renal function.
An ECG should be performed to look for:
An ECG should not delay the treatment of an acute exacerbation of COPD.
Antibiotics should only be used to treat exacerbations of COPD associated with a history of increased purulent sputum production or other features suggestive of pneumonia such as fever, raised inflammatory markers and signs of consolidation on chest X-ray.
Prescribe antibiotics according to local guidelines.
Hypovolaemic patients require fluid resuscitation:
After each fluid bolus, reassess for clinical evidence of fluid overload (e.g. auscultation of the lungs, assessment of JVP).
Repeat administration of fluid boluses up to four times (e.g. 2000ml or 1000ml in patients at increased risk of fluid overload), reassessing the patient each time.
Seek senior input if the patient has a negative response (e.g. increased chest crackles) or if the patient isn’t responding adequately to repeated boluses (i.e. persistent hypotension).
If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.
Make sure to re-assess the patient after any intervention.
In the context of an acute exacerbation of COPD, a patient’s consciousness level may be reduced secondary to hypoxia and/or hypercapnia.
Assess the patient’s level of consciousness using the AVPU scale:
If a more detailed assessment of the patient’s level of consciousness is required, use the Glasgow Coma Scale (GCS).
Assess the patient’s pupils:
Review the patient’s drug chart for medications which may cause neurological abnormalities (e.g. opioids, sedatives, anxiolytics).
Measure the patient’s capillary blood glucose level to screen for causes of a reduced level of consciousness (e.g. hypoglycaemia or hyperglycaemia).
It may be necessary to expose the patient during your assessment: remember to maintain dignity and respect throughout.
A blood glucose level may already be available from earlier investigations (e.g. ABG, venepuncture). The normal reference range for fasting plasma glucose is 4.0 – 5.8 mmol/l.
Hypoglycaemia is defined as a plasma glucose of less than 3.0 mmol/l. In hospitalised patients, a blood glucose ≤4.0 mmol/L should be treated if the patient is symptomatic.
If the blood glucose is elevated, check ketone levels which if also elevated may suggest a diagnosis of diabetic ketoacidosis (DKA).
Request a CT head if intracranial pathology is suspected after discussion with a senior.
Alert a senior immediately if you have any concerns about the consciousness level of a patient. A GCS of 8 or below warrants urgent expert help from an anaesthetist. In the meantime, you should re-assess and maintain the patient’s airway.
If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.
Make sure to re-assess the patient after any intervention.
