COPD Pt 2: Treatment and Managment Plan

“Patients suffering an exacerbation must have steroids to prevent a relapse. This can be Intravenously with us if they’re coming in, or by arranging contact with urgent or primary care for oral meds. ”

— General BroadCAST COPD Pt 2

The Hypoxic Drive

We discussed the hypoxic drive extensively on the podcast. for more information and references for what we talked about. Check out the link below.

Rebel EM: The Hypoxic Drive

All COPD patients should have their oxygen saturations targeted to be between 88-92%. If it goes below 88% we should increase supplemental oxygen, if it goes above 92% we should decrease supplemental oxygen.

COPD are high risk for t2 respiratory failure which is hypoxemia with hypercapnia so we should treat all patients with COPD this way until we can confirm they are not retaining co2 on blood gas.

That being said….. Hypoxeamia will kill quicker than hypercapnia, so oxygen to get to these levels must be given even in higher doses but sats over 92 should be warrant us titrating down.. If you need oxygen higher than 28% to maintain sats over 88% these patients are very unwell and should warrant a pre alert.

Sudden cessation of oxygen can cause rebound hypoxemia and can be life threatening, so titration down is a better approach.
Most ambulances will only have O2 driven nebuliser capability so because of the risks of hypercapnia we discussed earlier with oxygen these should be limited to 6 mins use at a time before a period off them and then re started…

6-8 L/min any higher or lower and liquid wont be aersolised correctly. If you ever need additional oxygen you can add nasal specs to a second oxygen source below the mask.

If a patient has an air driven nebuliser consider using this and then can supplement again with nasal oxygen if needed.

Hospital or Discharge?:

This can be a complexed decision. The NICE guidance offers a reasonable support tool with this. It is not exhaustive, and should be decided on an idividual basis as we discussed in the podcast. However, here are some useful things to consider.

Treatment:

In the podcast we talked in more detail about the role of SABAs and LAMAs in our practice. We’ve focused on Steroids more here, as this may be an area people are less familiar with.

Steriods:
Cortisol is a glucocorticoid naturally occurring hormone produced by the adrenal glands which has powerful anti-inflmatory and immunosuppressive effects. Naturally the form is cortisol, however it can also be sythenticialy increased

Glucocorticoids have powerful anti-inflammatory effects along with some immunosuppressive effects. Produced naturally in our bodies in the form of cortisol from the adrenal glands but can also be synthetically made and taken parentally e.g. hydrocortisone or enterally e.g. Prednisolone. They work by binding to glucocorticoid receptors resulting in down regulation of inflammatory cytokines whilst simultaneously upregulating anti-inflammatory genes [Hydrocortisone: Uses, Interactions, Mechanism of Action | DrugBank Online]. In COPD this mechanism of action predominantly results in decreased airway inflammatory response, reduced oedema caused during an exacerbation. Hence why steroids are given in exacerbations.

There is strong evidence In moderate to severe exacerbations of COPD oral steroids are advocated based upon the findings of multiple placebo controlled trials which have been systemically reviewed in the literature by guideline creators [Management of severe acute exacerbations of COPD: an updated narrative review | Multidisciplinary Respiratory Medicine | Full Text (biomedcentral.com)]. Steroids have demonstrated improvements in lung function, gaseous exchange and dyspnoea as well as lessening treatment failures, lowering relapse rates and shortening hospital admission duration.

It is for this reason that steroids are an essential part of the treatment for patients presenting with AECOPD and there use is therefore supported by major guidelines on the subject, including; the NICE COPD guideline [Recommendations | Chronic obstructive pulmonary disease in over 16s: diagnosis and management | Guidance | NICE] the joint European Respiratory Society/American Thoracic Society COPD Exacerbation guideline [Management of COPD exacerbations: a€European Respiratory Society/American Thoracic Society guideline (ersjournals.com)] and the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2022 guidelines 2022 GOLD Reports - Global Initiative for Chronic Obstructive Lung Disease - GOLD (goldcopd.org).

All of these bodies recommend steroid administration. Interestingly the evidence also suggests that no inferiority of oral vs IV administration in terms of benefit [Oral or IV Prednisolone in the Treatment of COPD Exacerbations - ScienceDirect] with most advocating oral prednisolone as the steroid of choice. They do all however advocate that IV hydrocortisone is equally as effective and beneficial for those patients who for whatever reason may not be able to take on oral Prednisolone. It is therefore standard initial treatment in patients with AECOPD to administer steroids after beginning bronchodilator therapy.

However the UK ambulance CPGs, despite listing acute exacerbation of asthma as an indication for Hydrocortisone treatment have never listed AECOPD as an indication. For many of us this was quite confusing given similar benefits achieved and the high evidence base recommendations for this intervention mentioned above in other guidelines.

Take away points:

COPD is a terminal condition that affects around 4% of the population.

It is most often caused by repeated exposure to noxious substances, often this is due to smoking, however this isn’t always the case and occupational exposure can be to blame. In about 1% of cases this is due to a rare genetic condition called alpha-1-antitrypsan deficiency.
COPD is an umbrella term for 2 respiratory pathologies, these are:
Chronic Bronchitis and Emphysema. Patients will have features of both diseases, however can tend to present as more one type, than the other.
Patients with COPD can have day to day symptoms managed well, and can have a very good quality of life. We will most often encounter them during an exacerbation, 70% of these are from a resultant RTI, but these can be from other causes, such as environmental triggers, Pulmonary embolism or pneumothorax, so we need to ensure our assessment is detailed to search for these.
Patients suffering an exacerbation will present to us with acute or semi-acute shortness of breath, they will often be wheezy and may have an accompanying cough. Remember Chest pain and haemoptysis Is rare in exacerbation, so if these are present, we should consider more sinister causes.
We’ve discussed oxygen’s part in managing these patients, as well as the risk of worsening CO2 retention if we aren’t cautious with our administration. But… hypoxia will kill your patients quicker, so ensure you give it if they need it. Aim for sats of 88-92% or their normal values if you know this.
Before giving a nebuliser to our patients, if appropriate consider getting them to demonstrate their inhaler technique, as this could be a teachable moment, but if nebs are required, we should administer Short acting beta agonists and Long acting anti muscarinics.
Patients suffering an exacerbation must have steroids to prevent a relapse. This can be Intravenously with us if they’re coming in, or by arranging contact with urgent or primary care for oral meds.
Not all patients need hospital admission, so we should consider if they are safe for discharge, and safety net them appropriately.