A few weeks back you learned about Cushing’s and Addison’s Disease, and you may recall that corticosteroids play a starring role in both disorders. So today we’ll be taking a deeper dive into the pharmacology of this very common class of medication. It’s used for a lot of disorders, has some pretty unique and significant side effects, and also comes with strict dosing schedules. Plus, it will most likely show up in your clinical rotations and definitely show up on your nursing school exams. So, let’s dive in!
What is a corticosteroid?
Before we get too far down the rabbit hole of corticosteroids, let’s talk about what they actually are. In the body, corticosteroids are sometimes referred to as the adrenocortical hormones because of where they are secreted (hint, it’s the adrenal glands!). They can be categorized into three subtypes: glucocorticoids, androgens and mineralocorticoids. Let’s break this down a bit further:
- Glucocorticoid: The primary one is cortisol (there are about 30 glucocorticoids!). Recall that cortisol is released in response to stress and play a key role in cellular metabolism.
- Androgens: The primary one is testosterone.
- Mineralocorticoids: The primary one is aldosterone, which plays an important function in sodium and water retention and potassium balance
What are exogenous corticosteroids used for?
When we say something is “exogenous” we mean that we are supplying it. Think “extra” and that’s a good way to remember that “exogenous” means we’re adding something extra into the boyd. On the other hand, the corticosteroids that the body produces on its own would be referred to as “endogenous.” So, why does the body need EXTRA corticosteroids?
Corticosteroids are used to treat a variety of conditions as well as adrenal insufficiency (remember our patient with Addison’s Disease?). Some other reasons a patient may receive corticosteroid therapy are:
- Chronic use of glucocorticoids (such as prednisone) can cause disruptions in the hormone feedback loop involving the pituitary gland and the secretion of ACTH. Recall that ACTH is the precursor hormone to cortisol secretion. In normal conditions, when cortisol levels are low, the pituitary gets the signal to secrete ACTH which tells the adrenal glands to release cortisol. So, instead of the pituitary receiving a signal that it needs MORE glucocorticoid, it gets a signal that the body has plenty of cortisol. This means that ACTH isn’t released and the adrenal glands don’t get the signal to release cortisol. Over time, the adrenal cortex shrinks and isn’t able to secrete cortisol effectively. We’ll talk about this more when we discuss dosing, but the result is the patient essentially can become dependent on exogenous glucocorticoids because the adrenal cortex is incapable of supplying the body with its cortisol needs. This is called “acquired adrenal insufficiency.”
- Addison’s disease or primary adrenal insufficiency (read more about it here).
- Autoimmune disorders such as lupus, vasculitis, rheumatoid arthritis, Crohn’s disease; the medication essentially suppresses the immune system so the body doesn’t attack itself with such gusto.
- Arthritis, to reduce inflammation and pain (check this)
- Rashes including those from poison oak, ivy, sumac (uroshiol)
- S/p transplant surgery to reduce incidence of organ rejection
- Cerebral edema
- Spinal cord injury
- Pre-term birth to prevent respiratory distress syndrome in the infant (given to mom)
Corticosteroids come in many different forms
Corticosteroids are really versatile drugs coming in both short- and long-acting formulations that can be given as tablets, in an IV or as an IM injection. Topical formulations are also available and are what you typically see used for dermatologic conditions (tell story about Tom and his nasty poison oak problem). You may also give patients corticosteroids via inhalation for the treatment of respiratory disorders, and there even nasal sprays available as well.
Some of the most common corticosteroids and their uses are:
- Prednisone: Autoimmune disorders such as lupus, multiple sclerosis and rheumatoid arthritis. Prednisone is available in PO form.
- Methylprednisolone: Systemic inflammation, multiple sclerosis, ARDS. Often given IV in critically ill patients, can also be given IM as well. Long-term use most likely taking PO.
- Dexamethasone: To reduce cerebral edema, often used after a stroke or brain injury. In the critical care environment, it is used to reduce airway edema prior to extubation. May also be used to prevent nausea with chemotherapy. Dexamethasone is available in PO, IM and IV form.
- Betamethasone: Given IM to moms who are in pre-term labor. Also used for adrenal insufficiency in PO form.
- Budesonide: Crohn’s disease may be treated with the PO form of this medication. It is also available as a nasal spray for allergic rhinitis and inhalation form used in asthma management.
- Hydrocortisone cream: Dermatologic inflammation and pruritis.
- Fluticasone: Used as maintenance therapy in asthma, not a “rescue” therapy. Also used as a nasal spray for nonallergic rhinitis.
So as you can see, there are a lot of different types of corticosteroids as well as uses. Rather than look at the side effects and implications for each one, let’s look at the broad strokes for each main type (systemic vs non-systemic). Sound good?
Side effects of corticosteroids
Systemic Corticosteroids typically have the larger side effect profile, so let’s start there first. The main thing you need to know about systemic corticosteroids is they suppress the immune system, so your patient will have an increased risk for infection. Also, with long-term use there can be a re-distribution of body fat that leads to the patient having what’s called a “moon face” and “buffalo hump”. It can also cause the patient to have mood swings, increased hunger, fluid retention, hypertension, delayed wound healing osteoporosis and hyperglycemia. Also, there is increased risk for peptic ulcers, which can bleed uncontrollably and thromboembolism which can occlude a pulmonary artery and be fatal.
Tapering off corticosteroids
Remember that negative feedback loop where the pituitary reacts to low levels of cortisol by sending out ACTH to tell the adrenal glands to amp up their production and release of cortisol? Let’s say you have a patient who has been on prednisone for awhile and whose adrenal glands have completely gone on a little adrenal vacation. They haven’t had to work in a while, and we all know how hard it is to get back into the swing of things once we get back from vacation, right?
So, when someone is being taken off corticosteroid therapy, we don’t just abruptly stop it. That would be like you flying home from Hawaii at 2am and getting up at 5am to work a 12 hour shift the next day. That would not work well at all. That’s why you ease back into things after a big trip. You might unpack that first day, do some laundry and collect the mail. Then maaaybe you go back to work after that. In other words, you ramp up slowly.
After being out of the glucocorticoid releasing game for a while, the adrenal glands need to ease back into it in order to meet the body’s needs. So that’s why we taper patients off glucocorticoids like prednisone. It gives the adrenal glands time to get back into gear. Otherwise, an abrupt discontinuation could leave the patient with no ability to meet their cortisol needs sending them straight into an addisonian crisis. This whole concept of tapering off corticosteroids WILL BE ON THE EXAM. It always is.
So let’s say you’re faced with the following scenario
Bob is 56 years old, and is being treated for a flare up of rheumatoid arthritis with prednisone. He started it eight weeks ago and is now presenting to the wound care clinic for a wound on his leg that just won’t heal. He’s gained ten pounds since beginning the prednisone therapy with no signs of edema. Vital signs are HR 81, RR 17, BP 166/82, O2 saturation 97% on RA; joint pain is rated as a 2 on 0-10 scale. As you are assessing his wound and comparing it to the assessment two weeks ago, he says, “These pills make me so edgy, I eat non-stop and I hate how round my face is. I can’t wait to get off of them next week.” The wound has not improved in the past two weeks, though it does not look infected at this time.
Based on this scenario, you could write some key care plan components, including:
- Risk for infection secondary to immunosuppression and presence of wound
- Impaired tissue integrity as evidenced by 2 cm x 1.5 cm wound at left medial malleolus
- Knowledge deficit related to drug dosing schedule as evidenced by patient statement “I can’t wait to get off of them next week.”
- Disturbed body image as evidenced by patient statement “I hate how round my face is.”
- Imbalanced nutrition/more than body requirements as evidenced by weight gain of ten pounds.
- Risk for excess fluid volume related to sodium retention secondary to prednisone therapy.
Now, of course, nursing is all about fixing problems. So the interventions you’ll need to implement will be aimed at the nursing diagnoses listed above.
- Risk for infection: Provide education about keeping wound clean, avoid people who are sick, not jumping into sewage-infested canals, you get the idea. Also teach patient the signs of infection such as fever, cough, purulent wound drainage, etc..
- Impaired tissue integrity: Provide education about wound care, teach patient to inspect skin daily for wounds, ensure patient understands when to return to wound clinic.
- Knowledge deficit: Provide education on medication tapering and importance of following MD instructions.
- Disturbed body image: Encourage patient to share his feelings, reassure patient that the “moon face” will subside once prednisone therapy is complete.
- Imbalanced nutrition/more than body requirements: Reassure patient that some initial weight gain is to be expected, instruct patient to weigh daily, provide patient with weight gain parameters, provide patient with dietary guidelines.
- Risk for excess fluid volume: Instruct the patient to weigh daily and report weight gain of two pounds or more in one day, monitor blood pressure, auscultate lung sounds, assess for edema.
And then of course, you’ll need to list your expected outcomes, which for infection risk could be something like:
- Prior to leaving clinic today, patient will be able to state three signs of wound infection.
- At next wound clinic appointment, wound will be free of signs of infection, patient will have normal VS.
Just the highlights
Your main takeaways for corticosteroids are:
- Risk for infection. This one is huge! You need to always be aware of this for any patient who is taking corticosteroids.
- Risk for impaired skin integrity and impaired wound healing. If these patients get a wound it’s going to be difficult to treat.
- Risk for hyperglycemia. If patient is diabetic, they can anticipate likely needing more insulin. Hyperglycemia leads to impaired tissue integrity as well, so your diabetic patient on corticosteroids could have some very persistent wounds.
- Risk for cushingoid appearance. This is the “moon face” and “buffalo hump” mentioned earlier.
- When discontinuing the medication, it MUST be tapered off! Otherwise, it puts the patient at risk for acute adrenal insufficiency.
Get this on audio in Episode 84!
I hope that helps you understand corticosteroids. Got questions? Share them in the comments below!