Oral corticosteroids in the management of chronic

rhinosinusitis with and without nasal polyps: Risks and

benefits
David M. Poetker, M.D., M.A.

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ABSTRACT

Background: Oral steroids are synthetic mimics of adrenal cortex hormones and are considered a staple in the management of chronic rhinosinusitis due
to their anti-inflammatory effects. Despite their common use, many providers are not familiar with the potential risks of the drugs.
Methods: Literature review.
Results: An overview of the existing data on the risks of oral steroids is presented as well as a review of the malpractice lawsuits with regard to oral steroid
use and a discussion of the data that support the use of oral steroids in patients with chronic rhinosinusitis with and those without nasal polyps.
Conclusion: It is essential for providers to be aware of the potential complications of a medication, the medical jurisprudence of the drugs, and the data
that support their use.
(Am J Rhinol Allergy 29, 339 342, 2015; doi: 10.2500/ajra.2015.29.4223)

ral steroids are a mainstay of treatment in the management of

sinonasal inflammatory disease, are commonly used, and are
considered by many rhinologists to constitute a key component of
maximal medical therapy.1 Their anti-inflammatory effects to treat
the inflammation associated with chronic rhinosinusitis (CRS) as well
as their antifibroblast effects to reduce postoperative scar formation
are the most common reasons for their widespread use.2 Despite their
common use, many providers are not familiar with the potential risks
of the drugs.
The objectives of this review were to present an overview of the
existing data on the risks of oral steroids. This was not intended to be
an exhaustive review because other articles exist that specifically
outline those risks.3 We plan to discuss what is known about specific
risks, review the lawsuits regarding oral steroid use, and finally,
discuss the data that support the use of oral steroids in patients with
CRS, with and without nasal polyps.

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Morphologic Changes

Redistribution of adipose tissue, a common effect associated with

prolonged oral steroids, is known as corticosteroid-induced lipodystrophy or cushingoid changes, and includes truncal obesity, facial
adipose tissue (moon facies), and dorsocervical adipose tissue (buffalo hump).4 The rate and incidence is variable but has been reported
to occur in 15% of patients in 3 months, with daily doses equivalent
to 1030 mg of prednisone.4 Higher doses and longer durations of
corticosteroids seem to increase the frequency of adipose tissue redistribution.5 The risk is reportedly higher in women, patients 50
years of age, and patients with either a high initial body mass index
or a high calorie intake.5

From the Division of Otolaryngology, Department of Surgery, Zablocki VA Medical

Center, Milwaukee, Wisconsin
D. Poetker is a speaker for Intersect ENT and a consultant for GlaxoSmithKline
Presented at the North American Rhinology and Allergy Conference, Boca Raton,
Florida, February 7, 2015
Address correspondence to David M. Poetker, M.D., Division of Rhinology and Sinus
Surgery, Department of Otolaryngology and Communication Sciences, Medical College
of Wisconsin, 9200 W Wisconsin Avenue, Milwaukee, WI 53226
E-mail address: dpoetker@mcw.edu
Copyright 2015, OceanSide Publications, Inc., U.S.A.

American Journal of Rhinology & Allergy

Steroids increase blood sugars by stimulating proteolysis, promoting gluconeogenesis, and inhibiting glucose uptake.6 In addition,
steroids cause an insulin resistance by decreasing the ability of adipocytes and hepatocytes to bind insulin. This effect can occur within
hours of beginning therapy but seems to decrease with prolonged
use.6 Synthetic steroids are many times more potent than natural
steroids at decreasing carbohydrate tolerance.6 Upon cessation of the
steroids, the inhibition of glucose uptake and metabolism usually
returns to normal.6 Despite their common use, the degree of hyperglycemia caused by steroids has not been clearly established.

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COMPLICATIONS OF STEROID USE

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Hyperglycemia

Infection

Although steroids increase circulating neutrophils by enhanced

release from bone marrow and reduced migration from blood vessels,
the number of lymphocytes, monocytes, basophils, and eosinophils
decrease due to a migration from the vascular bed to lymphoid
tissue.7 Steroids can impair neutrophil function by reducing their
adherence to vascular endothelium and their bactericidal activity;
inhibit antigen-presenting cells by limiting chemotaxis, phagocytosis,
and the release of cytokines; decrease the expression of inflammatory
mediators; and may inhibit B-cell production of immunoglobulins.7,8
Interestingly, steroid administration on an alternate day schedule has
been shown to reduce their negative impact on leukocyte function.8
Two large meta-analyses found that the rate of infections were
significantly higher in patients treated with steroids.9,10 Further review found that patients who received a daily dose of 10 mg per
day or a cumulative dose of 700 mg of prednisone did not have an
increased rate of infectious complications.10 Although the disease
processes for which the patients are being treated may themselves be
independent risk factors for infection, close review of the included
studies identified few patients with diseases known to increase risk
for infection.9,10 Additional studies demonstrated that patients treated
with glucocorticoids are at increased risk for developing invasive
fungal infections, pneumocystosis, and viral infections, especially in
patients who have undergone bone marrow transplantation.4,1115

Wound Healing
Steroids inhibit the natural wound healing process by decreasing
the influx of macrophages, which may decrease phagocytosis as well
as growth factor and/or cytokine production.1619 Steroids can also
delay reepithelialization, decrease the fibroblast response, slow capillary proliferation, and inhibit collagen synthesis and wound maturation.16,18,20

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Bone Metabolism

Adrenal Suppression

The role of steroids in bone loss is well described and may occur
through several different mechanisms. First, steroids reduce intestinal
calcium absorption; increase urinary calcium excretion, which stimulates parathyroid hormone production; and increase osteoclast activity and release calcium into the blood stream. In addition, steroids
inhibit osteoblast activity, which negatively impacts trabecular bone
formation.21,22 Corticosteroids also suppress the production of adrenal androgens, which decreases their beneficial effect on bone formation.22 Lastly, glucocorticoids have been found to cause apoptosis of
osteoblasts and osteocytes,23 which has been shown to occur within
several weeks of use but slows after 6 months.23
There are conflicting data as to whether a daily dose or a cumulative dose has a more significant clinical effect on bone density. Fracture risks have also been shown to increase based on dose, duration,
age, sex, and body weight.4 Studies have demonstrated that supplemental calcium and vitamin D as well as bisphosphonates can help
reduce the corticosteroid-induced loss of bone mineral density.4 Analysis of data indicates that these effects are reversible with cessation of
the steroids.24

In the normal, nonstressed adult, the adrenal gland secretes the

equivalent of 57 mg of prednisone per day.7,31 Exogenous steroids
increase the circulating corticosteroid levels, which can lead to a
negative feedback on the hypothalamic-pituitary-adrenal axis.32
There is a lack of consistency in the dose of exogenous steroids
required for adrenal suppression due to individual variability as well
as the specific synthetic corticosteroid administered.4,33 Postmortem
studies showed atrophy of adrenal glands after as few as 5 days of
corticosteroid therapy.4 Retrospective studies identified no definitive
cases of adrenal suppression with prednisone doses 5 mg per day,
even if that dose is taken for many months; however, when the doses
were increased to 10 mg daily for only 4 days, there was a significant
decrease in plasma cortisol.34,35 The incidence of clinically evident
adrenal insufficiency is unknown, yet it is believed to be much lower
than the incidence based on objective measures.4

Avascular Necrosis

Psychiatric

Corticosteroid use has also been associated with avascular necrosis

(AVN) or osteonecrosis. This complication has been correlated with
cumulative dose and has been seen primarily in the head of the
femur, although other bones can be affected.21 The etiology is not
understood but is thought to be due to decreased blood flow or
impaired perfusion of the bone.21,25,26
Two retrospective reviews of patients with AVN of the femoral
head outlined the steroid courses in those patients.27,28 The first
review had a mean cumulative dose of 850 mg of prednisone (range,
2903300 mg), and the mean duration of therapy was 20.5 days
(range, 639 days). The second review reported an AVN risk of 0.3%.
The mean cumulative dose was equivalent to 673 mg of prednisone
(range, 389990 mg of prednisone equivalents), and the mean duration was 20 days (range, 1527 days).28

Ophthalmic

The most commonly encountered ophthalmologic adverse effects

include posterior-subcapsular cataract formation and increased intraocular pressure or glaucoma.29 The incidence seems to be dependent
on dose and duration of steroid use, with most doses of 10 mg daily
for at least 1 year before the onset of cataract formation.29 How
steroids lead to cataracts is unclear. Theories include binding of lysine
residues that lead to opacities in the lens and coagulation of lens
proteins due to steroid impairment of the sodium-potassium pumps
of the lens.29
Increased intraocular pressure can lead to visual field loss, optic
disc cupping, and optic nerve atrophy. Steroids can cause significant
increases in intraocular pressure in 5% of the patients within the
first few weeks of therapy, with up to 36% of patients developing at
least a moderate (5 mm Hg or higher) increase in pressure with
prolonged use.22 The route of administration seems to play an important role, with topical ophthalmic and systemic administration having
very high correlations with the incidence of glaucoma. The exact
mechanism by which corticosteroids cause glaucoma is unknown.21,22

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Gastrointestinal
Large meta-analyses of randomized, placebo-controlled trials failed
to show an association between steroid use and peptic ulcer disease.9,30 Interestingly, these studies did find that patients who used
prednisone had peptic ulcertype symptoms more frequently than
did the control patients. The researchers hypothesized that this may
be due to the lower sensitivity of barium studies that detect ulcers in
the preendoscopic era.9

340

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The most common psychiatric manifestations of steroids include

agitation, anxiety, distractibility, fear, hypomania, indifference, insomnia, irritability, lethargy, mood lability, pressured speech, restlessness, and tearfulness. Severe reactions include mania, depression,
or a mixed state.36
There is a dramatic variability in the reported incidence of steroidinduced psychiatric adverse effects, reflective of the unpredictability
of these reactions. A meta-analysis reported an incidence of 27.6%
(range, 1362%) of individuals experienced mild-to-moderate psychiatric complications from corticosteroid use, whereas only 5.7% (range,
1.650%) reported severe complications.37
Steroid dose has been found to be the most significant risk factor,
with a reported 1.3% incidence in patients who received a daily
prednisone dose of 40 mg. That risk increased to 18.4% in those who
received 80 mg daily.38 The reduction of the dose resulted in resolution of symptoms. Interestingly, a past reaction is not predictive of
a future reaction, nor is past tolerance predictive of future tolerance.36
Additional studies have not been able to correlate a history of psychiatric illness with a psychiatric reaction to prednisone.39

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LITIGATION
Several studies reviewed specific litigation that involved steroid
use. The National Association of Insurance Commissioners, the state
officials who oversee the insurance industry, reported their malpractice claims in 1976. In their review, adrenal steroids accounted for
5.9% of claims.40 In 1977, the California Medical Association and the
California Hospital Association reviewed 20,000 patient charts to
look for both claims filed and events that had the potential for
compensation but claims were not filed. They found that adrenocorticoids were responsible for 7.6% of events.40 A review performed by
the Physician Insurers Association of America studied lawsuit data
provided by the liability insurance companies within their association.41 The association reviewed 117,000 claims and found that medication errors were the second most frequent reason for claims against
physicians and that steroids were the second most common drug
class implicated in the lawsuits, which involved 12% of the claims.
The Risk Management Foundation of the Harvard Medical Institution
analyzed the malpractice claims between 1990 and 1999.42 Three
percent of the medication-related claims involved corticosteroids.
A review of the WESTLAW computerized legal database (Thomson
Reuters, New York, NY) searched for all jury verdict reports that
involved steroid use from 1996 to 2008.43 Eighty-three cases that
involved steroid use were analyzed. The most common allegation
was AVN, which resulted from steroid use and accounted for 39% of
the cases. Changes in mood, including anxiety, depression, and psychosis, were the second most common allegation, in 16%. Infection
and vision change each accounted for 12% of the allegations from

SeptemberOctober 2015, Vol. 29, No. 5

steroid use. Thirty-four of the cases were either decided for the
plaintiff or settled with an average indemnity payment of $1.15
million. A more complete discussion of litigation associated with
steroid use can be found in the review by Poetker and Smith.44

7.

USE OF STEROIDS IN CRS

9.

Recently, an iterative review was performed that evaluated the data

that support the use of steroids in patients with CRS.45 The researchers initially evaluated the data that supported steroids in patients
with CRS and without nasal polyps by identifying four level-4 studies. Despite the common use of oral steroids for CRS without nasal
polyps, there is no study that evaluated its efficacy as a single agent
for CRS. In fact, there are no high-level studies that support steroid
use even as a component of a multidrug regimen. High-quality studies are needed to validate efficacy and proper dosing. Given the
potential risks of oral steroids, the expert panel thought that the use
of oral steroid in CRS without polyposis is optional. They indicated
that patients with more severe disease may have a more favorable
benefit-to-harm ratio than patients with mild disease.
When evaluating the use of oral steroids in patients with CRS and
with nasal polyps, 16 articles were identified,5065 5 of which had
level-2 evidence.6165 All the studies showed positive changes in the
majority of the parameters evaluated. Analysis of the data supports
the use of oral steroids in patients with CRS and with nasal polyps in
the immediate and short-term period. All the studies showed benefit
with very few adverse effects, and no severe adverse events were
reported. The researchers made a strong recommendation for the use
of oral steroids in the management of patients with CRS and with
nasal polyps, provided the use was short term. They further recommended the perioperative use of oral steroids in these patients, based
on two level-2 studies66,67 and one level-3 study,68 which showed
improved visualization during surgery and improved postoperative
courses.
Multiple treatment options exist for CRS, with each option carrying
varying degrees of success in the management of the disease.69 One
must keep in mind that all treatment options carry risks. These
include the risks of surgery as well as the risks of antibiotics.70,71 The
relative risks must be considered, weighed, and discussed. Ultimately, it is the patient who must accept these risks, and it is the
providers responsibility to educate the patient by ensuring that an
informed decision is made.

O
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CONCLUSION

8.

10.
11.

12.

13.
14.

15.

16.

O
N

In this review, I attempted to provide an overview of the existing

data of the risks of oral steroid use, the lawsuits associated with their
use, and the data that support the use of steroids in the CRS patient
population. No medication or intervention is without risk. Providers
need to be aware of the potential complications and the data that
support the use to provide the best care possible.

17.

18.
19.

20.

21.
22.

23.
24.

25.

26.

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