Nursing Research: Abstracting Information and Critiquing Medical Article
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Reviewing the Literature and Abstracting Information: Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients.
Glucocorticoid replacement therapy became available with the introduction of cortisone in 1949.
Severe illness and stress are known to activate the HPA axis and stimulate the release of ACTH
from the pituitary leading to increased cortisol release from the adrenal. (12)
This activation is considered essential and contributes to the maintenance of cellular and organ
homeostasis ( for example: adrenalectomized animals succumb quickly to hemorrhagic and sep
tic shock.) Adrenal replacement is protective against those stressors. (1,2)
Once considered rare in the ICU, adrenal failure has been increasingly reported in patients with a
variety of critical illnesses.Failure may be associated with structural adrenal, hypothalamic or
pituitary damage and many critically ill patients develop reversible failure of the HPA axis.
Despite the general agreement regarding the occurrence of adrenal failure in the critically ill, the
diagnosis and management of this disorder remains controversial. So how to diagnose Adrenal
insufficiency? Currently, adrenal insufficiency is best diagnosed with an Adrenocorticotrophic
Hormone (ACTH) stimulation test that reveals a rise of less than 9ug/dL or a baseline cortisol of
<10ug/dL (3,6). Although the 1ug/dL stimulation test may be more physiological and sensitive
than the 250ug/dL version, it is not currently recommended due to limited data (7). Free cortisol,
rather than the bound fraction, has been shown to be responsible for the physiologic hormonal
function at the cellular level (most true in patients with albumin below 2.5mg/dL). Unfortunately,
testing for free cortisol is not, currently, widely available and the normal range is still not well
defined (4,5).
How to treat without diagnosis? Annane et al randomized 300 patients in septic shock to hydro
cortisone with fludrocortisone or placebo (8). Their study demonstrated a 30% decrease in 28
day mortality but the benefit was limited to non-responders (delta cortisol <9).
The CORTICUS study (9) - A European multicenter (52), randomized, double-blind, placebo
controlled trial randomly assigned 499 patients to either : hydrocortisone(50mg IV Q6H) or
placebo. They did not find any difference in the 28 day mortality rate, nor did they find any
difference between ACTH stimulation test responders and non-responders.
However, they did find that patients who received hydrocortisone had a more rapid resolution of
shock. Who to treat?Treat patients in septic shock who are poorly responsive to fluid and/or
vasopressors, as those signs often correspond to adrenal insufficiency (recent data showed that
60% of patients with severe sepsis and septic shock are adrenally insufficient *Annane et al.
2006*).
Decision to treat in septic shock should not be based on total cortisol levels or response to
ACTH (as we have discussed above, they have poor accuracy).
Although HC treatment effects on mortality is not clear, it clearly results in faster resolution of
shock state. Additionally, other studies report a reduced incidence of PTSD and an improved
emotional well-being in survivors of septic shock who received steroids (10).
With so many unknowns, how could we safely and effectively implement HC therapy?
The ideal dose should be able to down regulate the pro-inflammatory response without harming
the immune system and disrupting wound healing. Current recommendations are based upon the
result of previously published studies which dont necessarily agree, thus further well-designed
studies are needed to define the proper dose and duration of therapy.
ADDENDUM: The current recommendations are as follow:
A dose of 200-300 mg hydrocortisone/day has been shown to suppress pro-inflammatory response,
but does not seem to be immunosuppressive. Based primarily on the CORTICUS study, the current
recommended dosing is
200mg/day in four divided doses, or as a bolus of 100mg followed by a continuous infusion of 10mg/hr.
Continuous infusion has been shown to result in better glycemic control.
Treatment should continue for 7 days followed by a slow taper.
Abrupt cessation of corticosteroid administration should be avoided due to rebound phenomena