adrenal insufficiency 2015
TRANSCRIPT
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Wellcome in our new group ..... Dr.SAMIR EL ANSARY
The incidence of adrenal insufficiency in the ICU population is 1 % to 6% and
may be as high as 74% for patients with septic shock.
However, no gold standard is agreed on for confirming adrenal insufficiency
among ICU patients, and, in many cases, uncertainty exists on how to
respond to this diagnosis.
Relative adrenal insufficiency
This is the most common and perplexing type of adrenal
insufficiency seen in patients in the ICU.
Patients with relative adrenal insufficiency may present with vasopressor dependency, acute
multiple organ dysfunction, hypothermia, or an inability to wean from mechanical ventilation.
Relative adrenal insufficiency
These patients can be identified by their limited response to
adrenal stimulation tests or lower-than-expected basal cortisol levels despite critical illness.
Acute adrenal crisis or insufficiency The acute clinical presentation typically
includes profoundhypotension, fever, and hypovolemia.
These patients will have very low
cortisol levels(< 3 mcg/dL).
Chronic adrenal insufficiency
Primary adrenal insufficiency (Addison disease)
The most common causes are autoimmune diseases (70%) and
tuberculosis (10%).
Rare causes include adrenal hemorrhage, adrenal metastasis,
cytomegalo virus, human immunodeficiency virus (HIV) disease,
amyloidosis, and sarcoidosis.
Secondary adrenal insufficiency
This condition is caused by inadequate production of
Adrenocorticotropic hormone (ACTH)
due to long-term use of exogenous steroids (most common cause),
hypopituitary state, or isolated ACTH deficiency.
ControversyEtomidate, an anesthetic agent often used for rapid-sequence intubation in critically ill
patients, increases the relative risk of adrenal insufficiency by more than 60%. Whether this increased risk of adrenal
insufficiency increases the risk of mortality for adult ICU patients remains controversial.
Clinical markers of acute adrenal insufficiency
Acute adrenal insufficiency presents with various combinations of
Hypotension, tachycardia, severe hypovolemia, respiratory failure,
nausea, vomiting, diarrhea, lethargy, and weakness.
Clinical markers of acute adrenal insufficiency
Patients with acute adrenal insufficiency due to chronic exogenous replacement
May not initially exhibitHypotension
because mineralocorticoid secretion can be intact until late-stage illness.
laboratory abnormalities associated with adrenal insufficiency.
Decreased Na , Cl , HCO3 ---- Increased K
Hyponatremia is most common.Low levels of chloride and bicarbonate and
high levels of potassium occur frequently.
Also seen are moderateeosinophilia, lymphocytosis,
hypercalcemia, and hypoglycemia.
The use of provocative adrenal stimulation tests in critically ill patients remains
controversial. Perhaps the most widely used protocol
identifies patients with septic shock as having relative
adrenal insufficiency if their baseline cortisol level is < 35 mcg/dL and they
respond to an ACTH stimulation test (250 mcg corticotropin) with a
bump in cortisol of < I0 mcgIdL .
The patients identified as nonresponders appeared to have a reduction in mortality
when given stress-dose steroids.
However, in a large subsequent study, no mortality benefit with stress-dose steroids was observed for patients with or without evidence of relative adrenal insufficiency.
Steroid use for "late acute respiratory distress syndrome"
is controversial.
In non-ICU patients In a nonstressed patient, a random cortisol level >20 mcg/dL may rule
out the diagnosis of adrenal insufficiency.
A random cortisol level < 3 mcg/dL confirms thediagnosis of adrenal
insufficiency.
How should one use the ACTH stimulation test?
Cortisol levels are measured before and 30 to 60 minutes after a supraphysiologic dose
of ACTH (250 mcg corticotropin given
intravenously). In patients who are not critically ill, a normal
response generates a poststimulation cortisol level of > 20 mcg/dL.
How should one use the ACTH stimulation test?
It isrecommended thatACTH stimulation tests should not be
used to determine whether adult patients with septic shock should
receive steroids.
Corticotropin-releasing hormone (CHR) stimulation
CHR is given to stimulate cortisol levels. Unlike the ACTH stimulation test, CHR stimulation can rule out central adrenal
insufficiency. A normal response generates a
poststimulation cortisol level > 20 mcg/dL or a 30- to 60-minute rise in cortisol 27 mcg/dL.
Should the low-doseACTH (1 mcg)
stimulation test be used?
This test may detect adrenal atrophy associated with adrenal insufficiency.
No consensus exists on how to determine the lower level that equates
with a normal cortisol response.
How does one distinguish between acute adrenal
insufficiency and other illness states in the ICU?
The clinical findings and laboratory findings among patients with acute adrenal
insufficiency are also common in the ICU population.
Distinguishing between adrenal insufficiency and other illnesses in critically ill patients requires clinical
suspicion and at least one of the following:
Failure to respond adequately to an adrenal stimulation test .
Inappropriately low basal cortisol levels .
An unequivocal clinical response to empiric exogenous steroids .
Should steroids be administered to ICU patients with a history of
long-term steroid use?
Patients' adrenals may become insufficient after taking the equivalent of 20 mg/day of
prednisone for just 5 days, but adrenal insufficiency is rare among patients taking steroids for <7 days.
Patients' adrenalsmay become insufficient
after taking very-low-dose steroids for months to years
> 5 mg/dayprednisone equivalent.
Fearing life-threatening adrenal impairment, many physicians give
stress doses (hydrocortisone 300-400 mglday
or equivalent)to critically ill ICU patients who
have received a course of steroids in the weeks or months before
their admission to the ICU.
Patient groups are at high risk for adrenal insufficiency
Patients with septic shockPatients taking chronic steroids.
Patients with HIV diseaseThe adrenal gland may be involved in >50%
of patients infected with HIV. However, because adrenal function requires <20%
of the gland to function, adrenalinsufficiency in this population is uncommon (3%).
Patient groups are at high risk for adrenal insufficiency
Patients with cancerEven when cancers metastasize to
the adrenal gland, adrenal dysfunction is uncommon.
Patient groups are at high risk for adrenal insufficiency
High-risk postoperative patientsPatients >55 years old, patients undergoing
major operations (e.g., coronary artery bypass grafting, abdominal aortic aneurysm
repair, Whipple procedure), patients with multiple trauma, and postoperative patients
requiring vasopressors or failing to wean from mechanical ventilation appear to be at
higher risk for adrenal insufficiency.
Do neurotrauma patients have special problems with adrenal
insufficiency?
Fifty percent of patients with moderate to severe traumatic head injury have cortisol levels less than15 mcg/dL.
This is especially true among patients receiving pentobarbital or propofol.
Do neurotrauma patients have special problems with adrenal
insufficiency?
These patients often require vasopressors. Thus monitoring cortisol levels in patients
with moderate to severe head injury may be warranted.
Steroid supplementation can be considered in patients with head trauma who have relative adrenal insufficiency
and sustained hypotension.
stress-dose steroids be used only among patients with septic shock whose blood
pressure is poorly responsive to both fluid resuscitation and
vasopressor therapy.
No randomized trials have been done to guide clinicians when confronted
with critically ill patients without septic shock who show evidence of relative
adrenal insufficiency, such as postoperative surgical patients,
patients with severe pancreatitis, and patients with moderate to severe
traumatic head injury.
The indicated therapies for ICU patients with
septic shock who may or may not have
adrenal insufficiency
Fluid resuscitation
Patients with septic shock typically require multiple large boluses of intravenous fluids
and often vasopressors to maintain effective arterial circulation.
If the patient's blood pressure responds poorly to fluids and
vasopressors, the administration of stress-dose steroids should be
initiated.
Steroid dosing
Administration of hydrocortisone, 300 to 400 mg/day given
intravenously in three or four divided doses
with or without fludrocortisone (50 mcg enterally every day), is
accepted practice.
Steroid duration
For adult patients with septic shock whose blood pressure is poorly responsive to
multiple intravenous fluid boluses for >1 to 2 hours, the author recommends
administration of stress-dose hydrocortisone
(300 mg/day) for 4 days.
If thepatient shows rapid clinical improvement,
the steroids may be stopped or tapered over 1 to 2 days. If significant hypotension recurs,
steroid dosing should return to the initial dose, and a
rapid taper can be undertaken after 7 days.
Steroid duration
For adult patients with septic shock whose blood pressure is poorly responsive to
multiple intravenous fluid boluses for >1 to 2 hours, the author recommends
administration of stress-dose hydrocortisone
(300 mg/day) for 4 days.
If thepatient shows rapid clinical
improvement, the steroids may be stopped or tapered over 1 to 2 days.
If significant hypotension recurs, steroid dosing should return to the
initial dose, and arapid taper can be undertaken after
7 days.
Should stress-dose steroid supplementation be strongly considered
in all patients with septic shock?
Because of conflicting studies, opinions on this point differ.
Yes, of courseA majority of patients with septic shock have
relative adrenal insufficiency. The mortality rate for such patients is 30% to
60%.
A landmark randomized control trial found an
absolute mortality reduction of 10% among patients with severe sepsis or septic shock and relative adrenal insufficiency who received stress-
dose steroids versus placebo.
This finding is supported by a recent systematic review that concluded that
prolonged low-dose steroid use reduces all-cause mortality among adult patients with
septic shock.
Steroid supplementation for most ICU patients with septic shock makes sense given the modest risk of a short course of low-dose
steroids.
NoThe data are too mixed
The Annane trial did not demonstrate across-the-board mortality reduction in the steroid
group with severe sepsis and septic shock.
The subsequent CORTICUSstudy showed no mortality benefit after
hydrocortisone therapy in patients with septic shock.
No mortality benefit of steroids was seen even among patients who met criteria for relative adrenal
insufficiency.
In addition, the steroid arm of the CORTICUS trial had significantly
more superinfections.
Early, smaller studies indicated a survival benefit from using
steroids in septic shock.
However, this benefit was not seen in meta-analysis of later
andlarger studies.
The Surviving Sepsis Campaign International Guidelines recommend using steroids for patients with septic shock unresponsive to
fluids and vasopressors.
This is largely a consensus-based recommendation rather than an evidence-
based conclusion. The scientific evidence to support even
this limited use of steroids in patients with septic shock is modest.
Relative adrenal insufficiency is common in ICU patients with septic shock, but its
clinical importance remains controversial.
2. To decide if and when a patient should receive hydrocortisone therapy for septic shock, there is no need to evaluate the
patient for relative adrenal insufficiency.
3. ICU patients with septic shock whose blood pressure does not respond to fluid
boluses and vasopressors should receive stress-dose steroids.
4. Critically ill ICU patients who recently received a prednisone equivalent to 25 mg/day for > 7 days should probably receive stress-dose steroid coverage.
GOOD LUCK
SAMIR EL ANSARYICU PROFESSOR
AIN SHAMSCAIRO
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Wellcome in our new group ..... Dr.SAMIR EL ANSARY