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emedicine.medscape.com

Adrenal Crisis
Updated: Mar 12, 2020
Author: Lisa Kirkland, MD, FACP, FCCM, MSHA; Chief Editor: George T Griffing, MD

Overview

Practice Essentials
Do not confuse acute adrenal crisis with Addison disease. In 1855, Thomas Addison described a syndrome of long-
term adrenal insufficiency that develops over months to years, with weakness, fatigue, anorexia, weight loss, and
hyperpigmentation as the primary symptoms. In contrast, an acute adrenal crisis can manifest with vomiting,
abdominal pain, and hypovolemic shock.[1, 2] When not promptly recognized, adrenal hemorrhage can be a cause of
adrenal crisis. Administration of glucocorticoids in supraphysiologic or stress doses is the only definitive therapy for
adrenal crisis.[3, 4, 5, 6] See the images below.

Computed tomographic (CT) scans of the abdomen show normal adrenal glands several months before the onset of
hemorrhage (upper panel) and enlarged adrenals 2 weeks after an acute episode of bilateral adrenal hemorrhage
(lower panel). The attenuation of the adrenal glands, indicated by arrows, is increased after the acute event.
Reproduced from Rao RH, Vagnucci AH, Amico JA: Bilateral massive adrenal hemorrhage: early recognition and
treatment. Ann Intern Med. Feb 1 1989;110(3):227-35 with permission from the journal.

Workup in adrenal crisis

Serum chemistry abnormalities are present in as many as 56% of patients. Hyponatremia is common (although not

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diagnostic); hyperkalemia, metabolic acidosis, and hypoglycemia also may be present. However, the absence of
laboratory abnormalities does not exclude the diagnosis of adrenal crisis.

Chest radiography can be used to assess for tuberculosis, histoplasmosis, malignant disease, sarcoid, and lymphoma.
Abdominal computed tomography (CT) scanning is used to visualize the adrenal glands for hemorrhage, atrophy,
infiltrative disorders, and metastatic disease. Adrenal hemorrhage appears as hyperdense, bilaterally enlarged adrenal
glands.

In primary adrenocortical failure, histologic evidence of infection, infiltrative disease, or another condition may be
demonstrated. Secondary adrenocortical insufficiency may cause atrophy of the adrenals or no histologic evidence at
all.

Management of adrenal crisis

Administration of glucocorticoids in supraphysiologic or stress doses is the only definitive therapy.[3, 4]

Dexamethasone does not interfere with serum cortisol assay and, thus, may be the initial drug of choice. However,
because dexamethasone has little mineralocorticoid activity, fluid and electrolyte replacement are essential.

A thorough search for a precipitating cause of adrenal crisis and administration of empiric antibiotics are indicated.
Reversal of coagulopathy should be attempted with fresh frozen plasma. Pressors (eg, dopamine, norepinephrine)
may be necessary to combat hypotension.

Pathophysiology
The adrenal cortex produces 3 steroid hormones: glucocorticoids (cortisol), mineralocorticoids (aldosterone, 11-
deoxycorticosterone), and androgens (dehydroepiandrosterone). The androgens are relatively unimportant in adults,
and 11-deoxycorticosterone is a fairly weak mineralocorticoid in comparison with aldosterone. The primary hormone of
importance in acute adrenal crisis is cortisol; adrenal aldosterone production is relatively minor.

Cortisol enhances gluconeogenesis and provides substrate through proteolysis, protein synthesis inhibition, fatty acid
mobilization, and enhanced hepatic amino acid uptake. Cortisol indirectly induces insulin secretion to counterbalance
hyperglycemia but also decreases insulin sensitivity. Cortisol exercises a significant anti-inflammatory effect by
stabilizing lysosomes, reducing leukocytic responses, and blocking cytokine production. Phagocytic activity is
preserved, but cell-mediated immunity is diminished, in situations of cortisol deficiency. Finally, cortisol facilitates free-
water clearance, enhances appetite, and suppresses adrenocorticotropic hormone (ACTH) synthesis.

Aldosterone is released in response to angiotensin II stimulation via the renin-angiotensin-aldosterone system,

hyperkalemia, hyponatremia, and dopamine antagonists. Its effect on its primary target organ, the kidney, is to promote
reabsorption of sodium and secretion of potassium and hydrogen. The mechanism of action is unclear; an increase in
the sodium- and potassium-activated adenosine triphosphatase (Na+/K+ ATPase) enzyme responsible for sodium
transport, as well as increased carbonic anhydrase activity, has been suggested. The net effect is to increase
intravascular volume. The renin-angiotensin-aldosterone system is unaffected by exogenous glucocorticoids, and
ACTH deficiency has a relatively minor effect on aldosterone levels.

Adrenocortical hormone deficiency results in the reverse of these hormonal effects, producing the clinical findings of
adrenal crisis.

Primary adrenocortical insufficiency occurs when the adrenal glands fail to release adequate amounts of these
hormones to meet physiologic needs, despite release of ACTH from the pituitary. Infiltrative or autoimmune disorders
are the most common cause, but adrenal exhaustion from severe chronic illness also may occur.

Secondary adrenocortical insufficiency occurs when exogenous steroids have suppressed the hypothalamic-pituitary-
adrenal (HPA) axis. Too rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may
induce cortisol requirements in excess of the adrenal glands' ability to respond immediately. In acute illness, a normal
cortisol level may actually reflect adrenal insufficiency because the cortisol level should be quite elevated.

Bilateral massive adrenal hemorrhage (BMAH) occurs under severe physiologic stress (eg, myocardial infarction,
septic shock, complicated pregnancy) or with concomitant coagulopathy or thromboembolic disorders.

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Hahner et al investigated the frequency and causes of, as well as the risk factors for, adrenal crisis in patients with
chronic adrenal insufficiency. Using a disease-specific questionnaire, the authors analyzed data from 444 patients,
including 254 with primary adrenal insufficiency and 190 with secondary adrenal insufficiency. At least one adrenal
crisis was reported by 42% of patients, including 47% of those with primary adrenal insufficiency and 35% of patients
with the secondary condition. GI infection and fever were the most common precipitating causes of crisis. Identified
risk factors for adrenal crisis were, for patients with primary adrenal insufficiency, concomitant nonendocrine disease,
and for patients with secondary adrenal insufficiency, female sex and diabetes insipidus.[7]

A study from the Netherlands, by Smans et al, of patients with adrenal insufficiency, found the existence of comorbidity
to be the most important risk factor for adrenal crisis, with infections being the most common precipitating factors.[8]

A Japanese study, by Iwasaku et al, found that of 504 patients with adrenal crisis, only about one third had preexisting
primary or central adrenal insufficiency. In the rest of the patients, comorbidities included cardiovascular disease
(31.6%), infection (18.8%), diabetes (16.5%), cancer (19.1%), hypothyroidism (7.0%), autoimmune disease (9.3%),
peptic ulcer (6.1%), chronic obstructive pulmonary disease or asthma (6.1%), and renal failure (6.1%).[9]

Epidemiology
Frequency

The incidence of primary adrenocortical insufficiency is variable and depends on the defining cortisol level and the
method of testing (ie, ACTH stimulation versus single random cortisol level). The underlying disease also is a factor.
Studies of critically ill patients with septic shock demonstrate a de novo (excluding patients with known adrenal
insufficiency or patients on glucocorticoid therapy) incidence ranging from 19-54%. Secondary adrenal insufficiency
has been demonstrated in 31% of patients admitted to a critical care unit.

Annane et al's landmark 2002 study found a very high rate, ie, 76% of all enrolled patients with septic shock. Of the
general perioperative population, in 62,473 anesthetic administrations, only 419 (0.7%) patients required glucocorticoid
supplementation and only 3 hypotensive events were thought to be attributable to glucocorticoid deficiency.[10]
Studies of patients undergoing cardiac or urologic surgery reveal an incidence of 0.01-0.1%. In a study of 2000
consecutive general hospital autopsies, only 22 (1.1%) revealed bilateral adrenal hemorrhage; however, as many as
15% of patients dying in shock have been demonstrated to have BMAH.

The aforementioned study from the Netherlands, by Smans et al, found the incidence of adrenal crisis among persons
with primary adrenal insufficiency to be 5.2 cases per 100 person-years, while in secondary adrenal insufficiency, the
incidence was reported as 3.6 cases per 100 person-years.[8]

In a study of Swiss patients with either primary or secondary adrenal insufficiency, Notter et al found the prevalence of
adrenal crisis to be 4.4 per 100 disease-years.[11]

According to a report by Chabre et al, the annual incidence of adrenal crisis in Europe is estimated to be 6-8 cases per
100 adrenal insufficiency patients.[12]

No description regarding racial data, sexual predilection, or age is available in the literature.

Mortality/Morbidity

In the absence of bilateral adrenal hemorrhage, the survival rate of patients with acute adrenal crisis that is diagnosed
promptly and treated appropriately approaches that of patients without acute adrenal crisis with similar severity of
illness. Patients who developed BMAH before the availability of hormonal testing or computed tomography (CT)
scanning rarely survived. In one series, patients who were diagnosed using CT scanning had an 85% rate of survival.
Because the true incidence of adrenal crisis and BMAH are unknown, the actual mortality rate also is unknown.

A Japanese study, by Ono et al, indicated that among patients with adrenal crisis, the risk of death is relatively high in
those who are older and have impaired consciousness and diabetes mellitus. In the study, of 799 patients with adrenal
crisis and concomitant primary or secondary adrenal insufficiency at hospital admission, 2.4% (19) suffered in-hospital
mortality, including 15 who were older than 60 years, 12 who had impaired consciousness at admission, and 13 who
received insulin therapy.[13]

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Presentation

History
History can include the following:

Prior steroid use: Use involves at least 20 mg daily of prednisone or its equivalent for at least 5 days within the
past 12 months. Patients receiving doses close to normal physiologic levels require only 1 month to recover
normal adrenal function.

Organisms associated with adrenal crisis (eg, Haemophilus influenzae, Staphylococcus aureus, Streptococcus
pneumonia, fungi)

Meningococcemia

Severe physiologic stress[14] (eg, sepsis, trauma, burns, surgery): In a retrospective review of patients from a
level 1 trauma center, Guillamondegui et al found that trauma patients with acute adrenal insufficiency who
were treated for the condition had shorter hospital stays and required fewer days in the intensive care unit and
on a ventilator than did untreated patients.[15] In addition, the authors concluded that recognition and treatment
of the condition can reduce trauma patient mortality by almost 50%.

Azotemia

Anticoagulants, hemorrhagic diathesis

Newborn, complicated pregnancy

Adrenocorticotropin therapy, known primary or secondary adrenocortical insufficiency

AIDS

Invasive or infiltrative disorders

Tuberculosis

Topical steroids: Risk of adrenal crisis occurs when used over a large surface area for a prolonged duration,
using occlusive dressings and a highly potent drug.

Inhaled steroids: Use of a high dose (>0.8mg/d) over a prolonged duration increases risk; fluticasone may
cause suppression at lower dose.

Congenital adrenal hyperplasia (CAH): A retrospective study by Rushworth et al indicated that in pediatric
patients with CAH, adrenal crises occur mostly in the younger ones. The study, which evaluated 573
admissions for medical problems in children with CAH, found that 21 of 37 adrenal crises occurred in patients
aged 1-5 years, with another six in children aged up to 1 year.[16]

Physical
See the list below:

Unexplained shock, usually refractory to fluid and pressor resuscitation

Nausea, vomiting, abdominal or flank pain

Hyperthermia or hypothermia

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Causes
See the list below:

Rapid withdrawal of long-term steroid therapy

Ketoconazole

Phenytoin

Rifampin

Mitotane

Septic shock

DDx

Differential Diagnoses
Septic Shock

Workup

Workup

Laboratory Studies
See the list below:

Serum chemistry: Abnormalities are present in as many as 56% of patients. Hyponatremia is common (although
not diagnostic); hyperkalemia, metabolic acidosis, and hypoglycemia also may be present. However, the
absence of laboratory abnormalities does not exclude the diagnosis of adrenal crisis.

Serum cortisol: Less than 20 mcg/dL in severe stress or after ACTH stimulation is indicative of adrenal
insufficiency.

ACTH test (diagnostic): Determine baseline serum cortisol, then administer ACTH 250 mcg intravenous push
(IVP), and then draw serum cortisol 30 and 60 minutes after ACTH administration. An increase of less than 9
mcg/dL is considered diagnostic of adrenal insufficiency.

CBC: Anemia (mild and nonspecific), lymphocytosis, and eosinophilia (highly suggestive) may be present.

Serum thyroid levels: Assess for autoimmune, infiltrative, or multiple endocrine disorders.

Cultures: Perform blood and other cultures as clinically indicated. Infection is a common cause of acute adrenal
crisis.

Imaging Studies

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See the list below:

Chest radiography: Assess for tuberculosis, histoplasmosis, malignant disease, sarcoid, and lymphoma.

Abdominal CT scanning: Visualize adrenal glands for hemorrhage (as in the image below), atrophy, infiltrative
disorders, and metastatic disease. Adrenal hemorrhage appears as hyperdense, bilaterally enlarged adrenal
glands.

Computed tomographic (CT) scans of the abdomen show normal adrenal glands several months before the
onset of hemorrhage (upper panel) and enlarged adrenals 2 weeks after an acute episode of bilateral adrenal
hemorrhage (lower panel). The attenuation of the adrenal glands, indicated by arrows, is increased after the
acute event. Reproduced from Rao RH, Vagnucci AH, Amico JA: Bilateral massive adrenal hemorrhage: early
recognition and treatment. Ann Intern Med. Feb 1 1989;110(3):227-35 with permission from the journal.

Other Tests
See the list below:

Electrocardiography

Prolongation of the QT interval can induce ventricular arrhythmias.

Deep negative T waves have been described in acute adrenal crisis.

Histologic Findings
Histology depends on the cause of the adrenal failure. In primary adrenocortical failure, histologic evidence of
infection, infiltrative disease, or other condition may be demonstrated. Secondary adrenocortical insufficiency may
cause atrophy of the adrenals or no histologic evidence at all, especially if due to exogenous steroid ingestion.

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Appearance of bilateral adrenal hemorrhage may be striking, as if bags of blood are replacing the glands.

Treatment

Medical Care
See the list below:

Administration of glucocorticoids in supraphysiologic or stress doses is the only definitive therapy.[3, 4]

Dexamethasone does not interfere with serum cortisol assay and, thus, may be the initial drug of choice.
However, because dexamethasone has little mineralocorticoid activity, fluid and electrolyte replacement
are essential.

A short ACTH stimulation test may be performed during resuscitation. Once complete, hydrocortisone
100 mg IV every 6 hours is the preferred treatment to provide mineralocorticoid support.

Delaying glucocorticoid replacement therapy while awaiting the results of the ACTH stimulation test is
inappropriate and dangerous.

In addition to corticosteroid replacement, aggressive fluid replacement with 5% or 10% intravenous dextrose
and saline solutions and treatment of hyperkalemia is mandatory. Fludrocortisone, a mineralocorticoid, may also
be given.

A thorough search for a precipitating cause and administration of empiric antibiotics are indicated. Reversal of
coagulopathy should be attempted with fresh frozen plasma.

Pressors (eg, dopamine, norepinephrine) may be necessary to combat hypotension.

Consultations
See the list below:

Endocrinologist

Infectious disease specialist

Critical care physician

Cardiologist

Surgeon

Other consultations as clinically indicated

Guidelines

Guidelines Summary
Society for Endocrinology

Guidelines from Britain’s Society for Endocrinology on the emergency management of adrenal crisis, published in

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2016, include the following diagnostic recommendations[17] :

Adrenal insufficiency should be ruled out in any acutely ill patient with signs or symptoms potentially suggestive
of acute adrenal insufficiency
Assess blood pressure and fluid balance status; if clinically feasible, measure blood pressure from supine to
standing to check for postural drop
Assess patient drug history; determine whether there has been glucocorticoid use
Perform appropriate blood tests: Sodium, potassium, urea, and creatinine; full blood counts; thyroid-stimulating
hormone and free thyroxine; paired serum cortisol and plasma ACTH
If the patient is hemodynamically stable, consider performing a short Synacthen test (serum cortisol at baseline
and 30 min after intravenous injection of 250 µg ACTH 1–24)
Serum/plasma aldosterone and plasma renin
Diagnostic measures should never delay prompt treatment of a suspected adrenal crisis

The guidelines include the following recommendations for emergency treatment[17] :

Administer hydrocortisone: Immediate bolus injection of 100 mg hydrocortisone intravenously or intramuscularly

followed by continuous intravenous infusion of 200 mg hydrocortisone per 24 hours (alternatively, 50 mg
hydrocortisone per intravenous or intramuscular injection every 6 h)
Rehydrate with rapid intravenous infusion of 1000 mL of isotonic saline infusion within the first hour, followed by
further intravenous rehydration as required (usually 4-6 L in 24 h; monitor for fluid overload in case of renal
impairment and in elderly patients)
Contact an endocrinologist for urgent review of the patient, advice on further tapering of hydrocortisone, and
investigation of the underlying cause of the disease, including the diagnosis of primary versus secondary
adrenal insufficiency
Tapering of hydrocortisone can be started after clinical recovery guided by an endocrinologist; in patients with
primary adrenal insufficiency, mineralocorticoid replacement must be initiated (starting dose 100 µg
fludrocortisone once daily) as soon as the daily glucocorticoid dose is below 50 mg of hydrocortisone every 24 
hours

Association of Anaesthetists, the Royal College of Physicians, and the Society for
Endocrinology

Guidelines released in 2020 by the Association of Anaesthetists, the Royal College of Physicians, and the Society for
Endocrinology examined perioperative glucocorticoid management in patients with adrenal insufficiency. With regard to
adrenal crisis, the guidelines state that surgical stress or illness places all glucocorticoid-dependent patients at risk for
this condition, the recognition and diagnosis of which are essential. If doubt exists as to the need for glucocorticoids in
patients with adrenal crisis, these agents should be provided, since short-term glucocorticoid administration produces
no long-term adverse consequences.[18]

Medication

Medication Summary
Corticosteroids are the mainstays of treatment. Other medications, such as pressors (eg, dopamine, norepinephrine)
or antibiotics, are administered as clinically indicated.

Corticosteroids

Class Summary

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These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the
body's immune response to diverse stimuli.

Dexamethasone (Decadron, Baldex, Dexone)

Used as empiric treatment of shock in suspected adrenal crisis or insufficiency until serum cortisol levels are drawn.

Hydrocortisone (Hydrocortone, Hydrocort)

DOC because of mineralocorticoid activity and glucocorticoid effects.

Cortisone (Cortone)
Oral DOC for patients with adrenocortical insufficiency.

Use in patients undergoing moderate stress surgery (eg, vascular bypass, total joint replacement) who can take PO
postoperatively.

Fludrocortisone (Florinef)
Acts on renal distal tubules to enhance reabsorption of sodium. Increases urinary excretion of both potassium and
hydrogen ions. The consequence of these 3 primary effects, together with similar actions on cation transport in other
tissues, appears to account for the spectrum of physiological activities characteristic of mineralocorticoids. Used in
adrenal insufficiency. Produces marked sodium retention and increased urinary potassium excretion.

Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol)

Usually third-line DOC for adrenal crisis because of lack of mineralocorticoid activity.

Consider use in patients with fluid overload, edema, or hypokalemia.

Vasopressors

Class Summary
These agents are potent vasoconstrictors, inotropes and chronotropes. They should be used with caution in
conjunction with corticosteroids and intravenous fluid support.

Norepinephrine (Levophed)
For protracted hypotension following adequate fluid-volume replacement. Stimulates beta1- and alpha-adrenergic
receptors, which in turn, increases cardiac muscle contractility and heart rate, as well as vasoconstriction. As a result,
systemic blood pressure and coronary blood flow increase. After obtaining a response, the rate of flow should be
adjusted and maintained at a low-normal blood pressure, such as 80-100 mm Hg systolic, sufficient to perfuse vital
organs.

Dopamine (Intropin)
Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose.

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Follow-up

Further Outpatient Care

See the list below:

Treat any underlying or precipitating disorder as clinically indicated.

Carefully monitor growth and development in pediatric patients.

Recommend medical tag or bracelet that alerts emergency personnel to adrenal gland insufficiency.

If exposed to chickenpox, prophylaxis with varicella-zoster immune globulin is indicated.

If exposed to measles, prophylaxis with immune globulin is indicated.

Closely observe for reactivation of tuberculosis in patients with latent disease.

Further Inpatient Care

See the list below:

Admit to ICU as clinically indicated.

Perform fluid resuscitation and hemodynamic monitoring as clinically indicated.

Monitor serum electrolytes, magnesium, and glucose every 4-6 hours until stable.

Search for precipitating cause of crisis (eg, infection, myocardial infarction, unreported exogenous
steroid use within 12 mo, autoimmune disorder).

Inpatient & Outpatient Medications

See the list below:

Taper steroid dose as outlined previously (see Medication).

Complications
See the list below:

Immunosuppression

Hypertension

Salt retention

Hypokalemia

Weight gain

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Delayed wound healing

Hyperglycemia

Metabolic alkalosis

Prognosis
See the list below:

Prognosis is the same as for patients without adrenal insufficiency if the condition is diagnosed and treated
appropriately.

Patient Education
See the list below:

Instruct patients regarding the importance of careful attention to health and fluid intake and to double
maintenance doses when ill until medical attention is obtained.

Avoid exposure to chickenpox or measles; if exposed, seek medical advice without delay.

Notify physician or seek medical attention for persistent nausea and vomiting, fatigue, and abdominal pain.

For excellent patient education materials, see eMedicineHealth's Thyroid & Metabolism Center and patient
education article Anatomy of the Endocrine System.

Questions & Answers

Overview

What is the difference between adrenal crisis and Addison disease?

Which hormones are involved in the pathophysiology of adrenal crisis?

What is the pathophysiology of adrenocortical insufficiency in adrenal crisis?

What is the incidence of adrenal crisis?

What is the mortality of adrenal crisis?

Presentation

What patient history is associated with adrenal crisis?

What is the presentation of adrenal crisis?

What causes adrenal crisis?

DDX

What are the differential diagnoses for Adrenal Crisis?

Workup

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Which lab studies are indicated in the workup of adrenal crisis?

Which imaging studies are indicated in the workup of adrenal crisis?

Which other tests are indicated in the workup of adrenal crisis?

What are the histologic findings in adrenal crisis?

Treatment

What is the medical treatment for adrenal crisis?

Which specialist consultations are indicated in the treatment of adrenal crisis?

Guidelines

What are the BSE guidelines on the diagnostic workup of adrenal crisis?

What are the BSE guidelines on the emergency treatment of adrenal crisis, as well as the AA/RCP/BSE adrenal crisis
guideline?

Medications

Which medications are used to treat adrenal crisis?

Which medications in the drug class Vasopressors are used in the treatment of Adrenal Crisis?

Which medications in the drug class Corticosteroids are used in the treatment of Adrenal Crisis?

Follow-up

What is the long-term care for patients with adrenal crisis?

What is the inpatient care for patients with adrenal crisis?

Which medications are indicated in the treatment of adrenal crisis?

What complications are associated with adrenal crisis?

What is the prognosis of adrenal crisis?

What is the patient education for adrenal crisis?

Contributor Information and Disclosures

Author

Lisa Kirkland, MD, FACP, FCCM, MSHA Assistant Professor, Department of Internal Medicine, Division of Hospital
Medicine, Mayo Clinic; Chair, Department of Critical Care, ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, FCCM, MSHA is a member of the following medical societies: American College of
Physicians, Society of Critical Care Medicine, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of
Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College
of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians,
American Diabetes Association, American Federation for Medical Research, American Heart Association, Central
Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

David M Klachko, MD, MEd Professor Emeritus, Department of Internal Medicine, Division of Endocrinology,
Diabetes, and Metabolism, University of Missouri-Columbia School of Medicine

David M Klachko, MD, MEd is a member of the following medical societies: Alpha Omega Alpha, Missouri State
Medical Association, American College of Physicians-American Society of Internal Medicine, American Diabetes
Association, American Federation for Medical Research, Endocrine Society, Sigma Xi

Disclosure: Nothing to disclose.

References

1. Loriaux DL, Fleseriu M. Relative adrenal insufficiency. Curr Opin Endocrinol Diabetes Obes. 2009 Aug 3. [Medline].

2. White K, Arlt W. Adrenal crisis in treated Addison's disease: a predictable but under-managed event. Eur J Endocrinol. 2010
Jan. 162(1):115-20. [Medline].

3. Arlt W. The approach to the adult with newly diagnosed adrenal insufficiency. J Clin Endocrinol Metab. 2009 Apr. 94(4):1059-
67. [Medline].

4. Hahner S, Allolio B. Therapeutic management of adrenal insufficiency. Best Pract Res Clin Endocrinol Metab. 2009 Apr.
23(2):167-79. [Medline].

5. Dineen R, Thompson CJ, Sherlock M. Adrenal crisis: prevention and management in adult patients. Ther Adv Endocrinol
Metab. 2019. 10:2042018819848218. [Medline].

6. Elshimy G, Alghoula F, Jeong JM. Adrenal Crisis. StatPearls. 2020 Jan. [Medline]. [Full Text].

7. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new
prevention strategies. Eur J Endocrinol. 2010 Mar. 162(3):597-602. [Medline].

8. Smans LC, Van der Valk ES, Hermus AR, Zelissen PM. Incidence of adrenal crisis in patients with adrenal insufficiency. Clin
Endocrinol (Oxf). 2016 Jan. 84 (1):17-22. [Medline].

9. Iwasaku M, Shinzawa M, Tanaka S, Kimachi K, Kawakami K. Clinical characteristics of adrenal crisis in adult population with
and without predisposing chronic adrenal insufficiency: a retrospective cohort study. BMC Endocr Disord. 2017 Sep 11. 17
(1):58. [Medline]. [Full Text].

10. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on
mortality in patients with septic shock. JAMA. 2002 Aug 21. 288(7):862-71. [Medline]. [Full Text].

11. Notter A, Jenni S, Christ E. Evaluation of the frequency of adrenal crises and preventive measures in patients with primary
and secondary adrenal insufficiency in Switzerland. Swiss Med Wkly. 2018 Jan 29. 148:w14586. [Medline]. [Full Text].

12. Chabre O, Goichot B, Zenaty D, Bertherat J. Group 1. Epidemiology of primary and secondary adrenal insufficiency:
Prevalence and incidence, acute adrenal insufficiency, long-term morbidity and mortality. Ann Endocrinol (Paris). 2017 Dec.
78 (6):490-4. [Medline].

13. Ono Y, Ono S, Yasunaga H, Matsui H, Fushimi K, Tanaka Y. Clinical features and practice patterns of treatment for adrenal
crisis: a nationwide cross-sectional study in Japan. Eur J Endocrinol. 2017 Mar. 176 (3):329-337. [Medline].

14. Weant KA, Sasaki-Adams D, Dziedzic K, et al. Acute relative adrenal insufficiency after aneurysmal subarachnoid

https://emedicine.medscape.com/article/116716-print Halaman 13 dari 14

 20/04/21 09.10

hemorrhage. Neurosurgery. 2008 Oct. 63(4):645-9; discussion 649-50. [Medline].

15. Guillamondegui OD, Gunter OL, Patel S, et al. Acute adrenal insufficiency may affect outcome in the trauma patient. Am
Surg. 2009 Apr. 75(4):287-90. [Medline].

16. Rushworth RL, Falhammar H, Munns CF, Maguire AM, Torpy DJ. Hospital Admission Patterns in Children with CAH:
Admission Rates and Adrenal Crises Decline with Age. Int J Endocrinol. 2016. 2016:5748264. [Medline]. [Full Text].

17. [Guideline] Arlt W, Society for Endocrinology Clinical Committee. SOCIETY FOR ENDOCRINOLOGY ENDOCRINE
EMERGENCY GUIDANCE: Emergency management of acute adrenal insufficiency (adrenal crisis) in adult patients. Endocr
Connect. 2016 Sep. 5 (5):G1-G3. [Medline]. [Full Text].

18. Woodcock T, Barker P, Daniel S, et al. Guidelines for the management of glucocorticoids during the peri-operative period for
patients with adrenal insufficiency: Guidelines from the Association of Anaesthetists, the Royal College of Physicians and the
Society for Endocrinology UK. Anaesthesia. 2020 Feb 3. [Medline]. [Full Text].

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