Adrenal Crisis Workup

  • Author: Lisa Kirkland, MD, FACP, CNSP, MSHA; Chief Editor: George T Griffing, MD   more...
 
Updated: Mar 8, 2010
 

Laboratory Studies

  • 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.
  • 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.
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Imaging Studies

  • 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 shoComputed 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.
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Other Tests

  • Electrocardiography
    • Prolongation of the QT interval can induce ventricular arrhythmias.
    • Deep negative T waves have been described in acute adrenal crisis.
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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. Appearance of bilateral adrenal hemorrhage may be striking, as if bags of blood are replacing the glands.

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, Endocrine Society, Missouri State Medical Association, and Sigma Xi

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

Don S Schalch, MD  Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor 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, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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

  3. 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. Mar 2010;162(3):597-602. [Medline].

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  10. Aono J, Mamiya K, Ueda W. Abrupt onset of adrenal crisis during routine preoperative examination in a patient with unknown Addison's disease. Anesthesiology. Jan 1999;90(1):313-4. [Medline].

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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.
Enlarged, dense, suprarenal masses
Table 1
TimingHydrocortisoneHydrocortisoneFludrocortisone
Routine daily20 mg PO at 8 am



10 mg PO at 4 pm



0.1 mg PO at 8 am
Day of operation10 mg/h continuous infusion
Postoperative day 15-7.5 mg/h continuous infusion
Postoperative day 22.5-5 mg/h continuous infusion
Postoperative day 32.5-5 mg/h continuous infusion or40 mg PO at 8 am



20 mg PO at 4 pm



0.1 mg PO at 8 am
Postoperative day 42.5-5 mg/h continuous infusion or40 mg PO at 8 am



20 mg PO at 4 pm



0.1 mg PO at 8 am
Postoperative day 540 mg PO at 8 am



20 mg PO at 4 pm



0.1 mg PO at 8 am
Postoperative day 620 mg PO at 8 am



20 mg PO at 4 pm



0.1 mg PO at 8 am
Postoperative day 720 mg PO at 8 am



10 mg PO at 4 pm



0.1 mg PO at 8 am
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