eMedicine Specialties > Endocrinology > Adrenal Gland

Adrenal Crisis: Treatment & Medication

Author: Lisa Kirkland, MD, FACP, CNSP, MSHA, Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital
Contributor Information and Disclosures

Updated: Aug 13, 2009

Treatment

Medical Care

  • Administration of glucocorticoids in supraphysiologic or stress doses is the only definitive therapy.5,6
    • 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 is indicated. Reversal of coagulopathy should be attempted with fresh frozen plasma.
  • Pressors (eg, dopamine, norepinephrine) may be necessary to combat hypotension.

Consultations

  • Endocrinologist
  • Infectious disease specialist
  • Critical care physician
  • Cardiologist
  • Surgeon
  • Other consultations as clinically indicated

Medication

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

Corticosteroids

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.

Adult

4-8 mg IV, followed by 16-24 mg/d as IV injection q4-6h or as continuous infusion

Pediatric

Not established

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin

Documented hypersensitivity; active bacterial or fungal infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use; may prolong coma in cerebral malaria


Hydrocortisone (Hydrocortone, Hydrocort)

DOC because of mineralocorticoid activity and glucocorticoid effects.

Adult

Septic shock: 50-100 mg IV q6h for 7 d, then discontinue or reduce to 50 mg IV q6h for 4 doses then taper by one half qd until discontinued or until prior maintenance dose
Major surgical stress (CABG, esophagogastrectomy): Following usual am dose, give 100 mg IV before induction, 50 mg IV q8h for 24 h, then taper by one half qd to maintenance
Moderate surgical stress (extremity vascular bypass, total joint replacement): Following usual am dose, give 50 mg IV before induction, 25 mg IV q8h for 24 hours, then taper by one half qd to maintenance

Pediatric

<12 years: 1-2 mg/kg IV bolus; follow with 25-150 mg/d divided q6-8h
>12 years: 1-2 mg/kg IV bolus; follow with 150-250 mg/d divided q6-8h

Corticosteroid clearance may decrease with estrogens

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes mellitus, and myasthenia gravis


Cortisone acetate (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.

Adult

Following intraoperative dose of hydrocortisone 50 mg IV, give 37.5 mg PO q12h for 2 d (as 25 mg PO qam and 12.5 mg PO qpm until stabilized)

Pediatric

Not established

Estrogen coadministration may increase corticosteroid levels; cortisone may increase digitalis toxicity secondary to hypokalemia; phenytoin, phenobarbital, rifampin, and ephedrine increase corticosteroid clearance; may inhibit response to coumarin anticoagulants; exacerbation of hypokalemia with potassium-depleting diuretics may occur

Documented hypersensitivity; viral, fungal, or tubercular skin lesions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, cirrhosis, nonspecific ulcerative colitis, osteoporosis, peptic ulcer, diabetes mellitus, and myasthenia gravis; may exacerbate existing emotional instability; may mask signs of GI peritonitis and sepsis; may impair growth and development in children; caution in peptic ulcer disease; caution in infections


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.

Adult

0.1-0.2 mg PO qd

Pediatric

0.05-0.1 mg PO qd

Antagonizes effects of anticholinergics; rifampin, hydantoins, and barbiturates decrease effects of fludrocortisone; decreases salicylate levels

Documented hypersensitivity; systemic fungal infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Taper dose gradually when therapy is discontinued; caution in Addison disease, potassium loss, and sodium and fluid retention


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.

Adult

4 mg IV equals 20 mg IV hydrocortisone
10-20 mg IV q6-8h equals 50-100 mg IV hydrocortisone q6-8h

Pediatric

Not established

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics; grapefruit juice increases prednisolone concentrations; methylprednisolone and cyclosporine mutually inhibit one another, resulting in increased plasma levels of each drug

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use; Depo-Medrol contains benzyl alcohol, which is potentially toxic when administered locally to neural tissue; administration of Depo-Medrol by other than indicated routes, including the epidural route, has been associated with reports of serious medical events including arachnoiditis, meningitis, paraparesis/paraplegia, sensory disturbances, bowel/bladder dysfunction, seizures, visual impairment (including blindness and ocular and periocular inflammation), and residue or slough at injection site

Vasopressors

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.

Adult

4-12 mcg/min IV infusion; titrate to desired perfusion status

Pediatric

0.1 mcg/kg/min IV; titrate to desired perfusion status

Enhances pressor response of norepinephrine by blocking reflex bradycardia; MAOIs, TCAs, antihistamines, guanethidine, ergot alkaloids, and methyldopa increase effects

Documented hypersensitivity; peripheral or mesenteric vascular thrombosis (ischemia may be increased and the area of the infarct extended)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Correct blood volume depletion, if possible, before administering norepinephrine therapy; extravasation may cause severe tissue necrosis and, thus, should be administered into a large vein; caution in occlusive vascular disease; extravasation can cause tissue necrosis


Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose.

Adult

0.5-20 mcg/kg/min IV infusion; titrate to desired perfusion status

Pediatric

Administer as in adults

Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects of dopamine

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure closely during the infusion; prior to infusion, correct hypovolemia with either whole blood or plasma because pressure may be helpful in detecting and treating hypovolemia; extravasation can cause tissue necrosis

More on Adrenal Crisis

Overview: Adrenal Crisis
Differential Diagnoses & Workup: Adrenal Crisis
Treatment & Medication: Adrenal Crisis
Follow-up: Adrenal Crisis
Multimedia: Adrenal Crisis
References
Further Reading

References

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  3. Weant KA, Sasaki-Adams D, Dziedzic K, et al. Acute relative adrenal insufficiency after aneurysmal subarachnoid hemorrhage. Neurosurgery. Oct 2008;63(4):645-9; discussion 649-50. [Medline].

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

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Keywords

adrenal crisis, adrenal insufficiency, cortisol, gland adrenal, adrenal, adrenal gland, cortisol levels, adrenal supplements, acute adrenal crisis, acute adrenal insufficiency, acute adrenocortical insufficiency, Addisonian crisis, adrenal apoplexy, aldosterone, primary adrenocortical insufficiency, secondary adrenocortical insufficiency, bilateral massive adrenal hemorrhage, BMAH, endocrine disorder

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.

Medical Editor

David M Klachko, MBBCh, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Missouri
David M Klachko, MBBCh 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

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.

 
 
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