Acute Adrenal Crisis

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Acute Adrenal Crisis

Acute life-threatening adrenocortical insufficiency with markedly reduced serum cortisol, which arises in a background of chronic adrenocortical insufficiency (Addison’s disease).  
Aetiology Infections, trauma, adrenal haemorrhage, tuberculosis, surgery, dehydration with salt deprivation, destruction of pituitary gland or evoked by replacing thyroid hormone in patients with hypothyroidism of hypothalamic or pituitary origin and underlying mild ACTH deficiency.
Triggers GI infection, fever
Clinical findings Hypotension, shock, fever, dehydration, anorexia, weakness, apathy, headache, vomiting, chills, tachycardia, sweating, abdominal pain
Lab Reduced Na+, increased K+, increased white cells, eosinophilia, hypoglycaemia
Management Pharmacologic doses of IV hydrocortisone, pressor support
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.

acute adrenal crisis

Acute adrenal insufficiency Endocrinology A life-threatening condition caused by an abrupt ↓ cortisol At risk Pts Those taking corticosteroids for prolonged periods–wks to months–eg with Addison's disease, especially if steroids are stopped abruptly Clinical Shock, hypotension, weakness, headache, vomiting, fever, chills, tachycardia, sweating Management Vasopressors, steroids Prevention Taper steroid withdrawal
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

Acute Adrenal Crisis

DRG Category:644
Mean LOS:4.9 days
Description:MEDICAL: Endocrine Disorders with CC

Acute adrenal crisis is a life-threatening endocrine emergency caused by a deficit of glucocorticoids (primarily cortisol) or mineralocorticoids (primarily aldosterone). The anterior pituitary gland produces adrenocorticotropic hormone (ACTH), which causes the adrenal cortex to produce more than 50 steroid hormones. Cortisol and aldosterone are the most physiologically active of these hormones. In primary adrenocortical insufficiency, glucocorticoid and mineralocorticoid function is lost. Acute adrenocortical insufficiency is a difficult diagnosis to make. Acute adrenal crisis rarely occurs without an accompanying serious injury or illness. The diagnosis is difficult because many of the signs and symptoms are nonspecific. However, when left untreated, someone with acute adrenal insufficiency has a very poor prognosis for survival. Any delay in disorder management while waiting for diagnostic confirmation may threaten the person’s life.

Glucocorticoids are cardiac stimulants that activate release of essential vasoactive substances. Without corticosteroids, stress results in hypotension, shock, and death. A deficiency of cortisol produces many metabolic abnormalities, such as decreases in glucose production, protein and fat metabolism, appetite, and digestion. Serious systemic effects include a decrease in vascular tone and a diminished effect of catecholamines, such as epinephrine and norepinephrine. Normally, a body under stress releases corticosteroids. Both the decrease in the vascular tone of the blood vessels and the decreased effect of catecholamines in an individual in an adrenal crisis can cause shock. The deficiency of aldosterone results in profound fluid and electrolyte imbalances: a decrease in sodium and water retention, a decrease in circulating blood volume, and an increase in both potassium and hydrogen ion reabsorption.


Acute adrenal insufficiency is most commonly caused by acute withdrawal of chronic corticosteroid therapy. It can also occur from immune destruction of the adrenal cortex or adrenal hemorrhage or from infiltration by metastatic carcinoma. Before signs and symptoms appear, at least 90% or more of the adrenal cortex is damaged. The disorders result in deficiencies of both glucocorticoid and mineralocorticoid hormones. Other causes include physiological stress including surgery, infection, burns, sepsis, anesthesia, fluid volume loss, trauma, asthma, hypothermia, alcohol abuse, myocardial infarction, fever, hypoglycemia, pain, and depression.

Genetic considerations

See Adrenal Insufficiency, p. 46.

Gender, ethnic/racial, and life span considerations

Primary adrenocortical insufficiency affects men and women equally, but women are affected two to three times more often by the idiopathic autoimmune form of adrenal insufficiency. In idiopathic autoimmune adrenal insufficiency, the diagnosis is most often discovered in the third to fifth decades of life, but acute adrenal crisis may occur at any age, without regard to gender, and may be associated with developmental or genetic abnormalities. Ethnicity and race have no known effects on the risk for acute adrenal crisis. In children, the most common cause of acute adrenal crisis is an overwhelming infection with Pseudomonas or meningococcal meningitis (also known as Waterhouse-Friderichsen syndrome). In adults, acute adrenal crisis is more commonly associated with hemorrhagic destruction because of anticoagulant therapy or aggravation of adrenal hypofunction during periods of major stress.

Global health considerations

In developed countries, the incidence in Western countries is 50 cases per 1 million persons. No data are available on Eastern countries or many developing nations.



Elicit a medication history, with particular attention to such medications as corticosteroids, phenytoin, barbiturates, anticoagulants, and rifampin. Note a history of cancer, autoimmune diseases requiring treatment with corticosteroids, or radiation to the head or abdomen. A family history of either Addison’s disease or an autoimmune disease may be important.

Inquire about a recent decrease in appetite, abdominal pain, weight loss, or salt craving. Often in crisis, the patient or family may describe fever, nausea, and vomiting. Determine if the patient has experienced signs and symptoms such as generalized fatigue, apathy, dizziness, weakness, headache, or changes in skin pigmentation. Some patients describe central nervous system effects such as confusion, irritability, psychoses, emotional lability, or even seizures. Women may describe a decreased libido and amenorrhea.

Physical examination

The patient appears to be critically ill with unexplained shock. Because of decreased fluid volume caused by a decrease in water reabsorption, the patient may arrive at the hospital with severe hypotension; tachycardia; decreased cardiac output; weak and rapid pulses; and cool, pale skin. Peripheral pulses may be weak and irregular. Urine output is usually quite low. The blood pressure may be very hard to maintain because a decrease in the catecholamines can result in decreased vascular tone. Other symptoms include nausea, vomiting, flank pain, and hypothermia.

An increase in skin pigmentation (bronze color) is noticeable in European Americans. Areas most often affected include the mucous membranes and areas over joints and scars. A loss of pubic hair may also occur from a decreased level of adrenal androgens.


Assess the patient’s and significant others’ ability to cope with a critical illness and the presence of a social network to support them.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Serum cortisol level6:00 to 8:00 a.m., 5–23 mcg/dLDecreasedDetermines the ability of the adrenal gland to produce glucocorticoids
Serum electrolytes and chemistriesSodium 136–145 mEq/L; potassium 3.5–5.1 mEq/L; blood urea nitrogen 5–20 mg/dL; glucose 70–105 mg/dLHyponatremia; hyperkalemia; azotemia; hypoglycemiaValues reflect sodium loss from a deficit in mineralocorticoids with loss of fluids and poor glucose control because of decreased gluconeogenesis
ACTH stimulation test; determine baseline serum cortisol, then administer 250 mcg ACTH intravenously and draw serum cortisol level 30–60 min laterNormal serum cortisol level (see above)Less than 20 mcg after ACTH stimulation; increase of less than 9 mcg/dL is diagnostic of adrenal insufficiencyNormal adrenal gland greatly increases production of cortisol when stimulated by ACTH

Other Tests: Blood and other cultures and sensitivities; computed tomography (CT) of the abdomen; complete blood count; skull x-rays; pituitary and adrenal imaging

Primary nursing diagnosis


Fluid volume deficit related to water loss and insufficient ability to reabsorb water


Fluid balance; Circulation status; Cardiac pump effectiveness; Hydration; Nutritional status


Fluid/electrolyte management; Hypoglycemia management; Intravenous therapy; Fluid monitoring; Medication administration

Planning and implementation


Pharmacologic treatment centers on fluid and electrolyte replacement and hormonal supplements (see Pharmacologic Highlights box). Fluid replacement with dextrose- and sodium-containing solutions allows for correction of hypovolemia and hypoglycemia. As much as 5 L or more of fluid may be needed to maintain an adequate blood pressure, circulation, and urine output and to replace the fluid deficit. Correct sodium, potassium, calcium, and glucose abnormalities. Always treat the underlying problem that precipitated the crisis.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
Dexamethasone4 mg IVCorticosteroidSubstitution therapy in deficiency state; drug does not interfere with serum cortisol assay; dangerous to delay glucocorticoid replacement while awaiting ACTH stimulation test results; drug does not have mineralocorticoid activity and therefore needs to be accompanied by fluid and electrolyte replacement
Hydrocortisone sodium succinate100 mg IV q 6–8 hrCorticosteroidSubstitution therapy in deficiency state

Other Therapies: Cortisone acetate (Cortone); fludrocortisone acetate (Florinef)


During the initial hours of managing a patient with acute adrenal crisis, the first priority is to maintain airway, breathing, and circulation. Patients who receive large amounts of room-temperature fluids are at risk for hypothermia. Keep the temperature of the room warm and the bed linens dry. If possible, keep the patient fully covered. During massive fluid replacement, administer warmed (body-temperature) fluids if possible.

Teach the patient on corticosteroids about the medication and the need to continue to take it until the physician tapers the dose and then finally discontinues it. Explain the symptoms of adrenal crisis to any patient who is undergoing anticoagulant therapy. Explain the effects of stress on the disease and the need for adjustment of medications during times of stress.

Patients with altered tissue perfusion require frequent skin care. If the patient is immobile, perform active and passive range-of-motion exercises at least every 8 hours. Encourage coughing and deep breathing to limit the complications from immobility. Provide small, frequent meals and make referrals to the dietitian early in the hospitalization.

Evidence-Based Practice and Health Policy

Wass, J.A. (2012). How to avoid precipitating an acute adrenal crisis. British Medical Journal, 345, e6333.

  • Prevention of acute adrenal crisis is a priority to avoid development of life-threatening complications.
  • Primary prevention recommendations include advising patients to double their regular hydrocortisone replacement doses during periods of illness and increased stress.
  • Secondary prevention recommendations include supplying patients with a medical alert bracelet and facilitating early admission and emergency treatment with parenteral administration of hydrocortisone as soon as patients recognize an impending crisis.

Documentation guidelines

  • Physical findings: Vital signs; pulmonary artery catheter pressure readings; monitoring of airway, breathing, circulation; urine output; mental status
  • Important changes in laboratory values: Plasma cortisol, serum glucose, serum sodium and potassium, pH, oxygen saturation
  • Presence of complications: Infection, cardiac dysrhythmias, fluid and electrolyte imbalance, weight loss
  • Response to therapy: Daily weights, appetite, level of hydration

Discharge and home healthcare guidelines

patient teaching.
Teach the patient and significant others about the disease and the factors that aggravate it. Provide suggestions about rest and activity and stress reduction. Explain the signs and symptoms that may lead to crisis.

Identify the stressors and the need to increase medication during times of stress. Teach the patient and family when the physician needs to be notified.

Teach the patient the name, dosage, action, and side effects of drugs and the need to continue using them for life. Provide written instruction about medications and follow-up physician’s appointments.

Diseases and Disorders, © 2011 Farlex and Partners
References in periodicals archive ?
Pakos, "CT diagnosis of acute adrenal insufficiency due to bilateral adrenal haemorrhage," European Journal of Radiology Extra, vol.
Hypotension refractory to fluids and requiring vasopressors is the most common feature of acute adrenal insufficiency. [23] In the present study, 100% patients (25 patients) have hypotension and 88% (22 patients) had weakness and fatigue and 72% (18 patients) had symptoms of nausea and vomiting.
Acute adrenal insufficiency occurs in patients who are unable to increase their production of cortisol during acute stress.
To illustrate possible diagnostic difficulties faced by endocrinologists, we use one case of POEMS syndrome with severe acute adrenal insufficiency to demonstrate the clinical course and the diagnostic challenge.
A 31-year-old male was admitted to the hospital with an acute adrenal insufficiency. Physical examination uncovered a marked hyperpigmentation on sun-exposed areas and predominant sensory neuropathy of the upper and lower limbs.
More recently acute adrenal insufficiency after TBI-based conditioning regimens has been reported in children [66, 67].
With the background of tuberculosis and acute adrenal insufficiency diagnosed by laboratory test, bilateral enlargement of adrenal glands was considered most consistent with tuberculosis in our patient.
Acute adrenal insufficiency as a manifestation of the anticardiolipin syndrome.
Introduction: Acute adrenal insufficiency (AI) is a condition frequently observed in critically ill trauma patients.
Patients can experience exacerbation of ischemic heart disease or acute adrenal insufficiency
Talbot (1996), (6) adrenal necrosis sometimes accompanied by haemorrhage may complicate shock and acute adrenal insufficiency may contribute to death.
The inability of the suppressed hypothalamic pituitary-adrenal (HPA) axis to respond to perioperative stress can lead to acute adrenal insufficiency and cardiovascular collapse.

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