Acute Adrenal Crisis
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
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 withdrawalAcute 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.
Causes
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.
Assessment
History
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.
Psychosocial
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
| Test | Normal Result | Abnormality With Condition | Explanation |
|---|---|---|---|
| Serum cortisol level | 6:00 to 8:00 a.m., 5–23 mcg/dL | Decreased | Determines the ability of the adrenal gland to produce glucocorticoids |
| Serum electrolytes and chemistries | Sodium 136–145 mEq/L; potassium 3.5–5.1 mEq/L; blood urea nitrogen 5–20 mg/dL; glucose 70–105 mg/dL | Hyponatremia; hyperkalemia; azotemia; hypoglycemia | Values 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 later | Normal serum cortisol level (see above) | Less than 20 mcg after ACTH stimulation; increase of less than 9 mcg/dL is diagnostic of adrenal insufficiency | Normal 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
Diagnosis
Fluid volume deficit related to water loss and insufficient ability to reabsorb waterOutcomes
Fluid balance; Circulation status; Cardiac pump effectiveness; Hydration; Nutritional statusInterventions
Fluid/electrolyte management; Hypoglycemia management; Intravenous therapy; Fluid monitoring; Medication administrationPlanning and implementation
Collaborative
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 Class | Dosage | Description | Rationale |
|---|---|---|---|
| Dexamethasone | 4 mg IV | Corticosteroid | Substitution 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 succinate | 100 mg IV q 6–8 hr | Corticosteroid | Substitution therapy in deficiency state |
Other Therapies: Cortisone acetate (Cortone); fludrocortisone acetate (Florinef)
Independent
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