Adrenal hypofunction Adrenal crisis

• Exhausted body stores of glucocorticoids in a patient with adrenal

Overview hypofunction after trauma, surgery, or other physiologic stress
• Primary adrenal hypofunction or insufficiency (Addison's disease) Incidence
originating within the adrenal gland and characterized by the Primary hypofunction
decreased
secretion of mineralocorticoids, glucocorticoids, and androgens • Primary adrenal hypofunction is relatively uncommon.
• Secondary adrenal hypofunction due to a disorder outside the • This disorder can occur at any age and in both sexes.
gland such Autoimmune Addison's disease
as impaired pituitary secretion of corticotropin and characterized • Autoimmune Addison's disease is most common in white females
by (genetic
decreased glucocorticoid secretion predisposition is likely).
• Adrenal crisis (addisonian crisis), a critical deficiency of • This disorder is more common in patients with a familial
mineralocorticoids and glucocorticoids generally following acute predisposition to
stress, autoimmune endocrine diseases.
sepsis, trauma, surgery, or the omission of steroid therapy in Age Factor
patients who
Most people with Addison's disease are diagnosed in their
have chronic adrenal insufficiency; a medical emergency that needs
immediate, vigorous treatment 20s to 40s.
Pathophysiology Complications
• Results from the partial or complete destruction of the adrenal • Hyperpyrexia
cortex • Psychotic reactions
• Manifests as a clinical syndrome in which the symptoms are • Deficient or excessive steroid treatment
associated
with deficient production of the adrenocortical hormones cortisol,
• Shock
aldosterone, and androgen • Profound hypoglycemia
• Results in high levels of corticotropin and corticotropin-releasing • Ultimate vascular collapse, renal shutdown, coma, and death (if
hormone untreated)
• Secondary adrenal hypofunction: Involves all zones of the cortex, Assessment
causing History
deficiencies of the adrenocortical hormones, glucocorticoids,
androgens, • Synthetic steroid use, adrenal surgery, or recent infection
and mineralocorticoids • Muscle weakness
• Cortisol deficiency: Causes decreased liver gluconeogenesis (the • Fatigue
formation
of glucose from molecules that aren't carbohydrates); resulting low
• Weight loss
blood • Craving for salty food
glucose levels can become dangerously low in patients who take • Decreased tolerance for stress
insulin
routinely • GI disturbances
• Aldosterone deficiency: Causes increased renal sodium loss and • Dehydration
enhances • Amenorrhea (in women)
potassium reabsorption
• Impotence (in men)
• Hypotension due to sodium excretion Physical findings
• Increased production of angiotensin II due to low plasma volume
and • Poor coordination
arteriolar pressure • Decreased axillary and pubic hair (in women)
• Androgen deficiency: May decrease hair growth in axillary and • Bronze coloration of the skin and darkening of scars
pubic areas • Areas of vitiligo
(less noticeable in men) as well as on the extremities of women
Causes • Increased pigmentation of mucous membranes
Primary hypofunction • Weak, irregular pulse
• Autoimmune process in which circulating antibodies react • Hypotension
specifically P.23
against the adrenal tissue Diagnostic test results
• Bilateral adrenalectomy Laboratory
• Family history of autoimmune disease (may predispose the patient • Rapid corticotropin stimulation test: Low corticotropin level
to indicates a
Addison's disease and other endocrinopathies) secondary disorder; elevated level indicates a primary disorder.
• Hemorrhage into the adrenal gland • Plasma cortisol level is less than 10 mcg/dl in the morning and
• Infection (histoplasmosis, cytomegalovirus) even lower
• Neoplasm in the evening.

• Tuberculosis (once the chief cause, now responsible for less than • Serum sodium and fasting blood glucose levels are decreased.
20% of • Serum potassium, calcium, and blood urea nitrogen levels are
adult cases) increased.
Secondary hypofunction • Hematocrit is elevated; lymphocyte and eosinophil counts are
• Abrupt withdrawal of long-term corticosteroid therapy increased.
• Hypopituitarism Imaging
• Removal of a corticotropin-secreting tumor • Chest X-ray shows a small heart.
• Computed tomography scan of the abdomen show adrenal • Intake and output
calcification (if
the cause is infectious).
Patient teaching
General
Treatment Be sure to cover:
General
• lifelong steroid therapy requirement
• I.V. fluids • symptoms of steroid overdose (swelling, weight gain) and steroid
Diet underdose (lethargy, weakness)
• Small, frequent, high-protein meals • possible need for dosage to be increased during times of stress or
Activity illness
(when the patient has a cold, for example)
• Periods of rest
Medications • possibility of adrenal crisis being precipitated by infection, injury,
or
• Lifelong corticosteroid replacement, usually with cortisone or profuse sweating in hot weather
hydrocortisone
• importance of carrying a medical identification card that states
• Oral fludrocortisone the
• Hydrocortisone patient is on steroid therapy (drug name and dosage should be
included on
• I.V. saline and glucose solutions (for adrenal crisis) the card)
• I.V. hydrocortisone replacement (for adrenal crisis) • how to give a hydrocortisone injection and to keep an emergency
Nursing considerations kit
containing hydrocortisone in a prepared syringe available for use in
Nursing diagnoses times
• Activity intolerance of stress
• Deficient fluid volume • stress management techniques.
• Disturbed body image Discharge planning
• Imbalanced nutrition: Less than body requirements • Refer the patient to the National Adrenal Diseases Foundation for
support
• Ineffective coping and information.
• Risk for imbalanced body temperature Resources
• Risk for impaired skin integrity Organizations
• Risk for infection National Adrenal Diseases Foundation:
Expected outcomes www.medhelp.org/nadf
The patient will: Selected references
Becker, K.L., et al. Principles and Practice of
• maintain joint mobility and range of motion Endocrinology and
• maintain an adequate fluid balance Metabolism, 3rd ed. Philadelphia: Lippincott Williams &
• verbalize feelings about changed body image Wilkins,
• consume required caloric intake 2004.
Greenspan, F.S., and Gardner, D.G. Basic and Clinical
• develop effective coping skills Endocrinology, 7th ed. New York: McGraw-Hill Book Co.,
• remain normothermic 2003.
• maintain skin integrity
• remain free from signs and symptoms of infection.
Nursing interventions
• Until onset of mineralocorticoid effect, encourage fluids to
replace
excessive fluid loss.
• Arrange for a diet that maintains sodium and potassium balances;
if the
patient is anorexic, suggest six small meals per day to increase
caloric
intake.
• Observe for cushingoid signs such as fluid retention around the
eyes and
face.
• Check for petechiae.
• If the patient receives glucocorticoids alone, observe for
orthostatic
hypotension or electrolyte abnormalities.
Monitoring
• Vital signs
• Signs of shock (decreased level of consciousness and urine output)
• Hyperkalemia before treatment; hypokalemia after treatment
• Cardiac rhythm
• Blood glucose levels
• Daily weight