Classifications: adrenal corticosteroid; mineralocorticoid; antiinflammatory agent; Therapeutic: antiinflammatory; corticosteroid
Pregnancy Category: C
0.1 mg tablets
Long-acting synthetic steroid with potent mineralocorticoid activity. Small doses produce marked sodium retention, increased
urinary potassium excretion, and elevated BP.
Synthetic corticosteroid replacement product for adrenocortical insufficiency.
Partial replacement therapy for adrenocortical insufficiency and for treatment of salt-losing forms of congenital adrenogenital
To increase systolic and diastolic blood pressure in patients with severe hypotension secondary to diabetes mellitus or to
Hypersensitivity to glucocorticoids, idiopathic thrombocytopenic purpura, psychoses, acute glomerulonephritis, viral or bacterial
diseases of skin, infections not controlled by antibiotics, active or latent amebiasis, hypercorticism (Cushing's syndrome),
smallpox vaccination or other immunologic procedures; pregnancy (category C). Topical steroids are contraindicated in presence
of varicella, vaccinia, on surfaces with compromised circulation, and in children <2 y.
Children; diabetes mellitus; chronic, active hepatitis positive for hepatitis B surface antigen; hyperlipidemia; cirrhosis;
stromal herpes simplex; glaucoma, tuberculosis of eye; osteoporosis; convulsive disorders; hypothyroidism; diverticulitis;
nonspecific ulcerative colitis; fresh intestinal anastomoses; active or latent peptic ulcer; gastritis; esophagitis; thromboembolic
disorders; CHF; metastatic carcinoma; hypertension; renal insufficiency; history of allergies; active or arrested tuberculosis;
systemic fungal infection; myasthenia gravis; lactation.
Route & Dosage
Adult: PO 0.1 mg/d, may range from 0.1 mg 3 times/wk to 0.2 mg/d
Child: PO 0.050.1 mg/d
Salt-Losing Adrenogenital Syndrome
Adult: PO 0.10.2 mg/d
Child: PO 0.050.1 mg/d
- Note: Concomitant oral cortisone or hydrocortisone therapy may be advisable to provide substitute therapy approximating normal adrenal
- Store in airtight containers at 15°30° C (59°86° F). Protect from light.
Adverse Effects (≥1%)CNS:
Vertigo, headache, nystagmus, increased intracranial pressure with papilledema (usually after discontinuation of medication),
mental disturbances, aggravation of preexisting psychiatric conditions, insomnia
, ataxia (rare). CV:
CHF, hypertension, thromboembolism
(rare), tachycardia. Endocrine:
Suppressed linear growth in children, decreased glucose tolerance; hyperglycemia, manifestations of latent diabetes
hypocorticism; amenorrhea and other menstrual difficulties. Special Senses:
Posterior subcapsular cataracts (especially in children), glaucoma
, exophthalmos, increased intraocular pressure with optic
nerve damage, perforation of the globe. Metabolic:
Hypocalcemia; sodium and fluid retention;
hypokalemia and hypokalemic alkalosis, negative nitrogen balance, decreased serum concentration of vitamins A and C. GI: Nausea,
increased appetite, ulcerative esophagitis, pancreatitis, abdominal distension, peptic ulcer
with perforation and hemorrhage,
(long-term use) Osteoporosis, compression fractures, muscle wasting and weakness, tendon rupture, aseptic necrosis of femoral
and humeral heads. Skin:
Skin thinning and atrophy, acne, impaired wound healing;
petechiae, ecchymosis, easy bruising; suppression of skin test reaction; hypopigmentation or hyperpigmentation, hirsutism,
acneiform eruptions, subcutaneous fat atrophy; allergic dermatitis, urticaria, angioneurotic edema, increased sweating. Body as a Whole: Anaphylactoid reactions
(rare), aggravation or masking of infections
; malaise, weight gain, obesity
Increased or decreased motility and number of sperm.
The antidiabetic effects of insulin
may be diminished; amphotericin B, diuretics
may increase potassium
may decrease prothrombin time; indomethacin, ibuprofen
can potentiate the pressor effect of fludrocortisone; anabolic steroids
increase risk of edema and acne; rifampin
may increase the hepatic metabolism of fludrocortisone.
Readily from GI tract. Peak:
1.7 h. Metabolism:
In liver. Half-Life:
Assessment & Drug Effects
- Monitor weight and I&O ratio to observe onset of fluid accumulation, especially if patient is on unrestricted salt intake
and without potassium supplement. Report weight gain of 2 kg (5 lb)/wk.
- Monitor and record BP daily. If hypertension develops as a consequence of therapy, report to physician. Usually, the dose
will be reduced to 0.05 mg/d.
- Check BP q46h and weight at least every other day during periods of dosage adjustment.
- Lab tests: Periodic serum electrolytes and ABGs during prolonged therapy.
- Monitor for S&S of hypokalemia and hyperkalemic metabolic alkalosis (see Appendix F).
- Monitor for signs of overdosage (hypercorticism): psychosis, excess weight gain, edema, congestive heart failure, ravenous
appetite, severe insomnia, and increase in BP.
- Note: Signs of insufficient dosage (hypocorticism) are loss of weight and appetite, nausea, vomiting, diarrhea, muscular weakness,
increased fatigue, and hypotension.
Patient & Family Education
- Report signs of hypokalemia (see Appendix F).
- Be aware of signs of potassium depletion associated with high sodium intake: Muscle weakness, paresthesias, circumoral numbness;
fatigue, anorexia, nausea, mental depression, polyuria, delirium, diminished reflexes, arrhythmias, cardiac failure, ileus,
- Advise patient to eat foods with high potassium content.
- Signs of edema should be reported immediately. Sodium intake may or may not require regulation, depending on individual needs
and clinical situation.
- Weigh daily under standard conditions and report steady weight gain.
- Report intercurrent infection, trauma, or unexpected stress of any kind promptly when taking maintenance therapy.
- Carry medical identification at all times. It needs to indicate medical diagnosis, medication(s), physician's name, address,
and telephone number.