HYDROCORTONE
Clinical safety rating: caution
Comprehensive clinical and safety monograph for HYDROCORTONE (HYDROCORTONE).
Hydrocortisone is a corticosteroid that binds to the glucocorticoid receptor, leading to anti-inflammatory and immunosuppressive effects by inhibiting phospholipase A2, reducing prostaglandin and leukotriene synthesis, and suppressing cytokine production.
| Metabolism | Hepatic via CYP3A4 and other microsomal enzymes; primarily metabolized by 11-beta-hydroxysteroid dehydrogenase and 5-alpha-reductase. |
| Excretion | Renal (primarily as inactive metabolites; <5% unchanged) and biliary/fecal (minor). |
| Half-life | Terminal elimination half-life: 1.5–2.5 hours (plasma), but biological half-life (duration of HPA axis suppression) is 8–12 hours. |
| Protein binding | ~90% bound to corticosteroid-binding globulin (CBG) and albumin. |
| Volume of Distribution | 0.3–0.5 L/kg; distributes widely into tissues, with high penetration into CSF. |
| Bioavailability | Oral: ~96% (rapid and complete); IM: 100% (by definition). |
| Onset of Action | IV: immediate (minutes); IM: 1–2 hours; oral: 1–2 hours; topical: variable (hours to days). |
| Duration of Action | Duration of HPA suppression: 8–12 hours after a single dose; clinical anti-inflammatory effects persist 24–48 hours. |
| Molecular Weight | 362.46 |
100-500 mg intravenously every 2-6 hours for initial management of adrenal insufficiency; oral maintenance: 20-30 mg daily in divided doses (e.g., 10 mg morning, 5 mg afternoon).
| Dosage form | TABLET |
| Renal impairment | No dose adjustment required for renal impairment. Not removed by hemodialysis. |
| Liver impairment | Child-Pugh Class A: no adjustment; Class B: reduce dose by 50%; Class C: reduce dose by 60% or consider alternative. |
| Pediatric use | Adrenal insufficiency: oral 8-10 mg/m²/day in 3 divided doses; IV/IM: 1-2 mg/kg/dose every 6-8 hours. Status asthmaticus: IV 4-8 mg/kg/day divided every 6 hours. |
| Geriatric use | Start at lowest effective dose (e.g., 10-15 mg/day oral). Monitor for hyperglycemia, hypertension, osteoporosis. Use lower initial doses due to increased risk of adverse effects. |
| 1st trimester | Corticosteroids are associated with a small increased risk of oral clefts; use only if clearly needed. |
| 2nd trimester | May cause fetal adrenal suppression with prolonged use; monitor for growth restriction. |
| 3rd trimester | Risk of neonatal adrenal suppression if used near term; use lowest effective dose. |
Clinical note
Comprehensive clinical and safety monograph for HYDROCORTONE (HYDROCORTONE).
| Placental transfer | Hydrocortisone crosses the placenta but is largely converted to inactive cortisone by placental 11β-HSD2; fetal exposure is limited. |
| Breastfeeding | Hydrocortisone is excreted into breast milk in low amounts; short-term use is considered compatible with breastfeeding. Monitor infant for adrenal suppression with high maternal doses. |
■ FDA Black Box Warning
None
| Serious Effects |
Systemic fungal infectionHypersensitivity to hydrocortisone or any component
| Precautions | Adrenal suppression, increased susceptibility to infections, masking of infection, Cushing's syndrome, osteoporosis, cataracts, glaucoma, hypertension, hypokalemia, growth retardation in children, and neuropsychiatric effects. |
| Food/Dietary | Avoid excessive grapefruit juice as it may increase hydrocortisone levels. Limit sodium intake to manage fluid retention and hypertension. Maintain adequate potassium intake (e.g., bananas, oranges) to counteract hypokalemia. No significant interaction with alcohol but it may exacerbate GI irritation. |
Loading safety data…
| Lactation Rating |
| L2 (Safer) |
| Teratogenic Risk | Corticosteroids including HYDROCORTONE are associated with a small increased risk of cleft palate (first trimester), fetal growth restriction, and adrenal suppression in neonates with prolonged maternal use. Second/third trimester use may cause fetal adrenal suppression but no specific malformation pattern. Risk must be weighed against maternal benefit. |
| Fetal Monitoring | Monitor maternal blood pressure, blood glucose (especially in diabetics), and signs of infection. Fetal growth should be assessed via ultrasound if prolonged use. Neonates exposed in utero should be monitored for adrenal insufficiency (e.g., hypoglycemia, hypotension) after birth. |
| Fertility Effects | Chronic high-dose corticosteroids may suppress endogenous cortisol, leading to oligomenorrhea or amenorrhea due to hypothalamic-pituitary-adrenal axis suppression. Effects are usually reversible upon dose reduction or discontinuation. No direct negative impact on fertility at typical therapeutic doses. |
| Clinical Pearls |
| Hydrocortisone is a short-acting glucocorticoid used for anti-inflammatory and immunosuppressive effects. In adrenal insufficiency, it is the preferred replacement therapy due to its mineralocorticoid activity at higher doses. For acute stress doses (e.g., surgery, trauma), increase to 50-100 mg IV q8h. Monitor serum potassium and glucose regularly. Taper doses to avoid adrenal crisis; do not stop abruptly. |
| Patient Advice | Take exactly as prescribed; do not stop without consulting your doctor. · Report any unusual weight gain, swelling, or severe headaches. · Avoid live vaccines during treatment. · Carry a medical alert card stating you are on steroid therapy. · In case of stress, infection, or surgery, you may need a dose adjustment. |