Corticosteroid
Hydrocortisone (Solu-Cortef)
Also called Solu-Cortef
Indications
- Adrenal crisis, including after pituitary apoplexy: treat before results return
- Stress dosing for surgery or critical illness in patients on long-term steroids
- Septic shock with an ongoing vasopressor need (off-label)
- Severe community-acquired pneumonia: SCCM 2024 recommends steroids, but trials conflict (off-label)
- Myxedema coma and thyroid storm, before or with thyroid treatment (off-label)
Dosing
| Where | Dose |
|---|---|
| Other common pushes | Hydrocortisone: 100 mg IV (adrenal crisis), then 200 mg/day |
| Corticosteroid equivalence | Hydrocortisone: 20 mg (short-acting; strong mineralocorticoid effect) |
On the quick cards
Mechanism of action
Hydrocortisone is cortisol. It binds the cytoplasmic glucocorticoid receptor, which sheds its heat-shock proteins, enters the nucleus and switches genes on (annexin-1, IκBα, β2 receptors, gluconeogenic enzymes) or off by tethering NF-κB and AP-1 (cytokines, COX-2, inducible NO synthase); these genomic effects take hours, while faster non-genomic effects help restore vascular responsiveness to catecholamines. It also binds the mineralocorticoid receptor as tightly as aldosterone: renal 11β-HSD2 normally oxidizes it to inactive cortisone, but above about 50 mg a day the enzyme is overwhelmed and sodium retention follows.
Pharmacology
- Cardiovascular: permissive for vascular tone; in septic shock it shortens shock and ventilation, but cut mortality only with fludrocortisone added (APROCCHSS 2018)
- Metabolic: hyperglycemia from gluconeogenesis and insulin resistance; protein breakdown
- Renal: sodium retention and potassium loss at stress doses; restores free-water excretion in cortisol deficiency, so sodium can rise fast
- Immune: lymphocytes and eosinophils fall and neutrophils rise within hours; fever and the WBC response are blunted
- Endocrine: the reference steroid, with glucocorticoid and mineralocorticoid potency both 1: 20 mg matches 4 mg of methylprednisolone or 0.75 mg of dexamethasone; suppresses ACTH
Pharmacokinetics
| Onset | IV: effects within 1 h (label); gene effects build over hours |
|---|---|
| Duration | Biologic effect 8–12 h, so stress doses go every 6–8 h or by infusion |
| Half-life | Plasma 1.5–2 h |
| Distribution | Vd about 0.5 L/kg (Derendorf 1991); placental 11β-HSD2 inactivates most of it |
| Protein binding | About 90%, mostly to CBG; CBG saturates at high levels and falls in sepsis, raising the free fraction |
| Metabolism | Kidney 11β-HSD2 to inactive cortisone; liver A-ring reduction and CYP3A4, then glucuronidation |
| Clearance | About 18 L/h; falls by more than half in critical illness (Boonen 2013) |
| Elimination | Urine as conjugates, very little unchanged; nearly complete within 12 h (label) |
| Routes | IV push (100 mg over 30 s; 500 mg or more over 10 min), infusion or IM |
Chemistry
- Cortisol (11β,17α,21-trihydroxypregn-4-ene-3,20-dione); the 11β-hydroxyl is essential, so cortisone needs 11β-HSD1 to become active
- Neutral and lipophilic, with no ionizable group at body pH; the 21-sodium succinate ester makes it water soluble, and esterases free it within minutes
- Solu-Cortef: preservative-free (2024 label), pH 7–8; dilute in D5W, NS or D5NS and use within 12 h (protect from light) or 24 h refrigerated
Adverse effects and cautions
In the one-pagers
- Shock Types at a GlanceDistributive shock: septic, anaphylactic, neurogenic, adrenal: Septic shock combines vasodilation (inducible nitric oxide, relative vasopressin deficiency), capillary leak, microcirculatory shunting and mitochondrial failure; septic cardiomyopathy can turn warm shock cold. The sequence: cultures and antimicrobials within 1 h; balanced crystalloid with reassessment (passive leg raise raising CO ≥10
- Pediatric Assessment and EmergenciesShock, fluids and sepsis (Phoenix 2024): For fluid-refractory septic shock start epinephrine or norepinephrine (PALS 2025, 2a), peripherally until central access is in (SSC); dopamine only if neither is available. Stress-dose hydrocortisone may be considered once vasoactives are needed (2b) and is given early for known adrenal insufficiency. Check glucose and ionized calcium.
- Vasopressors and InotropesSeptic shock order (SSC 2026): IV corticosteroids are suggested; the usual regimen is hydrocortisone 200 mg/day (SSC 2021 remark).
- Electrolyte ImbalancesHyponatremia: work-up by urine and volume: Low, renal: Over 30: Thiazides, salt wasting, adrenal insufficiency: Saline; stop the drug; hydrocortisone
- Medical Emergencies: Neuro, Endocrine, Blood and InfectionThyroid storm and myxedema coma: Rate control: beta blockade can precipitate collapse, especially with systolic heart failure; in the Japanese survey, nonselective beta blockers given to patients in Killip class IV failure were linked to deaths. The tachycardia is partly a response to fever and volume loss. NASEMSO lists hyperthyroidism among the causes of tachycardia and says AF rarely needs fiel
- Obstetric EmergenciesSepsis and venous thromboembolism: SMFM #47: antibiotics within 1 h, cultures, lactate, source control, 1–2 L of crystalloid, norepinephrine first, and no delivery for sepsis alone. Vasopressin at a fixed 0.03 units/min is a reasonable second pressor, and stress-dose hydrocortisone is held while antenatal steroids are given (Bauer and Pacheco 2025).
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In the algorithms
Other corticosteroid drugs
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Sources
- FDA label: Solu-Cortef (2024)
- Endocrine Society: primary adrenal insufficiency (2016)
- SCCM corticosteroid focused update (2024)
- Derendorf 1991 (pharmacokinetics)
For education and exam preparation only. Follow your institution’s protocols. Typical adult values for study. Follow your local protocols and medical direction.