Hydrocortisone (Cortisol): veterinary dose and monograph

At a glance

Drug class

Veterinary drug

Also known as

Cortisol, Solu-Cortef, Hydrocortisone sodium succinate

Species with doses

Dogs, Cats and Horses

General dose range

0.5–5 mg/kg IV q6–12h (acute) / replacement per protocol — check the species tables for the indication

Routes

IV, PO

Last reviewed

1 October 2026

Indications

• Addisonian (hypoadrenocortical) crisis — rapid IV glucocorticoid (with fluids/electrolyte correction)
• Physiologic glucocorticoid replacement (mimics cortisol; some mineralocorticoid effect)
• Relative adrenal insufficiency / vasopressor-refractory septic shock (low-dose IV)
• Topical dermatologic anti-inflammatory (mild)

Hydrocortisone (Cortisol) dose by species

Doses are per administration unless stated. mg/kg doses scale with body weight; per-animal, per-quarter and infusion-rate doses are shown as the reference writes them.

Dogs

• Addisonian crisis (intermittent IV): Plumb’s p.618 (Panciera 2009): hydrocortisone sodium succinate 2 mg/kg IV q6h or 2–4 mg/kg IV q8h. Provides gluco- and mineralocorticoid activity; give with aggressive fluids and electrolyte correction. Papich 5e: high ‘shock’ doses (50–150 mg/kg) are not recommended.
• Physiologic replacement (oral): Papich 5e: replacement 1–2 mg/kg PO q12h (anti-inflammatory 2.5–5 mg/kg q12h). Plumb’s 10e p.616 gives a LOWER oral regimen (next row). Adjust to clinical response; increase during stress.
• Long-term hypoadrenocorticism — oral (Plumb’s 10e): Plumb’s 10e p.616 (extra-label): when changing from parenteral to oral glucocorticoid after a crisis, most dogs start on an anecdotal 0.4–0.8 mg/kg PO once to twice a day; once stable, 0.4 mg/kg PO once to twice a day generally provides adequate supplementation. Usually combined with a mineralocorticoid (fludrocortisone or DOCP). REFERENCE CONFLICT: Papich 5e gives 1–2 mg/kg PO q12h (row above).
• Critical illness-related corticosteroid insufficiency (CIRCI): Plumb’s 10e p.617 (dogs/cats, extra-label): hydrocortisone sodium succinate 1–4.3 mg/kg/DAY divided into 4 equal doses IV every 6 hours or as a CRI; taper by 25% a day after the critical illness resolves and repeat an ACTH stimulation test. No strong veterinary evidence or consensus guideline exists for this use.
• Post-CPR haemodynamic instability: Plumb’s 10e p.617 (dogs/cats, extra-label): routine corticosteroids are not recommended after CPR; consider only if unstable despite fluids, inotropes and vasopressors — hydrocortisone sodium succinate 1 mg/kg IV, then 1 mg/kg IV every 6 hours or 0.15 mg/kg/hour IV CRI, tapered as the patient allows.
• Addisonian crisis (CRI): Papich 5e: 0.625 mg/kg/h IV CRI. Plumb’s p.618: 0.5 mg/kg/h until GI function returns (Church); 0.3 mg/kg/h (Panciera).
• Septic shock (relative adrenal insufficiency): Plumb’s p.618 (Crowe 2002): 0.08 mg/kg/h IV — low-dose infusion can shorten vasopressor need.

Cats

• Adrenal crisis (IV): Plumb’s 10e p.616 (dogs/cats, extra-label): acute adrenocortical insufficiency, after the ACTH stimulation test — hydrocortisone sodium succinate 2–4 mg/kg IV every 6 to 8 hours or 0.3–0.5 mg/kg/hour IV CRI, switching to oral steroid once eating and drinking. Papich 5e (dogs and cats): adrenal crisis 0.625 mg/kg/h CRI, anti-inflammatory 5 mg/kg IV q12h. Hypoadrenocorticism is uncommon in cats.
• Adrenal crisis / septic shock (CRI): Papich 5e (dogs and cats): adrenal crisis 0.625 mg/kg/h. Plumb’s p.618 (Crowe 2002): septic shock 0.08 mg/kg/h.

Horses

• Relative adrenal insufficiency (critically ill foals): Papich 5e: foals — replacement therapy for critical illness 1–3 mg/kg/day IV. Taper as the foal recovers; not for routine anti-inflammatory use.
• Glucocorticoid therapy (adult): Papich 5e: hydrocortisone sodium succinate 5 mg/kg IV q12h. Plumb’s p.618 (Robinson): 1–4 mg/kg as an IV infusion. Laminitis risk with glucocorticoids. ARCI Class 4.

Contraindications

Systemic fungal infection, uncontrolled infection, GI ulceration (relative). Congestive heart failure/hypertension/oedema (mineralocorticoid sodium retention). Diabetes (worsens control). Concurrent NSAIDs (GI ulceration). Abrupt withdrawal after prolonged use (HPA suppression). Known hypersensitivity.

Adverse effects

• Sodium/water retention, hypokalaemia, hypertension/oedema (mineralocorticoid effect)
• PU/PD, polyphagia; hyperglycaemia
• GI ulceration (esp. with NSAIDs); immunosuppression/delayed healing
• HPA-axis suppression with prolonged use

Drug interactions

• NSAIDs: additive GI ulceration
• Potassium-wasting diuretics: additive hypokalaemia
• Insulin/oral hypoglycaemics: antagonised (hyperglycaemia)
• CYP inducers/inhibitors: alter steroid levels; vaccines: reduced response

Pregnancy and lactation

Glucocorticoids can affect the fetus (and induce parturition in late pregnancy in some species) — use only when clearly needed (e.g. adrenal crisis).

Monitoring

• Electrolytes (Na/K) and blood pressure (mineralocorticoid effect)
• Blood glucose; signs of GI ulceration/infection
• In adrenal crisis: clinical/haemodynamic response, electrolytes, glucose
• Taper when discontinuing after prolonged use

Toxicity and overdose

Short-term high-dose or overdose: mineralocorticoid effects (sodium/water retention, hypokalaemia, hypertension/oedema) plus glucocorticoid effects (hyperglycaemia, GI ulceration, immunosuppression). Prolonged use causes iatrogenic hyperadrenocorticism and HPA suppression (needing taper). Its mineralocorticoid activity makes it more prone to fluid/electrolyte effects than prednisolone/dexamethasone.

Management: No specific antidote. Reduce/withhold; correct electrolytes (hypokalaemia) and manage fluid retention/hypertension; taper after prolonged use to avoid adrenal crisis. Supportive care; manage GI ulceration with protectants.

Clinical pearls

• The "physiologic" steroid — closest to natural cortisol with BOTH gluco- and mineralocorticoid activity; the go-to IV steroid for Addisonian crisis and for replacement, and a low-dose option in vasopressor-refractory septic shock
• Short-acting with salt-retaining effect — great for acute/replacement use, but a poor choice for sustained anti-inflammatory therapy (use prednisolone/dexamethasone there)
• Watch sodium/water retention and hypokalaemia (its mineralocorticoid activity) more than with other steroids
• Taper after prolonged use (HPA suppression) and cover stress with extra steroid in Addisonian patients

Mechanism of action

Binds cytoplasmic glucocorticoid receptors to modulate gene transcription — broad anti-inflammatory/immunosuppressive effects, metabolic effects (gluconeogenesis, protein/fat catabolism), and permissive support of vascular tone/catecholamine responsiveness (relevant in shock). Uniquely among common veterinary steroids it also has substantial MINERALOCORTICOID activity (binds the aldosterone receptor), promoting renal sodium retention and potassium excretion — hence its value as a near-physiologic replacement and in adrenal crisis.

Formulations and products

• Injection 100 / 250 mg vial (Na succinate, IV)
• Tablet 10 / 20 mg (oral replacement)
• Topical cream 1 % (dermatologic)
• Solu-Cortef — 100 / 250 mg vial (Na succinate), IV injection (human-label)
• Hydrocortisone tablet / cream — 10 / 20 mg tablet; 1 % cream, Tablet / cream (human-label)

Storage

Injection: reconstitute per label, use promptly; 15–30 °C. Tablets/cream: 15–30 °C, dry, protect from light.

Before you use this dose

Reference doses for veterinary professionals. Confirm the dose against the product label, the patient’s condition, current guidance and local regulations before use; the attending veterinarian remains responsible for every clinical decision.

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Frequently asked questions