1 vial 100mg


1 tablet 20mg

20 cents

  1. Relative corticosteroid insufficiency in patients with severe septic shock

  2. Adrenal insufficiency

  3. Steroid responsive inflammatory conditions

100mg/2ml vial plus benzyl alcohol diluent
Reconstitute by pressing down on the plastic activator. This forces the diluent into the lower compartment. Gently agitate to dissolve powder. To withdraw solution, remove the plastic tab covering the stopper. Wipe the top of the stopper with an alcohol swab. Insert drawing up needle through the centre of the stopper until the tip is just visible. Invert vial and withdraw dose.
Reconstituted solutions and solutions with concentrations not exceeding 1mg/ml are stable for up to 24 hours.
Compatible with the following IV fluids:
Normal saline 5% Dextrose Glucose and sodium chloride
Can be administered by infusion; however, preferred method in our ICU is administration by direct IV injection. Reconstituted solution is generally injection undiluted by slow IV injection.

Hydrocortisone 5mg and 20mg tablets (white)


Usual dose is 50mg 6 hourly for septic shock; however, many different dosage regimens exist for various indications (for most ICU indications 50mg 6 hourly is an appropriate dose)


0.5-4mg/kg 6 hourly

Dose as in normal renal function

Hydrocortisone is a naturally occurring steroid hormone which has glucocorticoid and mineralocorticoid properties


  1. The use of hydrocortisone sodium succinate sterile powder is contraindicated in premature infants because the 100, 250, 500and 1000 mg ACT-O-VIAL System contain benzyl alcohol. Benzyl alcohol has been reported to be associated with a fatal "Gasping Syndrome" in premature infants.

Steroid induced myopathy:
An acute myopathy has been observed with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular blocking drugs. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevations of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
Adrenal-insufficiency due to steroids:
In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting corticosteroids before, during, and after the stressful situation is indicated. Infections:
Corticosteroids may mask some signs of infection, and new infections may appear during their use.
Blood pressure:
Average and large doses of hydrocortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses.

There is an enhanced effect of corticosteroids in patients with hypothyroidism and in those with cirrhosis.
Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.

Laboratory Tests
No tests in addition to routine ICU tests are required

Drug/Laboratory Test Interactions
None known

The pharmacokinetic interactions listed below are potentially clinically important. Drugs that induce hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response.

Fluid and Electrolyte Disturbances:
Sodium retention; fluid retention; congestive heart failure in susceptible patients; potassium loss; hypokalemic alkalosis; hypertension.

Muscle weakness; steroid myopathy, loss of muscle mass; osteoporosis; tendon rupture, particularly of the Achilles tendon; vertebral compression fractures; aseptic necrosis of femoral and humeral heads; pathologic fracture of long bones.

Peptic ulcer with possible perforation and haemorrhage; pancreatitis; abdominal distention; ulcerative oesophagitis; increases in alanine transaminase (ALT, SGPT), aspartate transaminase (AST, SGOT) and alkaline phosphatase have been observed following corticosteroid treatment.
Impaired wound healing; thin fragile skin; petechiae and ecchymoses; facial erythema; increased sweating; may suppress reactions to skin tests.
Convulsions; increased intracranial pressure with papilloedema (pseudotumour cerebri) usually after treatment; vertigo; headache.
Menstrual irregularities; development of Cushingoid state; suppression of growth in children; secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery or illness; decreased carbohydrate tolerance; manifestations of latent diabetes mellitus; increased requirements for insulin or oral hypoglycaemic agents in diabetics.