The Dept of Anaesthesia & Intensive Care, CUHK thanks

for an unrestricted education grant
BASIC instructor/provider course, Hong Kong, July 2nd-4th
Other upcoming courses
Home Feedback Contents


Up ACE inhibitors Adenosine Anaphylaxis Antiarrhythmics Antibacterials Anticoagulants Anti-fibrinolytics Antifungals Antiplatelet drugs Anti-virals Beta2 agonists Ca antagonists Corticosteroids Erythropoietin Fosphenytoin Hydralazine Immunosuppressants Inotropes & vasopressors Insulin IV immunoglobulin Labetalol Mannitol Metoclopramide N-acetylcysteine Nesiritide Neuroleptic malignant syn Nitric oxide Nitroprusside Proton pump inhibitors Sedatives Serotonin syndrome Sucralfate Suxamethonium Theophylline Vasopressin


Mechanism of action

  • enter cells where they combine with steroid receptors in cytoplasm
  • combination enters nucleus where it controls synthesis of protein, including enzymes that regulate vital cell activities over a wide range of metabolic functions including all aspects of inflammation
  • formation of a protein that inhibits the enzyme phospholipase A2 which is needed to allow the supply of arachidonic acid. Latter is essential for the formation of inflammatory mediators
  • also act on cell membranes to alter ion permeability
  • also modify the production of neurohormones


Important to distinguish between physiological effects (replacement therapy) and pharmacological effects (occur at higher doses)


  • Na retention by renal tubule
  • increased K excretion in urine


  • CHO metabolism: increased gluconeogenesis, ± peripheral glucose uptake may be decreased with resultant hyperglycaemia ± glycosuria
  • protein metabolism: anabolism is decreased but catabolism continues unabated or is increased resulting in negative N balance and muscle wasting. Osteoporosis occurs, growth slows in children, skin atrophies (together with increased capillary fragility leads to bruising and striae), healing and fibrosis delayed
  • fat deposition: increased on shoulders, face and abdomen
  • inflammatory response depressed
  • allergic response depressed
  • antibody production reduced by large doses
  • lymphoid tissue reduced (including leukaemic lymphocytes)
  • decreased eosinophils
  • renal urate excretion increased
  • euphoria or psychotic states may occur. ? due to CNS electrolyte changes
  • anti-vitamin D action
  • reduction of hypercalcaemia (chiefly where this is due to increased absorption from gut: vit D intoxication, sarcoidosis)
  • increased urinary Ca excretion. Renal stones may form
  • growth reduction where new cells are being added (eg in children) but not where they are replacing cells as in adult tissues
  • suppression of HPA axis. NB steroid suppressed adrenal continues to secrete aldosterone
Normal daily secretion of hydrocortisone is 10-30 mg. Exogenous daily dose that completely suppresses cortex is 40-80 mg (or prednisolone 10-20 mg).

Individual steroids

Relative potencies





















  • prednisolone is standard choice for anti-inflammatory therapy. Can be given orally or IM
  • methylprednisolone used for IV pulsed therapy
  • dexamethasone longer acting.
  • fludrocortisone used to replace aldosterone where the adrenal cortex has been destroyed
  • beclomethasone and budesonide used by inhalation for asthma. About 90% of inhalation dose is swallowed and inactivated by first-pass hepatic metabolism (steroids listed above are protected from this by protein binding). The rest, which is absorbed from the mouth and lungs gives very low systemic plasma concentrations. Although risk of HPA axis suppression is very low it can happen.


Administration: PO/IM/IV/intra-articular/topical/inhaled. Absorption after oral administration is rapid. Maximum biological effect seen after 2-8 h

Distribution: high plasma protein binding (95% in case of hydrocortisone) to transcortin and when this is saturated to albumin (80% in the case of hydrocortisone). Concentration of transcortin is increased by oestrogens (eg pregnancy, oral contraceptives). In patients with very low serum albumin doses should be reduced due to reduced binding capacity

Elimination: hepatic and renal.t1/2 of most steroids 1-3 h. Prolonged in renal and hepatic disease and shortened by hepatic enzyme induction to an extent that may be clinically important

Adverse effects

In general serious unwanted effects are unlikely if daily dose is < 50 mg hydrocortisone or 10mg of prednisolone or equivalent

  • iatrogenic Cushings
  • avascular necrosis of bone
  • depression and psychosis
  • peptic ulceration
  • others include cataract (chronic use), glaucoma (prolonged use of eye drops), raised ICP and convulsions, blood hypercoagulability, menstrual disorders, fever
  • immunosuppression
  • HPA axis suppression: dependent on steroid used, dose, duration of administration and time of administration. Single morning dose of <20mg prednisolone does not usually cause suppression while 5mg in evening suppresses early morning activation of HPA axis

Use in pregnancy

  • teratogenic in animals
  • ? relationship between high dose steroids and cleft palate and other fetal abnormalities
  • adrenal insufficiency due to HPA axis suppression in newborn only occurs with high maternal doses
  • keep doses as low as possible in pregnancy
  • avoid fluorinated steroids (eg dexamethasone) as they are more teratogenic in animals

Treatment of intercurrent illness

  • maximum stress-induced output of cortisol is 200-300 mg/day
  • production following surgery tends to be much less. Based on normal cortisol production rates the recommended daily doses of hydrocortisone equivalent for different categories of surgery are:

Daily dose


Minor (eg hernia repair)

25 mg

1 day

Intermediate (eg cholecystectomy, colectomy, joint replacement)

50-75 mg

2 days

Major (eg oesophagectomy, cardiac surgery requiring CPB)

100-150 mg

2-3 days

If the patients maintenance dose exceeds recommended dose to cover surgical stress there is no evidence that any dose alteration is necessary and patient should continue to receive maintenance dose over the perioperative period.

In the case of perioperative complications continued glucocorticoid administration consistent with the postoperative stress response is appropriate

Further reading

Laurence DR, Bennett PN. Clinical Pharmacology, 7th ed, 1992

Chin R, Eagerton DC, Salem M. Corticosteroids. In Chernow B (ed). The pharmacological approach to the critically ill patient, 3rd ed, 1994 

© Charles Gomersall December 1999

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
Copyright policy    Contributors