ADMINISTRATION ROUTES:
PO, NG
ALTERNATIVE NAMES:
Apo-Prednisone
ICU INDICATIONS:
- Relative corticosteroid insufficiency in patients with severe septic shock
- Adrenal insufficiency
- Steroid responsive inflammatory conditions
PRESENTATION AND ADMINISTRATION:
PO / NG:
Prednisone sodium phosphate liquid 5 mg/mL Apo-prednisone 20 mg (pink), 20 mg (white), 5 mg, 1 mg
DOSAGE:
PO:
10 - 100 mg OD mane, or as divided dose
DOSAGE IN RENAL FAILURE AND RENAL REPLACEMENT THERAPY:
Dose as in normal renal function
DOSAGE IN PAEDIATRICS:
PO:
Acute asthma:
0.5 - 1 mg/kg for 24 hours, then every 12 hours for two doses, then 1 mg/kg OD
Moderate croup:
1 mg/kg stat. Can repeat in 12 hours
Severe croup:
4 mg/kg stat then 1 mg/kg TDS
CLINICAL PHARMACOLOGY:
Prednisone is a synthetic steroid hormone which has glucocorticoid and mineralocorticoid properties. Prednisone has no direct biological effects as it is a prodrug, requiring hepatic conversion into prednisolone before it is pharmacologically active. Prednisolone then binds to glucocorticoid receptors.
Prednisone has a half-life of 2 - 3 hours and is cleared by hepatic metabolism, with metabolites excreted in bile and urine.
The dose equivalence for 1 mg prednisone is hydrocortisone 4 mg (glucocorticoid activity) & 0.8 mg (mineralocorticoid activity)
CONTRAINDICATIONS:
- Systemic fungal infections
WARNINGS:
Steroid withdrawal:
As with all steroid treatment, before sudden cessation, dose and duration of treatment as well as the course of the underlying disease for which steroids were commenced should be taken into account. Adrenal suppression (decreased endogenous production of cortisol in the presence of exogenous steroids) may take some time to recover (weeks to months), resulting in physiological effects of steroid withdrawal. Dose reduction to physiological doses is recommended prior to cessation for patients considered at risk of steroid withdrawal.
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 (such as myasthenia gravis), or in patients receiving concomitant therapy with neuromuscular blocking drugs. This acute myopathy is generalised, 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 to 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.
PRECAUTIONS:
General:
There is an enhanced effect of corticosteroids in patients with hypothyroidism and in those with cirrhosis.
Psychological derangementmay 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
IMPORTANT DRUG INTERACTIONS IN ICU:
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.
ADVERSE REACTIONS:
Fluid and Electrolyte Disturbances:
Sodium retention, fluid retention, congestive heart failure in susceptible patients, potassium loss, hypokalemic alkalosis, hypertension
Musculoskeletal:
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
Gastrointestinal:
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
Dermatologic:
Impaired wound healing, thin fragile skin, petechiae and ecchymoses, facial erythema, increased sweating. May suppress reactions to skin tests
Neurological:
Convulsions, increased intracranial pressure with papilloedema (pseudotumour cerebri) usually after treatment, vertigo, headache
Endocrine:
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