GMP certified Best Quality B.P Hydrocortisone Sodium Succinate for
Injection, 100mg/vial, 50vials box, anti-inflammatory
Hydrocortisone Sodium Succinate Sterile Powder is an anti-inflammatory glucocorticoid that contains
hydrocortisone sodium succinate as the active ingredient.
SOLU-CORTEF Sterile Powder is available in several packages for
intravenous or intramuscular administration.
100 mg Plain—Vials containing hydrocortisone sodium succinate
equivalent to 100 mg hydrocortisone, 0.8 mg monobasic sodium
phosphate anhydrous, 8.73 mg dibasic sodium phosphate dried.
SOLU-CORTEF 100 mg plain does not contain diluent
(Single-Dose Vial) in four strengths:
Each 2 mL
Each 2 mL
Each 4 mL
Each 8 mL
The diluent, as part of the packaging presentation for the
ACT-O-VIAL® system, is comprised of Water for Injection only, and
does not contain any preservative.
When necessary, the pH of each formula was adjusted with sodium
hydroxide so that the pH of the reconstituted solution is within
the USP specified range of 7 to 8.
The chemical name for hydrocortisone sodium succinate is
monosodium salt, (11β)- and its molecular weight is 484.52.
The structural formula is represented below:
Hydrocortisone sodium succinate is a white or nearly white,
odorless, hygroscopic amorphous solid. It is very soluble in water
and in alcohol, very slightly soluble in acetone, and insoluble in
Glucocorticoids, naturally occurring and synthetic, are
adrenocortical steroids that are readily absorbed from the
Naturally occurring glucocorticoids (hydrocortisone and cortisone),
which also have salt-retaining properties, are used as replacement
therapy in adrenocortical deficiency states. Their synthetic
analogs are primarily used for their anti-inflammatory effects in
disorders of many organ systems.
Hydrocortisone sodium succinate has the same metabolic and
anti-inflammatory actions as hydrocortisone. When given
parenterally and in equimolar quantities, the two compounds are
equivalent in biologic activity. The highly water-soluble sodium
succinate ester of hydrocortisone permits the immediate intravenous
administration of high doses of hydrocortisone in a small volume of
diluent and is particularly useful where high blood levels of
hydrocortisone are required rapidly. Following the intravenous
injection of hydrocortisone sodium succinate, demonstrable effects
are evident within one hour and persist for a variable period.
Excretion of the administered dose is nearly complete within 12
hours. Thus, if constantly high blood levels are required,
injections should be made every 4 to 6 hours. This preparation is
also rapidly absorbed when administered intramuscularly and is
excreted in a pattern similar to that observed after intravenous
Glucocorticoids cause profound and varied metabolic effects. In
addition, they modify the body's immune response to diverse
Indications and usages
When oral therapy is not feasible, and the strength, dosage form,
and route of administration of the drug reasonably lend the
preparation to the treatment of the condition, the intravenous or
intramusculat use of SOLU-CORTEF Sterile Powder is indicated as
Control of severe or incapacitating allergic conditions intractable
to adequate trials of conventional treatment in asthma, atopic
dermatitis, contact dermatitis, drug hypersensitivity reactions,
perennial or seasonal allergic rhinitis, serum sickness,
Bullous dermatitis herpetiformis, exfoliative erythroderma, mycosis
fungoides, pemphigus, severe erythema multiforme (Stevens-Johnson
Primary or secondary adrenocortical insufficiency (hydrocortisone
or cortisone is the drug of choice; synthetic analogs may be used
in conjunction with mineralocorticoids where applicable; in
infancy, mineralocorticoid supplementation is of particular
importance), congenital adrenal hyperplasia, hypercalcemia
associated with cancer, nonsuppurative thyroiditis.Gastrointestinal diseases
To tide the patient over a critical period of the disease in
regional enteritis (systemic therapy) and ulcerative colitis.
Acquired (autoimmune) hemolytic anemia, congenital (erythroid)
hypoplastic anemia (Diamond Blackfan anemia), idiopathic
thrombocytopenic purpura in adults (intravenous administration
only; intramuscular administration is contraindicated), pure red
cell aplasia, select cases of secondary thrombocytopenia.
Trichinosis with neurologic or myocardial involvement, tuberculous
meningitis with subarachnoid block or impending block when used
concurrently with appropriate antituberculous chemotherapy.
For the palliative management of leukemias and lymphomas.
Acute exacerbations of multiple sclerosis; cerebral edema
associated with primary or metastatic brain tumor, or craniotomy.
Sympathetic ophthalmia, uveitis and ocular inflammatory conditions
unresponsive to topical corticosteroids.
To induce diuresis or remission of proteinuria in idiopathic
nephrotic syndrome, or that due to lupus erythematosus.
Berylliosis, fulminating or disseminated pulmonary tuberculosis
when used concurrently with appropriate antituberculous
chemotherapy, idiopathic eosinophilic pneumonias, symptomatic
As adjunctive therapy for short-term administration (to tide the
patient over an acute episode or exacerbation) in acute gouty
arthritis; acute rheumatic carditis; ankylosing spondylitis;
psoriatic arthritis; rheumatoid arthritis, including juvenile
rheumatoid arthritis (selected cases may require low-dose
maintenance therapy). For the treatment of dermatomyositis,
temporal arteritis, polymyositis, and systemic lupus erythematosus.
Hydrocortisone Sodium Succinate Sterile Powder is contraindicated in systemic fungal infections and
patients with known hypersensitivity to the product and its
Intramuscular corticosteroid preparations are contraindicated for
idiopathic thrombocytopenic purpura.
Hydrocortisone Sodium Succinate Sterile Powder is contraindicated for intrathecal administration.
Reports of severe medical events have been associated with this
route of administration.
Serious Neurologic Adverse Reactions with Epidural Administration
Serious neurologic events, some resulting in death, have been
reported with epidural injection of corticosteroids. Specific
events reported include, but are not limited to, spinal cord
infarction, paraplegia, quadriplegia, cortical blindness, and
stroke. These serious neurologic events have been reported with and
without use of fluoroscopy. The safety and effectiveness of
epidural administration of corticosteroids have not been
established, and corticosteroids are not approved for this use.
Injection of Hydrocortisone Sodium Succinatemay result in dermal and/or subdermal changes forming depressions
in the skin at the injection site. In order to minimize the
incidence of dermal and subdermal atrophy, care must be exercised
not to exceed recommended doses in injections. Injection into the
deltoid muscle should be avoided because of a high incidence of
Rare instances of anaphylactoid reactions have occurred in patients
receiving corticosteroid therapy/
Increased dosage of rapidly acting corticosteroids is indicated in
patients on corticosteroid therapy subjected to any unusual stress
before, during, and after the stressful situation.
Results from one multicenter, randomized, placebo-controlled study
with methylprednisolone hemisuccinate, an IV corticosteroid, showed
an increase in early (at 2 weeks) and late (at 6 months) mortality
in patients with cranial trauma who were determined not to have
other clear indications for corticosteroid treatment. High doses of
systemic corticosteroids, including SOLU-CORTEF, should not be used
for the treatment of traumatic brain injury.
Average and large doses of corticosteroids 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. Dietary salt
restriction and potassium supplementation may be necessary. All
corticosteroids increase calcium excretion.
Literature reports suggest an apparent association between use of
corticosteroids and left ventricular free wall rupture after a
recent myocardial infarction; therefore, therapy with
corticosteroids should be used with great caution in these
Hypothalamic-pituitary adrenal (HPA) axis suppression. Cushing's
syndrome, and hyperglycemia. Monitor patients for these conditions
with chronic use. Corticosteroids can produce reversible HPA axis
suppression with the potential for glucocorticosteroid
insufficiency after withdrawal of treatment. Drug induced secondary
adrenocortical insufficiency may be minimized by gradual reduction
of dosage. This type of relative insufficiency may persist for
months after discontinuation of therapy; therefore, in any
situation of stress occurring during that period, hormone therapy
should be reinstituted.nfections
Patients who are on corticosteroids are more susceptible to
infections than are healthy individuals. There may be decreased
resistance and inability to localize infection when corticosteroids
are used. Infection with any pathogen (viral, bacterial, fungal,
protozoan or helminthic) in any location of the body may be
associated with the use of corticosteroids alone or in combination
with other immunosuppressive agents.
These infections may be mild, but can be severe and at times fatal.
With increasing doses of corticosteroids, the rate of occurrence of
infectious complications increases. Corticosteroids may also mask
some signs of current infection. Do not use intra-articularly,
intrabursally or for intratendinous administration for local effect in the presence of acute local infection.
Corticosteroids may exacerbate systemic fungal infections and
therefore should not be used in the presence of such infections
unless they are needed to control drug reactions. There have been
cases reported in which concomitant use of amphotericin B and
hydrocortisone was followed by cardiac enlargement and congestive
Latent disease may be activated or there may be an exacerbation of
intercurrent infections due to pathogens, including those caused by
Amoeba, Candida, Cryptococcus, Mycobacterium, Nocardia,
Pneumocystis, and Toxoplasma.
It is recommended that latent amebiasis or active amebiasis be
ruled out before initiating corticosteroid therapy in any patient
who has spent time in the tropics or in any patient with
Similarly, corticosteroids should be used with great care in
patients with known or suspected Strongyloides (threadworm)
infestation. In such patients, corticosteroid-induced
immunosuppression may lead to Strongyloides hyperinfection and
dissemination with widespread larval migration, often accompanied
by severe enterocolitis and potentially fatal gram-negative
Corticosteroids should not be used in cerebral malaria. There is
currently no evidence of benefit from steroids in this condition.
The use of corticosteroids in active tuberculosis should be
restricted to those cases of fulminating or disseminated
tuberculosis in which the corticosteroid is used for the management
of the disease in conjunction with an appropriate antituberculous
If corticosteroids are indicated in patients with latent
tuberculosis or tuberculin reactivity, close observation is
necessary as reactivation of the disease may occur. During
prolonged corticosteroid therapy, these patients should receive
Administration of live or live, attenuated vaccines is
contraindicated in patients receiving immunosuppressive doses of
corticosteroids. Killed or inactivated vaccines may be
administered. However, the reponse to such vaccines cannot be
predicted.Immunization procedures may be undertaken in patients who
are receiving corticosteroids as replacement therapy (e.g., for
Chicken pox and measles can have a more serious or even fatal
course in pediatric and adult patients on corticosteroids. In
pediatric and adult patients who have not had these diseases,
particular care should be taken to avoid exposure. The contribution
of the underlying disease and/or prior corticosteroid treatment to
the risk is not known. If exposed to chicken pox, prophylaxis with
varicella zoster immune globulin (VZIG) may be indicated. If
exposed to measles, prophylaxis with immunoglobulin (IG) may be
indicated. (See the respective package inserts for complete VZIG
and IG prescribing information.) If chicken pox develops, treatment
with antiviral agents should be considered.
Reports of severe medical events have been associated with the
intrathecal route of administration.
Use of corticosteroids may produce posterior subcapsular cataracts,
glaucoma with possible damage to the optic nerves, and may enhance
the establishment of secondary ocular infections due to bacteria,
fungi, or viruses. The use of oral corticosteroids is not
recommended in the treatment of optic neuritis and may lead to an
increase in the risk of new episodes. Corticosteroids should be
used cautiously in patients with ocular herpes simplex because of
corneal perforation. Corticosteroids should not be used in active
ocular herpes simplex.
This product, like many other steroid formulations, is sensitive to
heat. Therefore, it should not be autoclaved when it is desirable
to sterilize the exterior of the vial. The lowest possible dose of
corticosteroid should be used to control the condition under
treatment. When reduction in dosage is possible, the reduction
should be gradual.
Since complications of treatment with glucocorticoids are dependent
on the size of the dose and the duration of treatment, a
risk/benefit decision must be made in each individual case as to
dose and duration of treatment and as to whether daily or
intermittent therapy should be used.
Kaposi's sarcoma has been reported to occur in patients receiving
corticosteroid therapy, most often for chronic conditions.
Discontinuation of corticosteroids may result in clinical
As sodium retention with resultant edema and potassium loss may
occur in patients receiving corticosteroids, these agents should be
used with caution in patients with congestive heart failure,
hypertension, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency may be
minimized by gradual reduction of dosage. This type of relative
insufficiency may persist for months after discontinuation of
therapy; therefore, in any situation of stress occurring during
that period, hormone therapy should be reinstituted. Since
mineralocorticoid secretion may be impaired, salt and/or a
mineralocorticoid should be administered concurrently. Metabolic
clearance of corticosteroids is decreased in hypothyroid patients
and increased in hyperthyroid patients. Changes in thyroid status
of the patient may necessitate adjustment in dosage.
Steroids should be used with caution in active or latent peptic
ulcers, diverticulitis, fresh intestinal anastomoses, and
non-specific ulcerative colitis, since they may increase the risk
of a perforation. Signs of peritoneal irritation following
gastrointestinal perforation in patients receiving corticosteroids
may be minimal or absent.
There is an enhanced effect due to decreased metabolism of
corticosteroids in patients with cirrhosis.
Corticosteroids decrease bone formation and increase bone
resorption both through their effect on calcium regulation (e.g.,
decreasing absorption and increasing excretion) and inhibition of
osteoblast function. This, together with a decrease in the protein
matrix of the bone secondary to an increase in protein catabolism,
and reduced sex hormone production, may lead to inhibition of bone
growth in pediatric patients and the development of osteoporosis at
any age. Special consideration should be given to patients at
increased risk of osteoporosis (i.e., postmenopausal women) before
initiating corticosteroid therapy.
Local injection of a steroid into a previously infected site is not
Although controlled clinical trials have shown corticosteroids to
be effective in speeding the resolution of acute exacerbations of
multiple sclerosis, they do not show that corticosteroids affect
the ultimate outcome or natural history of the disease. The studies
do show that relatively high doses of corticosteroids are necessary
to demonstrate a significant effect.
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 (e.g., pancuronium). This acute myopathy is generalized, may
involve ocular and respiratory muscles, and may result in
quadriparesis. Elevation of creatine kinase may occur. Clinical
improvement or recovery after stopping corticosteroids may require
weeks to years.
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.
Intraocular pressure may become elevated in some individuals. If
steroid therapy is continued for more than 6 weeks, intraocular
pressure should be monitored.
Information for Patients
Patients should be warned not to discontinue the use of
corticosteroids abruptly or without medical supervision, to advise
any medical attendants that they are taking corticosteroids, and to
seek medical advice at once should they develop fever or other
signs of infection.
Persons who are on corticosteroids should be warned to avoid
exposure to chicken pox or measles. Patients should also be advised
that if they are exposed, medical advice should be sought without
Aminoglutethimide may lead to a loss of corticosteroid-induced
Amphotericin B injection and potassium-depleting agents
When corticosteroids are administered concomitantly with
potassium-depleting agents (e.g., amphotericin B, diuretics),
patients should be observed closely for development of hypokalemia.
There have been cases reported in which concomitant use of
amphotericin B and hydrocortisone was followed by cardiac
enlargement and congestive heart failure.
Macrolide antibiotics have been reported to cause a significant
decrease in corticosteroid clearance
Concomitant use of anticholinesterase agents and corticosteroids
may produce severe weakness in patients with myasthenia gravis. If
possible, anticholinesterase agents should be withdrawn at least 24
hours before initiating corticosteroid therapy.
Coadministration of corticosteroids and warfarin usually results in
inhibition of response to warfarin, although there have been some
conflicting reports. Therefore, coagulation indices should be
monitored frequently to maintain the desired anticoagulant effect.
Because corticosteroids may increase blood glucose concentrations,
dosage adjustments of antidiabetic agents may be required.
Serum concentrations of isoniazid may be decreased.
Cholestyramine may increase the clearance of corticosteroids.
Increased activity of both cyclosporine and corticosteroids may
occur when the two are used concurrently. Convulsions have been
reported with this concurrent use.
Patients on digitalis glycosides may be at increased risk of
arrhythmias due to hypokalemia.
Estrogens, including oral contraceptives
Estrogens may decrease the hepatic metabolism of certain
corticosteroids, thereby increasing their effect.
Hepatic Enzyme Inducers (e.g., barbiturates, phenytoin,
Drugs that induce cytochrome P450 3A4 enzyme activity may enhance
the metabolism of corticosteroids and require that the dosage of
the corticosteroid be increased.
Hepatic Enzyme Inhibitors (e.g., ketoconazole, macrolide
antibiotics such as erythromycin and troleandomycin)
Drugs that inhibit cytochrome P450 3A4 have the potential to result
in increased plasma concentrations of corticosteroids.
Ketoconazole has been reported to significantly decrease the
metabolism of certain corticosteroids by up to 60%, leading to an
increased risk of corticosteroid side effects.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Concomitant use of aspirin (or other nonsteroidal anti-inflammatory
agents) and corticosteroids increases the risk of gastrointestinal
side effects. Aspirin should be used cautiously in conjunction with
corticosteroids in hypoprothrombinemia. The clearance of
salicylates may be increased with concurrent use of
Corticosteroids may suppress reactions to skin tests.
Patients on prolonged corticosteroid therapy may exhibit a
diminished response to toxoids and live or inactivated vaccines due
to inhibition of antibody response. Corticosteroids may also
potentiate the replication of some organisms contained in live
attenuated vaccines. Routine administration of vaccines or toxoids
should be deferred until corticosteroid therapy is discontinued if
Carcinogenesis, Mutagenesis, Impairment of Fertility
No adequate studies have been conducted in animals to determine
whether corticosteroids have a potential for carcinogenesis or
Steroids may increase or decrease motility and number of
spermatozoa in some patients.
Pregnancy Category C
Corticosteroids have been shown to be teratogenic in many species
when given in doses equivalent to the human dose. Animal studies in
which corticosteroids have been given to pregnant mice, rats, and
rabbits have yielded an increased incidence of cleft palate in the
offspring. There are no adequate and well-controlled studies in
pregnant women. Corticosteroids should be used during pregnancy
only if the potential benefit justifies the potential risk to the
fetus. Infants born to mothers who have received corticosteroids
during pregnancy should be carefully observed for signs of
Systemically administered corticosteroids appear in human milk and
could suppress growth, interfere with endogenous corticosteroid
production, or cause other untoward effects. Because of the
potential for serious adverse reactions in nursing infants from
corticosteroids, a decision should be made whether to continue
nursing or discontinue the drug, taking into account the importance
of the drug to the mother.
The efficacy and safety of corticosteroids in the pediatric
population are based on the well-established course of effect of
corticosteroids, which is similar in pediatric and adult
populations. Published studies provide evidence of efficacy and
safety in pediatric patients for the treatment of nephrotic
syndrome (>2 years of age) and aggressive lymphomas and
leukemias (>1 month of age). Other indications for pediatric use
of corticosteroids (e.g., severe asthma and wheezing) are based on
adequate and well-controlled trials conducted in adults, on the
premises that the course of the diseases and their pathophysiology
are considered to be substantially similar in both populations.
The adverse effects of corticosteroids in pediatric patients are
similar to those in adults . Like adults, pediatric patients should
be carefully observed with frequent measurements of blood pressure,
weight, height, intraocular pressure, and clinical evaluation for
the presence of infection, psychosocial disturbances,
thromboembolism, peptic ulcers, cataracts, and osteoporosis.
Pediatric patients who are treated with corticosteroids by any
route, including systemically administered corticosteroids, may
experience a decrease in their growth velocity. This negative
impact of corticosteroids on growth has been observed at low
systemic doses and in the absence of laboratory evidence of HPA
axis suppression (i.e., cosyntropin stimulation and basal cortisol
plasma levels). Growth velocity may therefore be a more sensitive
indicator of systemic corticosteroid exposure in pediatric patients
than some commonly used tests of HPA axis function. The linear
growth of pediatric patients treated with corticosteroids should be
monitored, and the potential growth effects of prolonged treatment
should be weighed against clinical benefits obtained and the
availability of treatment alternatives. In order to minimize the
potential growth effects of corticosteroids, pediatric patients
should be titrated to the lowest effective dose.
Clinical studies did not include sufficient numbers of subjects
aged 65 and over to determine whether they respond differently from
younger subjects. Other reported clinical experience has not
identified differences in responses between the elderly and younger
patients. In general, dose selection for an elderly patient should
be cautious, usually starting at the low end of the dosing range,
reflecting the greater frequency of decreased hepatic, renal, or
cardiac function, and of concomitant disease or other drug therapy.
The following adverse reactions have been reported with SOLU-CORTEF
or other corticosteroids:
Allergic reactions: Allergic or hypersensitivity reactions,
anaphylactoid reaction, anaphylaxis, angioedema.
Cardiovascular: Bradycardia, cardiac arrest, cardiac arrhythmias,
cardiac enlargement, circulatory collapse, congestive heart
failure, fat embolism, hypertension, hypertrophic cardiomyopathy in
premature infants, myocardial rupture following recent myocardial
infarction, pulmonary edema, syncope, tachycardia, thromboembolism,
Dermatologic: Acne, allergic dermatitis, burning or tingling
(especially in the perineal area, after intravenous injection),
cutaneous and subcutaneous atrophy, dry scaly skin, ecchymoses and
petechiae, edema, erythema, hyperpigmentation, hypopigmentation,
impaired wound healing, increased sweating, rash, sterile abscess,
striae, suppressed reactions to skin tests, thin fragile skin,
thinning scalp hair, urticaria.
Endocrine: Decreased carbohydrate and glucose tolerance,
development of cushingoid state, glycosuria, hirsutism,
hypertrichosis, increased requirements for insulin or oral
hypoglycemic agents in diabetes, manifestations of latent diabetes
mellitus, menstrual irregularities, secondary adrenocortical and
pituitary unresponsiveness (particularly in times of stress, as in
trauma, surgery, or illness), suppression of growth in pediatric
Fluid and electrolyte disturbances: Congestive heart failure in
susceptible patients, fluid retention, hypokalemic alkalosis,
potassium loss, sodium retention.
Gastrointestinal: Abdominal distention, bowel/bladder dysfunction
(after intrathecal administration), elevation in serum liver enzyme
levels (usually reversible upon discontinuation), hepatomegaly,
increased appetite, nausea, pancreatitis, peptic ulcer with
possible perforation and hemorrhage, perforation of the small and
large intestine (particularly in patients with inflammatory bowel
disease), ulcerative esophagitis.
Metabolic: Negative nitrogen balance due to protein catabolism.
Musculoskeletal: Aseptic necrosis of femoral and humeral heads,
Charcot-like arthropathy, loss of muscle mass, muscle weakness,
osteoporosis, pathologic fracture of long bones, postinjection
flare (following intra-articular use), steroid myopathy, tendon
rupture, vertebral compression fractures.
Neurologic/Psychiatric: Convulsions, depression, emotional
instability, euphoria, headache, increased intracranial pressure
with papilledema (pseudotumor cerebri) usually following
discontinuation of treatment, insomnia, mood swings, neuritis,
neuropathy, paresthesia, personality changes, psychic disorders,
vertigo. Arachnoiditis, meningitis, paraparesis/paraplegia, and
sensory disturbances have occurred after intrathecal administration
Ophthalmic: Exophthalmoses, glaucoma, increased intraocular
pressure, posterior subcapsular cataracts, rare instances of
blindness associated with periocular injections.
Other: Abnormal fat deposits, decreased resistance to infection,
hiccups, increased or decreased motility and number of spermatozoa,
injection site infections following non-sterile administration ,
malaise, moon face, weight gain.
Treatment of acute overdosage is by supportive and symptomatic
therapy. For chronic overdosage in the face of severe disease
requiring continuous steroid therapy, the dosage of the
corticosteroid may be reduced only temporarily, or alternate day
treatment may be introduced.
Dosage and Administarations
Because of possible physical incompatilitbilites, Hydrocortisone Sodium Succinate should not be diluted or mixed with other solutions.
Parenteral drug products should be inspected visually for
particulate matter and discoloration prior to administration,
whenever solution and container permit.
This preparation may be administered by intravenous injection, by
intravenous infusion, or by intramuscular injection, the preferred
method for initial emergency use being intravenous injection.
Following the initial emergency period, consideration should be
given to employing a longer acting injectable preparation or an
Therapy is initiated by administering Hydrocortisone Sodium Succinate Sterile Powder intravenously over a period of 30 seconds (e.g., 100
mg) to 10 minutes (e.g., 500 mg or more). In general, high dose
corticosteroid therapy should be continued only until the patient's
condition has stabilized, usually not beyond 48 to 72 hours. When
high dose hydrocortisone therapy must be continued beyond 48–72
hours, hypernatremia may occur. Under such circumstances, it may be
desirable to replace Hydrocortisone Sodium Succinate with a corticoid such as methylprednisolone sodium succinate which
causes little or no sodium retention.
The initial dose of Hydrocortisone Sodium Succinate Sterile Powder is 100 mg to 500 mg, depending on the specific
disease entity being treated. However, in certain overwhelming,
acute, life-threatening situations, administration in dosages
exceeding the usual dosages may be justified and may be in
multiples of the oral dosages.
This dose may be repeated at intervals of 2, 4, or 6 hours as
indicated by the patient's response and clinical condition.
It Should Be Emphasized that Dosage Requirements Are Variable and
Must Be Individualized on the Basis of the Disease Under Treatment
and the Response of the Patient. After a favorable response is noted, the proper maintenance dosage
should be determined by decreasing the initial drug dosage in small
decrements at appropriate time intervals until the lowest dosage
that maintains an adequate clinical response is reached. Situations
that may make dosage adjustments necessary are changes in clinical
status secondary to remissions or exacerbations in the disease
process, the patient's individual drug responsiveness, and the
effect of patient exposure to stressful situations not directly
related to the disease entity under treatment. In this latter
situation, it may be necessary to increase the dosage of the
corticosteroid for a period of time consistent with the patient's
condition. If after long-term therapy the drug is to be stopped, it
is recommended that it be withdrawn gradually rather than abruptly.
In the treatment of acute exacerbations of multiple sclerosis,
daily doses of 800 mg of hydrocortisone for a week followed by 320
mg every other day for one month are recommended.
In pediatric patients, the initial dose of hydrocortisone may vary
depending on the specific disease entity being treated. The range
of initial doses is 0.56 to 8 mg/kg/day in three or four divided
doses (20 to 240 mg/m2bsa/day). For the purpose of comparison, the
following is the equivalent milligram dosage of the various
These dose relationships apply only to oral or intravenous
administration of these compounds. When these substances or their
derivatives are injected intramuscularly or into joint spaces,
their relative properties may be greatly altered.
Preparation of Solutions 100 mg Plain
For intravenous or intramuscular injection, prepare solution by
aseptically adding not more than 2 mL of Bacteriostatic Water for
Injection or Bacteriostatic Sodium Chloride Injection to the
contents of one vial. For intravenous infusion, first prepare
solution by adding not more than 2 mL of Bacteriostatic Water for
Injection to the vial; this solution may then be added to 100 to
1000 mL of the following: 5% dextrose in water (or isotonic saline
solution or 5% dextrose in isotonic saline solution if patient is
not on sodium restriction).
DIRECTIONS FOR USING THE ACT-O-VIAL SYSTEM
Press down on plastic activator to force diluent into the lower
Gently agitate to effect solution.
Remove plastic tab covering center of stopper.
Sterilize top of stopper with a suitable germicide.
Insert needle squarely through center of stopper until tip is just
visible. Invert vial and withdraw dose.
Further dilution is not necessary for intravenous or intramuscular
injection. For intravenous infusion, first prepare solution as just
described. The 100 mg solution may then be added to 100 to 1000 mL
of 5% dextrose in water (or isotonic saline solution or 5% dextrose
in isotonic saline solution if patient is not on sodium
restriction). The 250 mg solution may be added to 250 to 1000 mL,
the 500 mg solution may be added to 500 to 1000 mL, and the 1000
mgsolution to 1000 mL of the same diluents. In cases where
administration of a small volume of fluid is desirable, 100 mg to
3000 mg of SOLU-CORTEF may be added to 50 mL of the above diluents.
The resulting solutions are stable for at least 4 hours and may be
administered either directly or by IV piggyback.
When reconstituted as directed, pH's of the solutions range from 7
to 8 and the tonicities are: 100 mg ACT-O-VIAL, 0.36 osmolar; 250
mg ACT-O-VIAL, 500 mg ACT-O-VIAL, and 1000 mg ACT-O-VIAL, 0.57
osmolar. (Isotonic saline=0.28 osmolar.)