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Depo-Medrone with Lidocaine


Methyprednisolone BP 4%, Lidocaine Hydrochloride BP 1%


White, sterile aqueous suspension for injection




Therapeutic indications
Corticosteroid (glucocorticoid). Depo-Medrone with Lidocaine is indicated in
conditions requiring a glucocorticoid effect: e.g. anti-inflammatory or antirheumatic. It is recommended for local use where the added anaesthetic effect
would be considered advantageous.
Depo-Medrone with Lidocaine may be used as follows:
Intra-articular administration
Rheumatoid arthritis
Osteo-arthritis with an inflammatory component
Periarticular administration
Intrabursal administration
Subacromial bursitis
Prepatellar bursitis
Olecranon bursitis
Tendon sheath administration

Therapy with Depo-Medrone with Lidocaine does not obviate the need for the
conventional measures usually employed. Although this method of treatment
will ameliorate symptoms, it is in no sense a cure and the hormone has no
effect on the cause of the inflammation.


Posology and method of administration
Depo-Medrone with Lidocaine should not be mixed with any other preparation
as flocculation of the product may occur. Parenteral drug products should be
inspected visually for particulate matter and discoloration prior to
administration whenever suspension and container permit. Depo-Medrone
with Lidocaine may be used by any of the following routes: intra-articular,
periarticular, intrabursal, and into the tendon sheath. It must not be used by the
intrathecal or intravenous routes (see Contra-indications and Side-effects)
Intra-articular: Rheumatoid arthritis, osteo-arthritis. The dose of DepoMedrone with Lidocaine depends on the size of the joint and the severity of
the condition. Repeated injections, if needed, may be given at intervals of one
to five or more weeks depending upon the degree of relief obtained from the
initial injection. A suggested dosage guide is: large joint (knee, ankle,
shoulder), 0.5 - 2 ml (20 - 80 mg of steroid); medium joint (elbow, wrist), 0.25
- 1 ml (10 - 40mg of steroid); small joint (metacarpophalangeal,
interphalangeal, stemoclavicular, acromioclavicular), 0.1 -0.25 ml (4 - 10 mg
of steroid).
Periarticular: Epicondylitis. Infiltrate 0.1 - 0.75 ml (4 - 30 mg of steroid) into
the affected area.
Intrabursal: Subdeltoid bursitis, prepatellar bursitis, olecranon bursitis. For
administration directly into bursae, 0.1 - 0.75 ml (4 - 30 mg of steroid). In
most acute cases, repeat injections are not needed.
Into the tendon sheath: Tendinitis, tenosynovitis, epicondylitis. For
administration directly into the tendon sheath, 0.1 - 0.75 ml (4 - 30 mg of
steroid). In recurrent or chronic conditions, repeat injections may be necessary.
For infants and children, the recommended dosage should be reduced, but
dosage should be governed by the severity of the condition rather than by strict
adherence to the ratio indicated by age or body weight.
When used according to instructions, there is no information to suggest that a
change in dosage is warranted in the elderly. However, treatment of elderly
patients, particularly if long-term, should be planned bearing in mind the more
serious consequences of the common side-effects of corticosteroids in old age
and close clinical supervision is required (see Other special warnings and

Special precautions should be observed when administering Depo-Medrone
Intra-articular injections should be made using precise, anatomical localisation
into the synovial space of the joint involved. The injection site for each joint is
determined by that location where the synovial cavity is most superficial and
most free of large vessels and nerves. Suitable sites for intra-articular injection
are the knee, ankle, wrist, elbow, shoulder, phalangeal and hip joints. The
spinal joints, unstable joints and those devoid of synovial space are not
suitable. Treatment failures are most frequently the result of failure to enter the
joint space. Intra-articular injections should be made with care as follows:
ensure correct positioning of the needle into the synovial space and aspirate a
few drops of joint fluid. The aspirating syringe should then be replaced by
another containing Depo-Medrone with Lidocaine. To ensure position of the
needle synovial fluid should be aspirated and the injection made.
After injection the joint is moved slightly to aid mixing of the synovial fluid
and the suspension. Subsequent to therapy care should be taken for the patient
not to overuse the joint in which benefit has been obtained. Negligence in this
matter may permit an increase in joint deterioration that will more than offset
the beneficial effects of the steroid.
Intrabursal injections should be made as follows: the area around the injection
site is prepared in a sterile way and a wheal at the site made with 1 percent
procaine hydrochloride solution. A 20 to 24 gauge needle attached to a dry
syringe is inserted into the bursa and the fluid aspirated. The needle is left in
place and the aspirating syringe changed for a small syringe containing the
desired dose. After injection, the needle is withdrawn and a small dressing
applied. In the treatment of tenosynovitis and tendinitis, care should be taken
to inject Depo-Medrone with Lidocaine into the tendon sheath rather than into
the substance of the tendon. Due to the absence of a true tendon sheath, the
Achilles tendon should not be injected with Depo-Medrone with Lidocaine.


Depo-Medrone with Lidocaine is contra-indicated where there is known
hypersensitivity to components or to any local anaesthetics of the amide type
and in systemic infection unless anti-infective therapy is employed.
Due to its potential for neurotoxicity, Depo-Medrone with Lidocaine must not
be given by the intrathecal route. In addition, as the product is a suspension it
must not be given by the intravenous route (see Side-effects).


Special warnings and precautions for use
Undesirable effects may be minimised by using the lowest effective
dose for the minimum period. Frequent patient review is required to
appropriately titrate the dose against disease activity (see Dosage and

Patients should carry 'Steroid Treatment' cards which give clear
guidance on the precautions to be taken to minimise risk and which
provide details of prescriber, drug, dosage and the duration of


Depo-Medrone with Lidocaine vials are intended for single dose use
only. Any multidose use of the product may lead to contamination.


Depo-Medrone with Lidocaine is not recommended for epidural,
intranasal, intra-ocular, or any other unapproved route of
administration. See Side-effects section for details of side-effects
reported from some non-recommended routes of administration.


Due to the absence of a true tendon sheath, the Achilles tendon should
not be injected with Depo-Medrone with Lidocaine.


While crystals of adrenal steroids in the dermis suppress inflammatory
reactions, their presence may cause disintegration of the cellular
elements and physiochemical changes in the ground substance of the
connective tissue. The resultant infrequently occurring dermal and/or
subdermal changes may form depressions in the skin at the injection
site and the possibility of depigmentation. The degree to which this
reaction occurs will vary with the amount of adrenal steroid injected.
Regeneration is usually complete within a few months or after all
crystals of the adrenal steroid have been absorbed. In order to
minimize the incidence of dermal and subdermal atrophy, care must be
exercised not to exceed recommended doses in injections. Multiple
small injections into the area of the lesion should be made whenever
possible. The technique of intra-articular injection should include
precautions against injection or leakage into the dermis.


Systemic absorption of methylprednisolone occurs following intraarticular injection of Depo-Medrone with Lidocaine. Systemic as well
as local effects can therefore be expected.


Intra-articular corticosteroids are associated with a substantially
increased risk of inflammatory response in the joint, particularly
bacterial infection introduced with the injection.
arthropathies have been reported particularly after repeated injections.
Appropriate examination of any joint fluid present is necessary to
exclude any bacterial infection, prior to injection.


Following a single dose of Depo-Medrone with Lidocaine, plasma
cortisol levels are reduced and there is evidence of hypothalamic-

pituitary-adrenal axis (HPA) suppression. This suppression lasts for a
variable period of up to 4 weeks. The usual dynamic tests of HPA axis
function can be used to diagnose evidence of impaired activity (e.g.
Synacthen test).

Adrenal cortical atrophy develops during prolonged therapy and may
persist for months after stopping treatment. In patients who have
received more than physiological doses of systemic corticosteroids
(approximately 6 mg methylprednisolone) for greater than 3 weeks,
withdrawal should not be abrupt. How dose reduction should be
carried out depends largely on whether the disease is likely to relapse
as the dose of systemic corticosteroids is reduced. Clinical assessment
of disease activity may be needed during withdrawal. If the disease is
unlikely to relapse on withdrawal of systemic corticosteroids, but there
is uncertainty about HPA suppression, the dose of systemic
corticosteroid may be reduced rapidly to physiological doses. Once a
daily dose of 6 mg methylprednisolone is reached, dose reduction
should be slower to allow the HPA-axis to recover.
Abrupt withdrawal of systemic corticosteroid treatment, which has
continued up to 3 weeks is appropriate if it considered that the disease
is unlikely to relapse. Abrupt withdrawal of doses up to 32 mg daily of
methylprednisolone for 3 weeks is unlikely to lead to clinically
relevant HPA-axis suppression, in the majority of patients. In the
following patient groups, gradual withdrawal of systemic
corticosteroid therapy should be considered even after courses lasting 3
weeks or less:
• Patients who have had repeated courses of systemic corticosteroids,
particularly if taken for greater than 3 weeks.
• When a short course has been prescribed within one year of
cessation of long-term therapy (months or years).
• Patients who may have reasons for adrenocortical insufficiency
other than exogenous corticosteroid therapy.
• Patients receiving doses of systemic corticosteroid greater than 32
mg daily of methylprednisolone.
• Patients repeatedly taking doses in the evening.


Since mineralocorticoid secretion may be impaired, salt and/or a
mineralocorticoid should be administered concurrently.


Because rare instances of anaphylactic reactions have occurred in
patients receiving parenteral corticosteroid therapy, appropriate
precautionary measures should be taken prior to administration,
especially when the patient has a history of drug allergy.


Corticosteroids may mask some signs of infection, and new infections
may appear during their use. Suppression of the inflammatory
response and immune function increases the susceptibility to fungal,
viral and bacterial infections and their severity.
The clinical

presentation may often be atypical and may reach an advanced stage
before being recognised.

Chickenpox is of serious concern since this normally minor illness may
be fatal in immunosuppressed patients. Patients (or parents of
children) without a definite history of chickenpox should be advised to
avoid close personal contact with chickenpox or herpes zoster and if
exposed they should seek urgent medical attention.
immunization with varicella/zoster immunoglobin (VZIG) is needed by
exposed non-immune patients who are receiving systemic
corticosteroids or who have used them within the previous 3 months;
this should be given within 10 days of exposure to chickenpox. If a
diagnosis of chickenpox is confirmed, the illness warrants specialist
care and urgent treatment. Corticosteroids should not be stopped and
the dose may need to be increased.


Live vaccines should not be given to individuals with impaired
immune responsiveness. The antibody response to other vaccines may
be diminished.


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 chemoprophylaxis.


This product contains benzyl alcohol. Benzyl alcohol has been
reported to be associated with a fatal "Gasping Syndrome" in
premature infants.


Care should be taken for patients receiving cardioactive drugs such as
digoxin because of steroid induced electrolyte disturbance/potassium
loss (see Side-effects).


The following precautions apply for parenteral corticosteroids:
Following intra-articular injection, a marked increase in pain
accompanied by local swelling, further restriction of joint motion,
fever, and malaise are suggestive of septic arthritis.
If this
complication occurs and the diagnosis of sepsis is confirmed,
appropriate antimicrobial therapy should be instituted.

No additional benefit derives from the intramuscular administration of DepoMedrone with Lidocaine. Where parenteral corticosteroid therapy for
sustained systemic effect is desired, plain Depo-Medrone should be used.
Local injection of a steroid into a previously infected joint is to be avoided.
Corticosteroids should not be injected into unstable joints.
Sterile technique is necessary to prevent infections or contamination.

Special precautions:
Particular care is required when considering the use of systemic
corticosteroids in patients with the following conditions and frequent patient
monitoring is necessary.

Osteoporosis (post-menopausal females are particularly at risk).


Hypertension or congestive heart failure.


Existing or previous history of severe affective disorders (especially
previous steroid psychosis).


Diabetes mellitus (or a family history of diabetes).


History of tuberculosis.


Glaucoma (or a family history of glaucoma).


Previous corticosteroid-induced myopathy.


Liver failure or cirrhosis.


Renal insufficiency.




Peptic ulceration.


Fresh intestinal anastomoses.


Predisposition to thrombophlebitis.


Abscess or other pyogenic infections.


Ulcerative colitis.




Myasthenia gravis.


Ocular herpes simplex, for fear of corneal perforation.




Patients and/or carers should be warned that potentially severe
psychiatric adverse reactions may occur with systemic steroids (see
section 4.8). Symptoms typically emerge within a few days or weeks of
starting treatment. Risks may be higher with high doses/systemic
exposure (see also section 4.5 Interaction with Other Medicaments and
Other Forms of Interaction that can increase the risk of side effects),

although dose levels do not allow prediction of the onset, type, severity
or duration of reactions. Most reactions recover after either dose
reduction or withdrawal, although specific treatment may be necessary.
Patients/carers should be encouraged to seek medical advice if
worrying psychological symptoms develop, especially if depressed
mood or suicidal ideation is suspected. Patients/carers should be alert
to possible psychiatric disturbances that may occur either during or
immediately after dose tapering/withdrawal of systemic steroids,
although such reactions have been reported infrequently.
Particular care is required when considering the use of systemic
corticosteroids in patients with existing or previous history of severe
affective disorders in themselves or in their first degree relatives. These
would include depressive or manic-depressive illness and previous
steroid psychosis.

Use in children: Corticosteroids cause growth retardation in infancy,
childhood and adolescence which may be irreversible. Treatment should be
limited to the minimum dosage for the shortest possible time.
Use in the elderly: The common adverse effects of systemic corticosteroids
may be associated with more serious consequences in old age, especially
osteoporosis, hypertension, hypokalaemia, diabetes, susceptibility to infection
and thinning of the skin. Close clinical supervision is required to avoid lifethreatening reactions.


Interaction with other medicinal products and other forms of interaction
Convulsions have been reported with concurrent use of methylprednisolone and
cyclosporin. Since concurrent administration of these agents results in a mutual
inhibition of metabolism, it is possible that convulsions and other adverse effects
associated with the individual use of either drug may be more apt to occur.

Drugs that induce hepatic enzymes, such as rifampicin, rifabutin, carbamazepine,
phenobarbitone, phenytoin, primidone, and aminoglutethimide enhance the
metabolism of cortico steroids and its therapeutic effects may be reduced.


Drugs such as erythromycin and ketoconazole may inhibit the metabolism of
corticosteroids and thus decrease their clearance.


Steroids may reduce the effects of anticholinesterases in myasthenia gravis. The
desired effects of hypoglycaemic agents (including insulin), antihypertensives
and diuretics are antagonised by corticosteroids, and the hypokalaemic effects of
acetazolamide, loop diuretics, thiazide diuretics and carbenoxolone are enhanced.


The efficacy of coumarin anticoagulants may be enhanced by concurrent
corticosteroid therapy and close monitoring of the INR or prothrombin time is

required to avoid spontaneous bleeding.



The renal clearance of salicylates is increased by corticosteroids and steroid
withdrawal may result in salicylate intoxication. Salicylates and non-steroidal
anti-inflammatory agents should be used cautiously in conjunction with
corticosteroids in hypothrombinaemia.


Steroids have been reported to interact with neuromuscular blocking agents such
as pancuronium with partial reversal of the neuromuscular block.

Fertility, Pregnancy and lactation
The ability of corticosteroids to cross the placenta varies between individual
drugs, however, methyiprednisolone does cross the placenta.
Administration of corticosteroids to pregnant animals can cause abnormalities
of foetal development including cleft palate, intra-uterine growth retardation
and affects on brain growth and development. There is no evidence that
corticosteroids result in an increased incidence of congenital abnormalities,
such as cleft palate in man, however, when administered for long periods or
repeatedly during pregnancy, corticosteroids may increase the risk of intrauterine growth retardation. Hypoadrenalism may, in theory, occur in the
neonate following prenatal exposure to corticosteroids but usually resolves
spontaneously following birth and is rarely clinically important. As with all
drugs, corticosteroids should only be prescribed when the benefits to the
mother and child outweigh the risks. When corticosteroids are essential,
however, patients with normal pregnancies may be treated as though they were
in the non-gravid state.
The use of local anaesthetics such as lidocaine during labour and delivery may
be associated with adverse effects on mother and foetus. Lidocaine readily
crosses the placenta.
Corticosteroids are excreted in small amounts in breast milk, however, doses
of up to 40 mg daily of methylprednisolone are unlikely to cause systemic
effects in the infant. Infants of mothers taking higher doses than this may have
a degree of adrenal suppression, but the benefits of breastfeeding are likely to
outweigh any theoretical risk.
It is not known whether lidocaine is excreted in human breast milk.


Effects on ability to drive and use machines
None stated.


Undesirable effects
The incidence of predictable undesirable side-effects associated with the use of
corticosteroids, including hypothalamic-pituitary-adrenal suppression correlates
with the relative potency of the drug, dosage, timing of administration and
duration of treatment (See other special warnings and precautions).
Side-effects for the Depo-Medrone component may be observed including:
allergic reactions, hypopigmentation or hyperpigmentation, subcutaneous and
cutaneous atrophy, sterile abscess, post injection flare (following intraarticular use), charcot-like arthropathy.
GASTRO-INTESTINAL - Dyspepsia, peptic ulceration with perforation and
haemorrhage, abdominal distension, oesophageal ulceration, oesophageal
candidiasis, acute pancreatitis, perforation of bowel.
Increases in alanine transaminase (ALT, SGPT) aspartate transaminase (AST,
SGOT) and alkaline phosphatase have been observed following corticosteroid
treatment. These changes are usually small, not associated with any clinical
syndrome and are reversible upon discontinuation.
ANTI-INFLAMMATORY AND IMMUNOSUPPRESSIVE EFFECTS Increased susceptibility and severity of infections with suppression of clinical
symptoms and signs, opportunistic infections, may suppress reactions to skin
tests, recurrence of dormant tuberculosis (see Other special warnings and
MUSCULOSKELETAL - Proximal myopathy, osteoporosis, vertebral and
long bone fractures, avascular osteonecrosis, tendon rupture, aseptic necrosis,
muscle weakness.
retention, potassium loss, hypertension, hypokalaemic alkalosis, congestive
heart failure in susceptible patients.
DERMATOLOGICAL - Impaired healing, petechiae and ecchymosis, thin
fragile skin, skin atrophy, bruising, striae, telangiectasia, acne.
ENDOCRINE/METABOLIC - Suppression of the hypothalamo-pituitaryadrenal axis; growth suppression in infancy, childhood and adolescence;
menstrual irregularity and amenorrhoea. Cushingoid facies, hirsutism, weight
gain, impaired carbohydrate tolerance with increased requirement for
antidiabetic therapy, negative nitrogen and calcium balance. Increased
NEUROPSYCHIATRIC - A wide range of psychiatric reactions including
affective disorders (such as irritable, euphoric, depressed and labile mood

psychological dependence and suicidal thoughts), psychotic reactions
(including mania, delusions, hallucinations and aggravation of schizophrenia),
behavioural disturbances, irritability, anxiety, sleep disturbances, and
cognitive dysfunction including confusion and amnesia have been reported for
all corticosteroids. Reactions are common and may occur in both adults and
children. In adults, the frequency of severe reactions was estimated to be 56%. Psychological effects have been reported on withdrawal of
corticosteroids; the frequency is unknown. Increased intra-cranial pressure
with papilloedema in children (pseudotumour cerebri) has been reported,
usually after treatment withdrawal of methylprednisolone.
OPHTHALMIC - Increased intra-ocular pressure, glaucoma, papilloedema,
cataracts with possible damage to the optic nerve, corneal or scleral thinning,
exacerbation of ophthalmic viral or fungal disease, exophthalmos.
GENERAL - Leucocytosis, hypersensitivity including anaphylaxis, thromboembolism, nausea, vertigo.
WITHDRAWAL SYMPTOMS - Too rapid a reduction of corticosteroid
dosage following prolonged treatment can lead to acute adrenal insufficiency,
hypotension and death. However, this is more applicable to corticosteroids
with an indication where continuous therapy is given (see Other special
warnings and precautions).
A 'withdrawal syndrome' may also occur including, fever, myalgia, arthralgia,
rhinitis, conjunctivitis, painful itchy skin nodules and loss of weight.
Side-effects for the Lidocaine component include:
CENTRAL NERVOUS SYSTEM - Lightheadedness, nervousness,
apprehension, euphoria, confusion, dizziness, drowsiness, tinnitus, blurred or
double vision, vomiting, sensation of heat, cold, numbness, twitching, tremors,
convulsions, loss of consciousness, respiratory depression, respiratory arrest.
CARDIOVASCULAR SYSTEM - Bradycardia, hypotension, cardiovascular
collapse, cardiac arrest.
anaphylactic reactions.









Usual systemic corticoid adverse reactions, headache,
meningismus, meningitis, paraplegia, spinal fluid abnormalities, nausea,
vomiting, sweating, arachnoiditis, convulsions.
Extradural: Wound dehiscence, loss of sphincter control.
Intranasal: Permanent/temporary blindness, allergic reactions, rhinitis.

Ophthalmic (Subconjunctival): Redness and itching, abscess, slough at
injection site, residue at injection site, increased intra-ocular pressure,
decreased vision - blindness, infection.
Miscellaneous: Scalp, tonsillar fauces, sphenopalatine ganglion: blindness.


There is no clinical syndrome of acute overdosage with Depo-Medrone with
Lidocaine. Following overdosage the possibility of adrenal suppression should
be guarded against by gradual diminution of dose levels over a period of time.
In such event the patient may require to be supported during any further
traumatic episode.




Pharmacodynamic properties
Methylprednisolone acetate is a synthetic glucocorticoid with the actions and
use of natural corticosteroids. However the slower metabolism of the synthetic
corticosteroid with their lower protein-binding affinity may account for their
increased potency compared with the natural corticosteroids.
Lidocaine has the actions of a local anaesthetic.


Pharmacokinetic properties
No pharmacokinetic studies have been performed with the combination product of
methylprednisolone and lidocaine, however, data are provided from pharmacokinetic
studies performed with the individual product components methylprednisolone and
One in-house study of eight volunteers determined the pharmacokinetics of a single
40 mg intramuscular dose of Depo-Medrone. The average of the individual peak
plasma concentrations was 14.8 ± 8.6 ng/mL, the average of the individual peak times
(tmax) was 7.25 ± 1.04 hours, and the average area under the curve (AUC) was
1354.2 ± 424.1 ng/mL x hrs (Day 1-21).
Pharmacokinetics of lidocaine after synovial absorption following intra-articular
bolus injection in patients with knee joint arthroscopy was studied with different

maximum concentration (Cmax) values reported. The Cmax values are 2.18 µg/mL at 1
hour (serum) and 0.63 µg/mL at 0.5 hour (plasma) following administration of
lidocaine doses of 7 mg/kg and 400 mg, respectively. Other reported serum Cmax
values are 0.69 µg/mL at 5 minutes and 0.278 µg/mL at 2 hours following
administration of lidocaine doses of 25 mL of 1% and 20 mL of 1.5%, respectively.
Pharmacokinetic data of lidocaine after intra-bursa and intra-cyst administrations for
local effect are not available.
Methylprednisolone is widely distributed into the tissues, crosses the blood-brain
barrier, and is secreted in breast milk. Its apparent volume of distribution is
approximately 1.4 L/kg. The plasma protein binding of methylprednisolone in
humans is approximately 77%.
The plasma protein binding of lidocaine is concentration-dependent, and binding
decreases as concentration increases. At concentrations of 1 to 5 µg/mL, 60%-80%
lidocaine is protein bound. Binding is also dependent on the plasma concentration of
the α1-acid glycoprotein.
Lidocaine has a volume of distribution at steady state of 91 L.
Lidocaine readily crosses the placenta, and equilibrium of unbound drug
concentration is rapidly reached. The degree of plasma protein binding in the foetus is
less than in the mother, which results in lower total plasma concentrations in the
In humans, methylprednisolone is metabolized in the liver to inactive metabolites; the
major ones are 20α-hydroxymethylprednisolone and 20βhydroxymethylprednisolone. Metabolism in the liver occurs primarily via the
CYP3A4. (For a list of drug interactions based on CYP3A4-mediated metabolism,
see section 4.5.)
Methylprednisolone, like many CYP3A4 substrates, may also be a substrate for the
ATP-binding cassette (ABC) transport protein p-glycoprotein, influencing tissue
distribution and interactions with other medicines modulated by P-gp.
Lidocaine is mainly metabolized by the liver. The main metabolites of lidocaine are
monoethylglycine xylidide, glycinexylidide, 2,6-dimethylaniline, and 4-hydroxy-2,6dimethylaniline. The lidocaine N-dealkylation to monoethylglycine xylidide is
considered to be mediated by both CYP1A2 and CYP3A4. The metabolite 2,6dimethylaniline is converted to 4-hydroxy-2,6-dimethylaniline by CYP2A6 and

The mean elimination half-life for total methylprednisolone is in the range of 1.8 to
5.2 hours. Total clearance is approximately 5 to 6 mL/min/kg.
The clearance of lidocaine in plasma following intravenous bolus administration is 9
to 10 mL/min/kg.
The elimination half life of lidocaine following intravenous bolus injection is
typically 1.5 to 2 hours.
The pharmacological actions of monoethylglycine xylidide and glycinexylidide are
similar to but less potent than those of lidocaine. Monoethylglycine xylidide has a
half life of approximately 2.3 hours and glycinexylidide has a half life of about 10
hours and may accumulate after long-term administration.
Only 3% of lidocaine is excreted unchanged by the kidneys. About 73% of lidocaine
appears in the urine as 4-hydroxy-2,6-dimethylaniline metabolite.
Special Population
No pharmacokinetic studies have been performed for methylprednisolone in special
Special Population
Hepatic impairment
Following intravenous administration, the half life of lidocaine has approximately 3fold increase in patients with liver impairment. Pharmacokinetic data of lidocaine
after intra-articular, intra-bursa and intra-cyst administrations for local effect are not
available in hepatic impairment.
Renal impairment
Mild to moderate renal impairment (CLcr 30-60 mL/min) does not affect lidocaine
pharmacokinetics but may increase the accumulation of glycinexylidide metabolite
following intravenous administration. However, lidocaine clearance decreases about
half and its half life is approximately doubled with increased accumulation of
glycinexylidide metabolite in patients with severe renal impairment (Clcr <30
The pharmacokinetics of lidocaine and its main metabolite of monoethylglycine
xylidide are not altered significantly in haemodialysis patients who receive an
intravenous dose of lidocaine.
Pharmacokinetic data of lidocaine after intra-articular, intra-bursa and intra-cyst
administrations for local effect are not available in renal impairment.
No dosing adjustments are necessary in renal failure. Methylprednisolone is


Preclinical safety data

Based on conventional studies of safety pharmacology and repeated dose toxicity, no
unexpected hazards were identified. The toxicities seen in the repeated-dose studies
were those expected to occur with continued exposure to exogenous adrenocortical
Mutagenic potential:
There was no evidence of a potential for genetic and chromosome mutations when
tested in limited studies performed in bacteria and mammalian cells.
Carcinogenic potential:
Long-term studies in animals have not been performed to evaluate carcinogenic
potential, as the drug is indicated for short-term treatment only. There were no signs
indicative of carcinogenic activity in studies conducted to date.
Reproductive toxicity:
Reproductive fertility studies in animals have not been performed to evaluate
specifically the potential of impairment of fertility. There is no evidence that
corticosteroids impair fertility.
An increased frequency of cleft palate was observed among the offspring of mice
treated during pregnancy with methylprednisolone in doses similar to those typically
used for oral therapy in humans.
An increased frequency of cardiovascular defects and decreased body weight were
observed among the offspring of pregnant rats treated with methylprednisolone in a
dose that was similar to that used for oral therapy in humans but was toxic to the
mothers. In contrast, no teratogenic effect was noted in rats with doses <1-18 times
those typically used for oral therapy in humans in another study. High frequencies of
foetal death and a variety of central nervous system and skeletal anomalies were
reported in the offspring of pregnant rabbits treated with methylprednisolone in doses
less than those used in humans. The relevance of these findings to the risk of
malformations in human infants born to mothers treated with methylprednisolone in
pregnancy is unknown. Safety margins for the reported teratogenic effects are

Carcinogenic potential:
Long-term studies in animals have not been performed to evaluate carcinogenic
Mutagenic potential:
Genotoxicity studies were carried out with lidocaine and its metabolites. The
Salmonella microsomal assay (Salmonella typhimurium strains TA100, TA98, and
TA1538 with 1, 10, 100 and 500 mg/plate), with or without metabolic activation, with
lidocaine and its metabolites monoethylglycinexylidine, N-hydroxylidocaine, Nhydroxy-monoethylglycinexylidine, 2,6-xylidine, 2,6dimethylphenylhydroxylamine, did not reveal any mutagenic activity. However,
metabolite 2,6-dimethylaniline, has been shown to have mutagenic and carcinogenic
Reproductive toxicity:

Lidocaine has not been shown to affect male or female fertility.

Methylprednisolone plus Lidocaine
Carcinogenic potential:
Long-term studies in animals have not been performed to evaluate carcinogenic
The toxicity of lidocaine was not significantly altered in rats that were treated with the
combination of lidocaine and methylprednisolone.
Mutagenic potential:
Genotoxicity studies have not been conducted with the combination of
methylprednisolone and lidocaine (see above for genotoxicity as it pertains to the
individual drugs).
Reproductive toxicity:
Reproductive toxicity studies have not been conducted with the combination of
methylprednisolone and lidocaine (see above for reproductive toxicity as it
pertains to the individual drugs).




List of excipients
Sodium chloride, myristyl-garnma-picolinium chloride, benzyl alcohol,
macrogol, sodium hydroxide, hydrochloric acid and water for injection.




Shelf life
24 months.


Special precautions for storage
Store below 25 °C. Protect from freezing.


Nature and contents of container
Glass vials with rubber cap containing 1 or 2 ml of suspension.


Special precautions for disposal


Pfizer Limited
Ramsgate Road
CT13 9NJ
United Kingdom


PL 00057/0964


MA granted: 03 March 1981
MA renewed: 25 November 1991



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Source: Medicines and Healthcare Products Regulatory Agency

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