Source: Health Products Regulatory Authority (IE) Revision Year: 2021 Publisher: Pfizer Healthcare Ireland, 9 Riverwalk, National Digital Park, Citywest Business Campus, Dublin 24, Ireland
Depo-Medrone with Lidocaine is contraindicated:
Administration of live or live attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids (see section 4.4).
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 section 4.2).
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 should not be administered by any route other than those listed. It is critical that, during administration of Depo-Medrone with Lidocaine, appropriate technique be used and care taken to assure proper placement of drug.
Severe medical events have been reported in association with the intrathecal/epidural routes of administration (see section 4.3 and 4.8). Appropriate measures must be taken to avoid intravascular injection.
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.
Adrenal cortical atrophy develops during prolonged therapy and may persist for months after stopping treatment. Withdrawal of corticosteroids after prolonged therapy must therefore always be gradual to avoid acute rebound exacerbation of disease, acute adrenal insufficiency or polyarteritis being tapered off over weeks or months according to the dose and duration of treatment.
During prolonged therapy any intercurrent illness, trauma, anaesthesia or surgical procedure will require a temporary increase in dosage. In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting corticosteroids before, during and after the stressful situation is indicated. If corticosteroids have been stopped following prolonged therapy they may need to be temporarily re-introduced.
The following precautions apply for parenteral corticosteroids:
Intra-articular corticosteroids are associated with a substantially increased risk of inflammatory response in the joint, particularly bacterial infection introduced with the injection. Charcot-like 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.
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.
Systemic absorption of methylprednisolone occurs following intra-articular injection of Depo-Medrone with Lidocaine. Systemic as well as local effects can therefore be expected.
Intra-synovial injection of a corticosteroid may produce systemic, as well as local effects. No additional benefit derives from the intramuscular administration of methylprednisolone acetate with lidocaine. Where parenteral corticosteroid therapy for sustained systemic effect is desired, plain methylprednisolone acetate 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.
Since complications of treatment with glucocorticoids are dependent on the amount 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.
Benzyl alcohol is also potentially toxic when administered locally to neural tissue (see also section 4.4, Excipient information).
Corticosteroids may increase susceptibility to infection, may mask some signs of infection, and new infections may appear during their use. There may be decreased resistance and inability to localize infection when corticosteroids are used. Infections with any pathogen including viral, bacterial, fungal, protozoan or helminthic organisms, in any location in the body, may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect cellular immunity, humoral immunity, or neutrophil function. 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.Do not use intra-synovial, intrabursal or intratendinous administration for local effect in the presence of acute infection.
Persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. Chickenpox and measles, for example, can have a more serious or even fatal course in non-immune children or adults on corticosteroids.
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. Passive 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.
Measles can have a more serious or even fatal course in immunosuppressed patients. In such children or adults, particular care should be taken to avoid exposure to measles. If exposed, prophylaxis with intramuscular pooled immunoglobulin (IVIG) may be indicated. Exposed patients should be advised to seek medical advice without delay.
Live vaccines should not be given to individuals with impaired immune responsiveness. The antibody response to other vaccines may be diminished (see section 4.3).
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.
Kaposi’s sarcoma has been reported to occur in patients receiving corticosteroid therapy. Discontinuation of corticosteroids may result in clinical remission.
The role of corticosteroids in septic shock has been controversial, with early studies reporting both beneficial and detrimental effects. More recently, supplemental corticosteroids have been suggested to be beneficial in patients with established septic shock who exhibit adrenal insufficiency. However, their routine use in septic shock is not recommended. A systematic review of short-course, high-dose corticosteroids did not support their use. However, meta-analyses, and a review suggest that longer courses (5-11 days) of low-dose corticosteroids might reduce mortality, especially in patients with vasopressor-dependent septic shock.
Allergic reactions may occur. Because rare instances of skin reactions and anaphylactic/anaphylactoid reactions have occurred in patients receiving corticosteroid therapy, appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of drug allergy.
Pharmacologic doses of corticosteroids administered for prolonged periods may result in hypothalamic-pituitary-adrenal (HPA) suppression (secondary adrenocortical insufficiency). The degree and duration of adrenocortical insufficiency produced is variable among patients and depends on the dose, frequency, time of administration, and duration of glucocorticoid therapy. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should be administered concurrently.
A steroid “withdrawal syndrome”, seemingly unrelated to adrenocortical insufficiency, may also occur following abrupt discontinuance of glucocorticoids. This syndrome includes symptoms such as: anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, desquamation, myalgia, weight loss, and/or hypotension. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels.
Because glucocorticoids can produce or aggravate Cushing’s syndrome, glucocorticoids should be avoided in patients with Cushing’s disease.
There is an enhanced effect of corticosteroids on patients with hypothyroidism.
Corticosteroids, including methylprednisolone, can increase blood glucose, worsen pre-existing diabetes, and predispose those on long-term corticosteroid therapy to diabetes mellitus.
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.
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), 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.
Corticosteroids should be used with caution in patients with seizure disorders.
Corticosteroids should be used with caution in patients with myasthenia gravis (also see myopathy statement in
There have been reports of epidural lipomatosis in patients taking corticosteroids, typically with long-term use at high doses.
Prolonged use of corticosteroids may produce posterior subcapsular cataracts and nuclear cataracts (particularly in children), exophthalmos, or increased intraocular pressure, which may result in glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses.
Corticosteroids should be used cautiously in patients with ocular herpes simplex, because of possible corneal perforation.
Corticosteroid therapy has been associated with central serous chorioretinopathy, which may lead to retinal detachment.
Visual disturbance may be reported with systemic and topical corticosteroid use. If a patient presents with symptoms such as blurred vision or other visual disturbances, the patient should be considered for referral to an ophthalmologist for evaluation of possible causes which may include cataract, glaucoma or rare diseases such as central serous chorioretinopathy (CSCR) which have been reported after use of systemic and topical corticosteroids. Central serous chorioretinopathy, may lead to retinal detachment.
Adverse effects of glucocorticoids on the cardiovascular system, such as dyslipidaemia and hypertension, may predispose treated patients with existing cardiovascular risk factors to additional cardiovascular effects, if high doses and prolonged courses are used. Accordingly, corticosteroids should be employed judiciously in such patients and attention should be paid to risk modification and additional cardiac monitoring if needed.
Systemic corticosteroids should be used with caution, and only if strictly necessary, in cases of congestive heart failure.
Corticosteroids should be used with caution in patients with hypertension.
Thrombosis including venous thromboembolism has been reported to occur with corticosteroids. As a result corticosteroids should be used with caution in patients who have or may be predisposed to thromboembolic disorders.
High doses of corticosteroids may produce acute pancreatitis.
There is no universal agreement on whether corticosteroids per se are responsible for peptic ulcers encountered during therapy; however, glucocorticoid therapy may mask the symptoms of peptic ulcer so that perforation or haemorrhage may occur without significant pain (see section 4.8). Glucocorticoid therapy may mask peritonitis or other signs or symptoms associated with gastrointestinal disorders such as perforation, obstruction or pancreatitis. In combination with NSAIDs, the risk of developing gastrointestinal ulcers is increased (see section 4.5).
Corticosteroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess or other pyogenic infection. Caution must also be used in diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer when steroids are used as direct or adjunctive therapy.
Drug induced liver injury including acute hepatitis or liver enzyme increase can result from cyclical pulsed IV methylprednisolone (usually at initial dose > 1 g/day). Rare cases of hepatotoxicity have been reported. The time to onset can be several weeks or longer. In the majority of case reports resolution of the adverse events has been observed after treatment was discontinued. Therefore, appropriate monitoring is required.
Corticosteroids should be used with caution in patients with liver failure or cirrhosis.
An acute myopathy has been reported 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 anticholinergics, such as neuromuscular blocking drugs (e.g., pancuronium). 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.
Osteoporosis is a common but infrequently recognized adverse effect associated with a long-term use of large doses of glucocorticoid.
Corticosteroids should be used with caution in patients with renal insufficiency (see section 5.2).
Average and large doses of hydrocortisone or cortisone 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.
Systemic corticosteroids are not indicated for, and therefore should not be used to treat, traumatic brain injury, a multicenter study revealed an increased mortality at 2 weeks and 6 months after injury in patients administered methylprednisolone sodium succinate compared to placebo. A causal association with methylprednisolone sodium succinate treatment has not been established.
Care should be taken for patients receiving cardioactive drugs such as digoxin because of steroid induced electrolyte disturbance/potassium loss (see section 4.8).
Corticosteroids should be used with caution in patients with a predisposition to thrombophlebitis.
Aspirin and nonsteroidal anti-inflammatory agents should be used cautiously in conjunction with corticosteroids.
This medicinal product contains less than 1 mmol sodium (23 mg) per dose, i.e. essentially ‘sodium-free’.
Pheochromocytoma crisis, which can be fatal, has been reported after administration of systemic corticosteroids. Corticosteroids should only be administered to patients with suspected or identified pheochromocytoma after an appropriate risk/benefit evaluation.
Caution is required in patients with systemic sclerosis because an increased incidence of scleroderma renal crisis has been observed with corticosteroids, including methylprednisolone.
Co‑treatment with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic side-effects. The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid side-effects, in which case patients should be monitored for systemic corticosteroid side-effects (see section 4.5).
Corticosteroids cause growth retardation in infancy, childhood and adolescence which may be irreversible. Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed. Treatment should be limited to the minimum dosage for the most serious indications and shortest possible time. The use of such a regimen should be restricted to those most serious indications.
Infants and children on prolonged corticosteroid therapy are at special risk from raised intracranial pressure.
High doses of corticosteroids may produce pancreatitis in children.
Depo-Medrone with Lidocaine contains benzyl alcohol (see section 2). The preservative benzyl alcohol may cause hypersensitivity reactions. Intravenous administration of benzyl alcohol has been associated with serious adverse events and death in paediatric patients including neonates (“gasping syndrome”). Although normal therapeutic doses of this product ordinarily deliver amounts of benzyl alcohol that are substantially lower than those reported in association with the “gasping syndrome”, the minimum amount of benzyl alcohol at which toxicity may occur is not known. Benzyl alcohol containing formulations should only be used in neonates if it is necessary and if there are no alternatives possible. Premature and low-birth weight neonates may be more likely to develop toxicity. Benzyl alcohol containing formulations should not be used for more than 1 week in children under 3 years of age unless necessary. It is important to consider the total quantity of benzyl alcohol received from all sources, and high volumes should be used with caution and only if necessary, especially in patients with liver or kidney impairment, as well as in pregnant or breast-feeding women, because of the risk of accumulation and toxicity (metabolic acidosis).
Depo-Medrone with Lidocaine contains less than 1 mmol sodium (23 mg) in each vial, that is to say essentially ‘sodium‑free’.
Methylprednisolone is a cytochrome P450 enzyme (CYP) substrate and is mainly metabolized by the CYP3A enzyme. CYP3A4 is the dominant enzyme of the most abundant CYP subfamily in the liver of adult humans. It catalyzes 6β-hydroxylation of steroids, the essential Phase I metabolic step for both endogenous and synthetic corticosteroids. Many other compounds are also substrates of CYP3A4, some of which (as well as other drugs) have been shown to alter glucocorticoid metabolism by induction (upregulation) or inhibition of the CYP3A4 enzyme.
CYP3A4 INHIBITORS – Drugs that inhibit CYP3A4 activity generally decrease hepatic clearance and increase the plasma concentration of CYP3A4 substrate medications, such as methylprednisolone. In the presence of a CYP3A4 inhibitor, the dose of methylprednisolone may need to be titrated to avoid steroid toxicity.
CYP3A4 INDUCERS – Drugs that induce CYP3A4 activity generally increase hepatic clearance, resulting in decreased plasma concentration of medications that are substrates for CYP3A4. Co-administration may require an increase in methylprednisolone dosage to achieve the desired result.
CYP3A4 SUBSTRATES – In the presence of another CYP3A4 substrate, the hepatic clearance of methylprednisolone may be affected, with corresponding dosage adjustments required. It is possible that adverse events associated with the use of either drug alone may be more likely to occur with co-administration.
1. Convulsions have been reported with concurrent use of methylprednisolone and cyclosporin (CYP3A4 inhibitor and substrate). 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.
2. Drugs that induce hepatic enzymes, such as rifampicin (antibiotic CYP3A4 inducer), rifabutin, carbamazepine (anticonvulsant CYP3A4 inducer and substrate), phenobarbitone and phenytoin (anticonvulsants CYP3A4 inducers), primidone and aminoglutethimide (aromatase inhibitor) enhance the metabolism of corticosteroids and its therapeutic effects may be reduced. Aminoglutethimide- induced adrenal suppression may exacerbate endocrine changes caused by prolonged glucocorticoid treatment.
3. Antibiotics/Antimycotics – Drugs such as erythromycin (macrolide antibacterial CYP3A4 inhibitor and substrate), itraconazole and ketoconazole (antifungal CYP3A4 inhibitors and substrates) may inhibit the metabolism of corticosteroids and thus decrease their clearance.
Troleandomycin (CYP3A4 inhibitor), as well as clarithromycin, erythromycin, itraconazole and ketoconazole (CYP3A4 inhibitors and substrates) increase the effects and the side effects of methylprednisolone.
The acetylation rate and clearance of isoniazid (CYP3A4 inhibitor), an antibacterial drug, can be increased by methylprednisolone.
4. Steroids may reduce the effects of anticholinesterases in myasthenia gravis. An acute myopathy has been reported with the concomitant use of high doses of corticosteroids and anticholinergics, such as neuromuscular blocking drugs. (see section 4.4).
Antagonism of the neuromuscular blocking effects of pancuronium and vecuronium has been reported in patients taking corticosteroids. This interaction may be expected with all competitive neuromuscular blockers.
The desired effects of hypoglycaemic agents (including insulin), anti-hypertensives and diuretics are antagonised by corticosteroids, and the hypokalaemic effects of acetazolamide, loop diuretics, thiazide diuretics and carbenoxolone are enhanced.
5. The effect of methylprednisolone on oral anticoagulants is variable. 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 and to maintain the desired anticoagulant effects.
There are also reports of diminished effects of anticoagulants when given concurrently with corticosteroids.
6. There may be increased incidence of gastrointestinal bleeding and ulceration when corticosteroids are given with NSAIDs (see section 4.4).
Methylprednisolone may increase the clearance of high-dose aspirin, which can lead to decreased salicylate serum levels.
Discontinuation of methylprednisolone treatment can lead to raised salicylate serum levels, which could lead to an increased risk of salicylate toxicity.
7. Antidiabetics – Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required.
8. Antiemetics – Aprepitant and fosaprepitant (CYP3A4 inhibitors and substrates)
9. Antivirals – HIV protease inhibitors: Indinavir and ritonavir (CYP3A4 inhibitors and substrates) may increase plasma concentrations of corticosteroids. Corticosteroids may induce the metabolism of HIV-protease inhibitors resulting in reduced plasma concentrations.
10. Calcium channel blocker – Diltiazem (CYP3A4 inhibitor and substrate).
11. Contraceptives (oral) - Ethinylestradiol/norethindrone (CYP3A4 inhibitors and substrate).
12. Other immunosuppressants like cyclophosphamide and tacrolimus are substrates of CYP3A4.
13. Potassium-depleting agents -When corticosteroids are administered concomitantly with potassium-depleting agents (e.g. diuretics), patients should be observed closely for development of hypokalaemia. There is also an increased risk of hypokalaemia with concurrent use of corticosteroids with amphotericin B, xanthenes, or beta2 agonists.
14. Grapefruit juice – CYP3A4 inhibitor.
15. Pharmacokinetic enhancers (cobicistat) - CYP3A4 INHIBITORS, which are used to treat HIV infections.
Corticosteroids have been shown to impair fertility in animal studies (see section 5.3).
Corticosteroids cross the placenta. Animal studies have shown reproductive toxicity (see section 5.3). Although observational studies in humans do not support an association between systemic corticosteroids use during pregnancy and the risk of congenital malformations or oral cleft, a risk cannot be excluded due to the limited amount of data from the use of systemic corticosteroids in pregnant women. Since adequate human reproductive studies have not been done with methylprednisolone acetate, this medicinal product should be used during pregnancy only after a careful benefit‑risk assessment for the mother and foetus.
Published studies found an increased incidence of low birth weights in infants born of mothers receiving corticosteroids. In humans, the risk of low birth weight appears to be dose related and may be minimized by administering lower corticosteroid doses.
Cataracts have been observed in infants born to mothers treated with long-term corticosteroids during pregnancy. Neonates of mothers who received corticosteroid therapy during pregnancy should be observed for signs of hypo-adrenalism and appropriate measures instituted if such signs exist, although neonatal adrenal insufficiency appears to be rare in infants who were exposed in utero to corticosteroids. Patients with pre-eclampsia or fluid retention require close monitoring. There are no known effects of corticosteroids on labour and delivery.
Lidocaine readily crosses the placenta. The use of local anaesthetics such as lidocaine during labour and delivery may be associated with adverse effects on mother and foetus.
Since adequate human reproductive studies have not been done with methylprednisolone acetate with lidocaine, this medicinal product should be used during pregnancy only after a careful assessment of the benefit risk ratio to the mother and fetus.
Depo-Medrone with Lidocaine contains benzyl alcohol as a preservative. Benzyl alcohol can cross the placenta (see section 4.4).
Methylprednisolone is excreted in breast milk and infants of mothers taking pharmacological doses of steroids should be monitored carefully for signs of adrenal suppression.
Corticosteroids distributed into breast milk may interfere with endogenous glucocorticoid production in nursing infants.
Lidocaine is excreted in human breast milk.
This medicinal product should be used during breast feeding only after a careful assessment of the benefit risk ratio to the mother and infant.
Depo-Medrone with Lidocaine contains benzyl alcohol as a preservative (see section 4.4).
The effect of corticosteroids on the ability to drive or use machinery has not been systematically evaluated. Undesirable effects, such as dizziness, vertigo, visual disturbances, and fatigue are possible after treatment with corticosteroids. If affected, patients should not drive or operate machinery.
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 section 4.4).
CERTAIN SIDE-EFFECTS REPORTED WITH SOME CONTRAINDICATED AND NON‑RECOMMENDED ROUTES OF ADMINISTRATION:
| MedDRA System Organ Class | Frequency | Undesirable Effects |
|---|---|---|
| Infections and infestations | Not Known | Opportunistic infectione; Infectione; Injection site infection; Peritonitisc,e; Recurrence of dormant tuberculosis |
| Immune system disorders | Not Known | Drug hypersensitivitye, Anaphylactic reaction; Anaphylactoid reactione |
| Neoplasms benign, malignant and unspecified (including cysts and polyps) | Not Known | Kaposi’s sarcoma; Phaeochromocytoma crisis |
| Blood and lymphatic system disorders | Not Known | Leukocytosis |
| Endocrine disorders | Not Known | Cushingoide; Hypopituitarisme; Steroid 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 section 4.4). A 'withdrawal syndrome' may also occur including, fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful itchy skin nodules and loss of weight. |
| Metabolism and nutrition disorders | Not Known | Metabolic acidosise; Sodium retentione; Fluid retentione; Alkalosis hypokalaemice; Dyslipidaemiae; Glucose tolerance impairede; Increased appetite (which may result in Weight increased)e; Increased requirements for insulin (or oral hypoglycemic agents in diabetics)a,e; Lipomatosise |
| Psychiatric disorders | Not Known | Affective disordere (including Depressed moode, Euphoric mood, Affect labilitye, Drug dependencee, Suicidal ideatione), Psychotic disordere (including Maniae, Delusion, Hallucination, and Schizophrenia [aggravation of]); Confusional state; Mental disorder; Anxiety; Personality changee; Mood swingse; Abnormal behavioure; Insomniae; Irritabilitye; Nervousnessd |
| Nervous system disorders | Not Known | Intracranial pressure increased (with Papilloedema [Benign intracranial hypertension])e; Seizure; Amnesiae; Cognitive disordere; Dizziness; Headachee; Epidural lipomatosise |
| Eye disorders | Not Known | Exophthalmose; Chorioretinopathye; Cataracte; Glaucomae; rare instances of blindness associated with intralesional therapy around the face and heada; Increased intra-ocular pressure, with possible damage to the optic nerve; Corneal or scleral thinning; Exacerbation of ophthalmic viral or fungal disease; Diplopiad; Vision blurredd (see section 4.4) |
| Ear and labyrinth disorders | Not Known | Vertigoe; Tinnitusd |
| Cardiac disorders | Not Known | Cardiac arrestd; Cardiac failure congestive (in susceptible patients)e; Bradycardiad |
| Vascular disorders | Not Known | Circulatory collapsed; Thrombosise; Hypertensione; Hypotension; Thrombotic events |
| Respiratory, thoracic and mediastinal disorders | Not Known | Respiratory arrestd; Respiratory depressiond; Pulmonary embolisme, Hiccupse |
| Gastrointestinal disorders | Not Known | Peptic ulcerb,e; Gastric |
| Hepatobiliary disorders | Not known | Hepatitis, Increase of liver enzymes |
| Skin and subcutaneous tissue disorders | Not Known | Angioedemae; Petechiaee; Ecchymosise; Skin atrophye; Skin striaee; Skin hyperpigmentatione; Skin hypopigmentatione; Skin lesiond; Hirsutisme; Rashe; Erythemae; Prurituse; Urticaria; Acnee; Hyperhidrosise |
| Musculoskeletal and connective tissue disorders | Not Known | Muscular weaknesse; Osteonecrosise; Pathological fracturee; Muscle atrophye; Osteoporosis; Myopathye; Neuropathic arthropathye; Arthralgia; Growth retardatione; Myalgiae; Muscle twitchingd |
| Reproductive system and breast disorders | Not Known | Menstruation irregulare |
| General disorders and administration site conditions | Not Known | Injection site reactione; Abscess sterilee; Impaired healinge; Oedemad Oedema peripherale; Fatiguee; Malaisee; Feeling coldd Feeling hotd |
| Investigations | Not Known | Intraocular pressure increasede; Alanine aminotransferase increasede; Aspartate aminotransferase increasede; Blood alkaline phosphatase increasede; Carbohydrate tolerance decreasede; Blood potassium decreasede; Urine calcium increasede; suppression of reactions to skin testsa,e; Blood urea increasede |
| Injury, poisoning and procedural complications | Not Known | Tendon rupturee; Spinal compression fracturee. Systemic corticosteroids are not indicated for, and therefore should not be used to treat, traumatic brain injury. |
a Not a MedDRA Preferred term.
b Peptic ulcer perforation and Peptic ulcer haemorrhage.
c Peritonitis may be the primary presenting sign or symptom of a gastrointestinal disorder such as perforation, obstruction or pancreatitis (see section 4.4).
d Reported for lidocaine only.
e Reported for methylprednisolone acetate only.
Intrathecal / Epidural: Usual systemic corticoid adverse reactions, headache, meningismus, meningitis, paraparesis, / paraplegia, spinal fluid abnormalities, nausea, vomiting, sweating, arachnoiditis, functional gastrointestinal disorder / bladder dysfunction, seizure, sensory disturbances.
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.
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via HPRA Pharmacovigilance Website: www.hpra.ie.
In the absence of stability studies this medicinal product must not be mixed with other medicinal products.
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