Side effects
There may be a decrease in immunological reactivity, leading to exacerbation of chronic foci of infection. To avoid these side effects, it is advisable to use a suspension of hydrocortisone acetate in combination with antimicrobial agents. During treatment, there may be an exacerbation of ulcerative lesions of the skin and gastrointestinal tract, increased blood and intraocular pressure, slower wound healing, the appearance of hyperglycemia, sodium retention in the body and increased excretion of potassium and calcium with the possibility of developing edema and osteoporosis, increased blood clotting, and menstrual irregularities.
Nosological classification (ICD-10)
- A41.9 Septicemia, unspecified
- A49.9 Bacterial infection, unspecified
- C95.0 Acute leukemia of unspecified cell type
- C95.9 Leukemia, unspecified
- D59 Acquired hemolytic anemia
- D69.3 Idiopathic thrombocytopenic purpura
- D70 Agranulocytosis
- E05.5 Thyroid crisis or coma
- E06 Thyroiditis
- E27.1 Primary adrenal insufficiency
- E27.2 Addison's crisis
- E83.5.0* Hypercalcemia
- G93.6 Cerebral edema
- J44 Other chronic obstructive pulmonary disease
- J45 Asthma
- J46 Status asthmaticus
- J98.8.0* Bronchospasm
- L30.9 Dermatitis, unspecified
- M13.9 Arthritis, unspecified
- M19.9 Arthrosis, unspecified
- M24.5 Joint contracture
- M35.9 Systemic connective tissue disorders, unspecified
- M65.9 Synovitis and tenosynovitis, unspecified
- M71.9 Bursopathy, unspecified
- M77.0 Medial epicondylitis
- M77.1 Lateral epicondylitis
- M79.0 Rheumatism, unspecified
- R57.9 Shock, unspecified
- T78.2 Anaphylactic shock, unspecified
- T78.4 Allergy, unspecified
Note!
Description of the drug Hydrocortisone acetate suspension. d/in. 25mg/ml amp. 2ml No. 10 on this page is a simplified author’s version of the apteka911 website, created on the basis of the instructions for use.
Before purchasing or using the drug, you should consult your doctor and read the manufacturer's original instructions (attached to each package of the drug). Information about the drug is provided for informational purposes only and should not be used as a guide to self-medication. Only a doctor can decide to prescribe the drug, as well as determine the dose and methods of its use.
Directions for use and doses
IM (deep) into the gluteal muscle at a dose of 50–300 mg to 1000–1500 mg/day. Before use, the contents of the ampoules must be shaken until a homogeneous suspension is formed.
For acute, life-threatening conditions, 100–150 mg is administered every 4 hours for 48 hours; then - every 8-12 hours. Children - every 4 hours 1-2 mg/kg, the optimal daily dose is 6-9 mg/kg.
5–25 mg (0.1–1 ml (depending on the size of the joint)) is injected into the joint cavity once a week. 3–5 injections per course. The effect of the drug begins 6–25 hours after administration and lasts several days or weeks
What rules should you follow if you have been prescribed hormone injections into a joint?
If you cannot do without hormone injections, remember this:
- Keep a break of at least 2 weeks between injections. The drug does not start working instantly, so you need to wait a while for the doctor to evaluate its effectiveness.
- Remember that the first injection is the most effective. If there is no relief after the first injection, avoid repeated injections in the same place. It would be more correct to change the injection site or choose a different drug.
- You should not give hormone injections to one knee more than 4-5 times, as the risk of complications increases. Each time, the likelihood of needle injury, infection, or ligament damage increases.
Hormone injections are a last resort for arthrosis
In the video you will see how a synovial fluid prosthesis is injected into the knee joint in a medical office:
HYDROCORTISONE-RICHTER susp. d/injection 125 mg vial. 5 ml
Interaction
Hydrocortisone increases the toxicity of cardiac glycosides (due to the resulting hypokalemia, the risk of developing arrhythmias increases).
Accelerates the elimination of acetylsalicylic acid, reduces the content of its metabolites in the blood (with its abolition, the concentration of salicylates in the blood increases and the risk of side effects increases). When used simultaneously with live (attenuated) vaccines and against the background of other types of immunizations, it increases the risk of viral activation and the development of infections. Increases the metabolism of isoniazid, mexiletine (especially in “fast acetylators”), which leads to a decrease in their plasma concentrations. Increases the risk of developing the hepatotoxic effect of paracetamol (induction of “liver” enzymes and the formation of a toxic metabolite of paracetamol).
Hypokalemia caused by hydrocortisone may increase the severity and duration of muscle blockade due to muscle relaxants.
In high doses, it reduces the effect of somatropin.
Hydrocortisone reduces the effect of oral hypoglycemic drugs.
Strengthens the anticoagulant effect of coumarin derivatives.
Weakens the effect of vitamin D on calcium absorption in the intestinal lumen. Ketoconazole (reduces clearance) increases the toxicity of hydrocortisone.
Thiazide diuretics, carbonic anhydrase inhibitors, other glucocorticoids and amphotericin B increase the risk of hypokalemia, sodium-containing drugs - edema and increased blood pressure. Nonsteroidal anti-inflammatory drugs and ethanol increase the risk of ulceration of the gastrointestinal tract (GIT) mucosa and bleeding. In combination with non-steroidal anti-inflammatory drugs for the treatment of arthritis, it is possible to reduce the dose of hydrocortisone due to the additive therapeutic effect.
Indomethacin, displacing hydrocortisone from its connection with albumin, increases the risk of developing its side effects.
Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis.
The therapeutic effect of hydrocortisone is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin and other inducers of “liver” microsomal enzymes (increased metabolic rate). Mitotane and other steroid synthesis inhibitors may necessitate an increase in the dose of hydrocortisone.
The clearance of hydrocortisone increases against the background of thyroid hormone preparations.
Immunosuppressants increase the risk of developing infections and lymphoma or other lymphoproliferative disorders associated with Epstein-Barr virus.
Estrogens (including oral estrogen-containing contraceptives) reduce the clearance of hydrocortisone, prolong T1/2 and their therapeutic and toxic effects. The appearance of hirsutism and acne is facilitated by the simultaneous use of hydrocortisone and steroid hormonal drugs - androgens, estrogens, anabolic steroids, oral contraceptives. Tricyclic antidepressants may increase the severity of depression caused by taking hydrocortisone (not indicated for the treatment of these side effects).
The risk of developing cataracts increases when used in conjunction with other glucocorticoids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine.
Simultaneous administration with nitrates, m-anticholinergics (including antihistamines, tricyclic antidepressants) increases intraocular pressure.
In what cases are hormones prescribed?
In the later stages of arthrosis of the hip joint or any other, when pain almost always bothers the patient and painkillers do not help, a stronger remedy may be prescribed. This is an emergency treatment measure that can quickly relieve pain and improve well-being. Unfortunately, this coin also has a downside, especially if you resort to this method more often than necessary.
Kenalog, diprospan and other corticosteroid drugs quickly stop inflammation, eliminate edema and swelling. However, they do not cure arthrosis at all, do not restore nutrition to the cartilage and do not improve the condition of the joint. This is only an ambulance - a powerful blow to the body, especially if you resort to such treatment for osteoarthritis too often.
No organism can withstand frequent injections of hormonal drugs.
Drug interactions
The effectiveness of Hydrocortisone when used systemically can be reduced by drugs of the following pharmacological groups:
- Antihistamines.
- Diuretics.
- Anticonvulsants.
Taking this drug together with non-steroidal anti-inflammatory drugs significantly increases the risk of drug ulcers.
Hydrocortisone reduces the effectiveness of glucose-lowering medications, and its simultaneous use with amphotericin B provokes the development of cardiovascular failure.
Is there an alternative?
Hormone injections reduce pain due to arthrosis of the ankle, knee, and hip, but also have a negative effect on the body. They are especially dangerous in case of diabetes mellitus, arterial hypertension, stomach ulcers, and also if the patient’s kidney function is impaired. In addition, corticosteroids only temporarily relieve pain, which means that a person will need a larger dose each time.
Instead of harmful corticosteroids, which also do not cure, you can choose other therapeutic methods:
- injections of chondroprotectors, which are aimed at restoring damaged cartilage tissue and normalizing metabolism in the joint (the course ranges from 3 to 15 injections);
- injection of a synovial fluid prosthesis, such as Noltrex, which expands the damaged cartilage surfaces, mixes with the joint fluid and returns the joint to normal functioning.
The course of injections of synovial fluid prosthesis is 2-5 procedures. After this, you can forget about arthrosis for 1-1.5 years. The drug based on hyaluronic acid or synthetic Noltrex is safe for the gastrointestinal tract and other body systems and will not harm diabetics or people with high blood pressure.
If you are experiencing severe joint pain, do not rush to relieve it with hormones. Consider a future-proof treatment option instead of drugging your body with corticosteroids for a long time.
Side effects and symptoms of overdose
Hydrocortisone when administered intramuscularly, intravenously and intraarticularly can provoke the appearance of edema, the development of heart failure, arrhythmia, osteoporosis and bone fractures, medicinal ulcers of the digestive tract, increased blood and intracranial pressure, muscle cramps, a decrease in the body's defenses, Itsenko-Cushing syndrome.
Skin ointment most often causes the following undesirable reactions: local redness, irritation, dryness, itching, burning, swelling and atrophy.
Use of the ophthalmic form of Hydrocortisone can lead to mixed injection, eyelid eczema, exophthalmos, cataracts, hormonal glaucoma, and corneal perforation.
An overdose of the drug is manifested by increased side effects, the appearance of dyspeptic syndrome and a violation of the general condition of the body.
In such a situation, it is important to gradually discontinue hydrocortisone and carry out competent symptomatic therapy.
Indications and contraindications for the use of Hydrocortisone
As a component of systemic and replacement therapy, the drug is indicated for the following conditions: adrenal insufficiency, shock of various origins, hepatic coma, allergic laryngeal edema, status asthmaticus, exacerbation of Crohn's disease and ulcerative colitis, gouty, rheumatoid and psoriatic arthritis, SLE, dermatomyositis.
Local use of the drug is indicated for eczema, various dermatitis, psoriasis, scabies, and insect bites.
Eye ointment is used to treat chronic or allergic blepharoconjunctivitis, acute keratitis, anterior and posterior uveitis, and burns of the ocular surface.
Contraindications to the systemic administration of Hydrocortisone are a history of allergic reactions, epilepsy, hypertensive crisis, Itsenko-Cushing syndrome and disease, osteoporosis, peptic ulcer and duodenal ulcer, diabetes mellitus type 1 and 2, HIV infection, pregnancy, lactation, and childhood.
Skin ointment should not be used for malignant neoplasms, syphilis, tuberculosis, viral, fungal and bacterial local infections.
The ophthalmic form of Hydrocortisone should not be prescribed for violations of the integrity of the cornea, infectious diseases, or trachoma.
Hydrocortisone
Interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids (GCS) are found in all tissues, especially in the liver) to form a complex that induces the formation of proteins (including enzymes that regulate vital processes in cells).
Protein metabolism: reduces the amount of globulins in plasma, increases albumin synthesis in the liver and kidneys (with an increase in the albumin/globulin ratio), reduces synthesis and increases protein catabolism in muscle tissue.
Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation occurs mainly in the shoulder girdle, face, abdomen), leads to developed hypercholesterolemia.
Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase (increasing the flow of glucose from the liver into the blood); increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases (activation of gluconeogenesis); promotes the development of hyperglycemia. Water-electrolyte metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (mineralocorticoid activity), reduces the absorption of Ca2+ from the gastrointestinal tract, causes “leaching” of calcium from the bones and increases its renal excretion, reduces bone mineralization.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by zosinophils and mast cells; inducing the formation of lipocortins and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes (especially lysosomal) and organelle membranes. Acts on all stages of the inflammatory process: inhibits the synthesis of prostaglandins (Pg) at the level of arachidonic acid (lipocortin inhibits phospholipase A2, suppresses the liberation of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes, which contribute to the processes of inflammation, allergies, etc.), the synthesis of “pro-inflammatory cytokines" (interleukin 1, tumor necrosis factor alpha, etc.); increases the resistance of the cell membrane to the action of various damaging factors.
The immunosuppressive effect is caused by the involution of lymphoid tissue, inhibition of the proliferation of lymphocytes (especially T lymphocytes), suppression of the migration of B cells and the interaction of T and B lymphocytes, inhibition of the release of cytokines (interleukin-1, 2; interferon gamma) from lymphocytes and macrophages and decreased antibody formation.
The antiallergic effect develops as a result of a decrease in the synthesis and secretion of allergic mediators, inhibition of the release of histamine and other biologically active substances from sensitized mast cells and basophils, a decrease in the number of circulating basophils, T- and B-lymphocytes, mast cells, suppression of the development of lymphoid and connective tissue, decreased sensitivity of effector cells to mediators, allergies, inhibition of antibody formation, changes in the body's immune response.
In obstructive diseases of the respiratory tract, the effect is mainly due to inhibition of inflammatory processes, prevention or reduction of the severity of swelling of the mucous membranes, reduction of eosinophilic infiltration of the submucosal layer of the bronchial epithelium and deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucosa. Increases the sensitivity of beta-adrenergic receptors of small and medium-sized bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by reducing its production.
Suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous corticosteroids. Inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
