For the treatment of severe infections caused by bacteria susceptible to amikacin (see section 5.1), when less toxic antimicrobial agents are ineffective: nosocomial lower respiratory tract infections, including severe pneumonia, intra-abdominal infections, including peritonitis, complicated and recurrent urinary tract infections, skin and soft tissue infections, including poorly healing wound inf

AMIKACIN B. BRAUN 10MG/ML Solution for infusion: Roztwór do infuzji 5 mg/ml

All aminoglycosides have the potential to induce ototoxicity, renal toxicity, and neuromuscular blockade. These toxicities occur more frequently in patients with renal impairment, in patients treated with other ototoxic or nephrotoxic medicinal products, and in patients treated for prolonged periods and/or with doses higher than recommended (see section 4.4). Adverse reactions fo

Hypersensitivity to amikacin or other aminoglycosides or to any of the excipients listed in section 6.1. A history of hypersensitivity or severe toxic reactions to aminoglycosides may, due to the known cross-sensitivity of patients to medicinal products in this class, contraindicate the use of any aminoglycoside.

AMIKACIN B. BRAUN 10MG/ML Solution for infusion

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AMIKACIN B. BRAUN 10MG/ML Solution for infusion — Description, Dosage, Side Effects | PillsCard

Pharmacotherapeutic group: Other aminoglycosides, ATC code: J01GB06 Amikacin is a semi-synthetic aminoglycoside antibiotic derived from kanamycin.‍‍‍‍‍‍‍‍‍‍‍‍‍ It is obtained by acylation of the C-1 amino group in the 2-deoxystreptamine moiety with amino-hydroxybutyric acid. Mechanism of action Amikacin acts by inhibiting protein synthesis at the bacterial ribosome through interaction with ribosomal RNA and, in susceptible microorganisms, subsequent inhibition of reproduction. The result is a bactericidal effect. Pharmacokinetic/pharmacodynamic relationship Of the pharmacokinetic/pharmacodynamic parameters, the most important predictor of the bactericidal effect of amikacin is the ratio of peak serum concentration (Cmax) to the minimum inhibitory concentration (MIC) for the given pathogen. A Cmax/MIC ratio of 8:1 or 10:1 is considered effective for bacterial killing and prevention of regrowth. Amikacin exhibits a post-antibiotic effect both in vitro and in vivo. The post-antibiotic effect permits prolongation of the dosing interval without loss of efficacy against most Gram-negative bacilli. Mechanism(s) of resistance Resistance to amikacin may develop through the following mechanisms: Enzymatic inactivation: The most common mechanism of resistance is enzymatic modification of aminoglycoside molecules. These are mediated by acetyltransferases, phosphotransferases, or nucleotidyltransferases, which are primarily encoded on plasmids. Due to its resistance to degradation by aminoglycoside-inactivating enzymes, amikacin has been shown to be effective against many bacterial species resistant to aminoglycosides. Reduced penetration and active efflux: This resistance mechanism is observed in Pseudomonas aeruginosa. Recent data indicate the emergence of a similar resistance mechanism in Acinetobacter spp. Target structure alteration: Ribosomal modifications are only occasionally observed as a cause of resistance. Partial cross-resistance between amikacin and other aminoglycosides exists. Susceptibility testing breakpoints The European Committee on Antimicrobial Susceptibility Testing (EUCAST) has established the following interpretive criteria for minimum inhibitory concentration (MIC) susceptibility testing of amikacin: https://www.ema.europa.eu/documents/other/minimum-inhibitory-concentration-mic-breakpoints_en.xlsx Spectrum of activity of amikacin: The prevalence of acquired resistance may vary geographically and over time for selected species. Local resistance data are desirable, particularly when treating severe infections. Where necessary, expert advice should be sought when the local prevalence of resistance is such that the utility of the drug is questionable in at least some types of infection. Generally susceptible species Aerobic Gram-positive microorganisms Staphylococcus aureus Staphylococcus haemolyticusStaphylococcus hominis 0 Aerobic Gram-negative microorganisms Acinetobacter pittii Citrobacter freundii Citrobacter koseri Enterobacter cloacae Escherichia coli Klebsiella aerogenes Klebsiella oxytoca Klebsiella pneumoniae Morganella morganii Proteus mirabilis Proteus vulgaris 0 Pseudomonas aeruginosa 1 Salmonella enterica 0 Serratia liquefaciens 0 Serratia marcescens Shigella spp. Species for which acquired resistance may be a problem Aerobic Gram-positive microorganisms Staphylococcus epidermidis Aerobic Gram-negative microorganisms Acinetobacter baumannii Intrinsically resistant organisms Aerobic Gram-positive microorganisms Enterococcus spp. Streptococcus spp. Aerobic Gram-negative microorganisms Burkholderia cepacia Stenotrophomonas maltophilia Anaerobes Bacteroides spp. Prevotella spp. Other microorganisms Chlamydia spp. Chlamydophila spp. Mycoplasma spp. Ureaplasma urealyticum 1 In specific patient populations, e.g. patients with cystic fibrosis, the proportion of resistant isolates is ≥10%. 0 At the time of publication of these tables, no updated data were available. Susceptibility is assumed based on primary literature, standard reference works, and treatment guidelines. Additional information: Aminoglycosides are suitable in combination with other antibiotics against Gram-positive cocci.

⚠️ Warnings

Caution is required when administering to patients: with renal impairment, with hearing or vestibular impairment, with neuromuscular disorders (e.g.‍‍‍‍‍‍‍‍‍‍‍‍‍ myasthenia gravis, parkinsonism, as muscle weakness may be exacerbated due to the curare-like effect that amikacin may potentially exert on the neuromuscular junction), and patients treated with other aminoglycosides immediately prior to amikacin use. Patients treated with parenteral aminoglycosides should be under close clinical observation because of the potential ototoxicity and nephrotoxicity associated with their use. Toxic effects of aminoglycosides, including amikacin, are more common in patients with renal impairment, when high doses are administered, and during prolonged treatment. The safety of treatment exceeding 14 days has not been established. Other factors that increase the risk of aminoglycoside toxicity include advanced age and dehydration. Neuro/ototoxicity Neurotoxicity, manifesting as vestibular and/or bilateral auditory ototoxicity, may occur in patients treated with aminoglycosides. The risk of aminoglycoside-induced ototoxicity is higher in patients with renal impairment and in patients, including those who are otherwise healthy, whose therapy is extended to 5–7 days. High-frequency deafness usually appears first and can only be detected by audiometric testing. Vertigo may occur, which may be indicative of vestibular damage. Other manifestations of neurotoxicity may include numbness, tingling, muscle twitching, and convulsions. Patients with mitochondrial DNA mutations (particularly the 1555 A-to-G nucleotide substitution in the 12S rRNA gene) are at increased risk of ototoxicity, even when aminoglycoside serum levels remain within the recommended range during treatment. Alternative treatment options should be considered for these patients. In patients with a family history of relevant mutations or aminoglycoside-induced deafness, alternative treatment or genetic testing should be considered before administration. Patients who develop cochlear or vestibular damage may not experience any symptoms during treatment that would warn them of developing eighth-nerve toxicity, and complete or partial irreversible bilateral deafness or severe vertigo may occur after discontinuation of the product. See also section 4.8. Aminoglycoside-induced ototoxicity is usually irreversible. Neuromuscular toxicity Neuromuscular blockade and respiratory paralysis have been reported following parenteral injection, topical application (such as orthopaedic or abdominal irrigation or local treatment of empyema), and oral use of aminoglycosides. The possibility of respiratory paralysis should be considered regardless of the route of aminoglycoside administration, particularly in patients concomitantly receiving medicinal products that cause neuromuscular blockade. See also section 4.5. If neuromuscular blockade occurs, calcium salts may reverse respiratory paralysis; however, mechanical ventilation may still be necessary. Neuromuscular blockade and muscle paralysis have been demonstrated in laboratory animals given high doses of amikacin. Renal toxicity Aminoglycosides are potentially nephrotoxic. Renal toxicity is independent of the plasma sample obtained at peak concentration (Cmax). The risk of nephrotoxicity is higher in patients with renal impairment and in patients receiving high doses or undergoing prolonged therapy. Patients must be well hydrated during treatment, and renal function should be assessed by standard methods before starting therapy and daily during treatment. See section 4.2. Reduction of daily doses and/or extension of the dosing interval is required in the event of signs of renal dysfunction, such as: cylindruria, presence of leukocytes or erythrocytes in urine, albuminuria, decreased creatinine clearance, decreased urine specific gravity, hyperazotaemia, increased BUN, rise in serum creatinine, and oliguria. Treatment should be discontinued if azotaemia increases or if there is a progressive decrease in urine output. Patient monitoring Renal function and eighth cranial nerve function should be carefully monitored, particularly in patients with known or suspected renal impairment at the start of therapy, as well as in patients whose renal function is initially normal but who develop renal impairment during therapy. Serum amikacin concentrations should be monitored when possible to ensure adequate levels and to prevent potentially toxic levels. Urine should be examined for decreased specific gravity, increased protein excretion, and the presence of cells or sediment. Blood urea nitrogen, serum creatinine, or creatinine clearance should be measured at regular intervals. Serial audiograms should be obtained when possible in patients old enough to be tested, particularly high-risk patients. Evidence of ototoxicity (dizziness, vertigo, tinnitus, roaring in the ears, and hearing loss) or nephrotoxicity requires discontinuation of treatment or dose adjustment. See section 4.8. Amikacin treatment should be discontinued upon the occurrence of tinnitus, subjective hearing deterioration, or when serial audiograms demonstrate significant loss of high-frequency tone perception. As with other antibiotics, the use of amikacin may result in overgrowth of non-susceptible organisms. If this occurs, appropriate therapy should be initiated. Aminoglycosides applied locally as part of a surgical procedure are rapidly and almost completely absorbed (with the exception of the urinary bladder). Irreversible deafness, renal failure, and death caused by neuromuscular blockade have been reported in connection with aminoglycoside irrigation of the surgical field (regardless of extent). Macular infarction has been reported following intravitreal administration of amikacin (injection into the eye), leading in some cases to permanent loss of vision. Elderly patients Elderly patients may have reduced renal function that may not be apparent from routine screening tests such as BUN or serum creatinine. Determination of creatinine clearance may be more useful. Monitoring of renal function during aminoglycoside therapy is particularly important in elderly patients. Paediatric population Administration of aminoglycosides to premature and neonatal infants requires caution due to the renal immaturity of these patients, resulting in prolongation of the serum half-life of these drugs. Special warnings/precautions concerning excipients This medicinal product contains 354 mg of sodium per 100 ml, equivalent to 17.7% of the WHO recommended maximum daily dietary intake of sodium for an adult, which is 2 g sodium. Interference with laboratory tests When cephalosporins are administered concurrently, serum creatinine tests may yield falsely elevated values. In samples (e.g. serum, cerebrospinal fluid, etc.) collected for aminoglycoside testing, mutual inactivation of amikacin and beta-lactam antibiotics may continue, leading to inaccurate results. Samples should therefore be analysed immediately after collection, or frozen, or the beta-lactam antibiotics must be inactivated by the addition of beta-lactamase. Inactivation of aminoglycosides is clinically significant only in patients with severe renal impairment.

AMIKACIN B. BRAUN 10MG/ML Solution for infusion

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