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Side effects

Side effects of gentamicin toxicity vary between people. Side effects may become apparent shortly after or up to months after gentamicin is administered (they need citation?). Symptoms of gentamicin toxicity include:

  • Balance difficulty
  • Bouncing, unsteady vision
  • Ringing in the ears (tinnitus)
  • Difficulty multi-tasking, particularly when standing ( They need Citations?)

Nephrotoxicity is a problem in 10-25% of patients who receive aminoglycosides, and gentamicin is one of the most nephrotoxic of the class. [1] The risk of nephrotoxicity can be affected by the dose, frequency, duration of therapy, and concurrent use of certain medications such as NSAIDs, diuretics, cisplatin, cyclosporin, cephalosporin, amphotericin, iodide contrast media, and vancomycin . [1]

Patient factors that increase risk of nephrotoxicity include: [1]

  • increased age
  • reduced renal function
  • pregnancy
  • hypothyroidism
  • hepatic dysfunction
  • volume depletion
  • metabolic acidosis
  • sodium depletion

Clinicians observe for kidney dysfunction in patients on gentamicin by monitoring the rate that kidneys clear a molecule called creatinine, blood electrolyte levels, and concentrations of other chemical in the blood.[1]

Psychiatric symptoms related to gentamicin can occur. These include anorexia, confusion, depression, disorientation and visual hallucinations.[2]

A number of factors and determinants should be taken into account when using gentamicin, including differentiation between empirical and directed therapy which will affect dosage and treatment period.[3] Many medical practitioners freely administer gentamicin as an antibiotic without advising people of the severe and permanent potential ramifications of its use.

Inner ear[edit]

Aminoglycosides are toxic to the sensory cells of the ear, but they vary greatly in their relative effects on hearing versus balance. Gentamicin is a vestibulotoxin, and can cause permanent loss of equilibrioception, caused by damage to the vestibular apparatus of the inner ear, usually if taken at high doses or for prolonged periods of time, but there are well documented cases in which gentamicin completely destroyed the vestibular apparatus after three to five days.[citation needed] A small number of affected individuals have a normally harmless mutation in their mitochondrial DNA encoding the 12S ribosomal RNA (m.1555 A>G), that allows the gentamicin to affect their cells.[4] The cells of the ear are particularly sensitive to this, sometimes causing complete hearing loss.[5] However, gentamicin is sometimes used intentionally for this purpose in severe Ménière's disease, to disable the vestibular apparatus. These side effects are most common when the drug is administered via drops directly to the ear.

Kidneys[edit]

Prevention of nephrotoxicity includes judicious use of IV fluids to correct and avoid volume depletion, correction of hypokalemia and hypomagnesemia. Once daily dosing has been shown to be less toxic than multiple daily doses. Gentamicin is usually dosed by ideal body weight. Various formulae exist for calculating gentamicin dosage. Trough and peak serum levels of gentamicin are monitored during treatment to individualize therapy and prevent excess exposure.[6]

Gentamicin, like other aminoglycosides, causes nephrotoxicity by inhibiting protein synthesis in renal cells. This mechanism specifically causes necrosis of cells in the proximal tubule, resulting in acute tubular necrosis which can lead to acute renal failure.[7]

  1. ^ a b c d Lopez-Novoa, Jose M.; Quiros, Yaremi; Vicente, Laura; Morales, Ana I.; Lopez-Hernandez, Francisco J. (2011-01-01). "New insights into the mechanism of aminoglycoside nephrotoxicity: an integrative point of view". Kidney International. 79 (1): 33–45. doi:10.1038/ki.2010.337. ISSN 1523-1755. PMID 20861826.
  2. ^ Giannini, A.J.; Black, H.R. (1978). Psychiatric, Psychogenic and Somatopsychic Disorders Handbook. Garden City, New York: Medical Examination Publishing Co. pp. 136–137. ISBN 0-87488-596-5.
  3. ^ Cite error: The named reference ap01 was invoked but never defined (see the help page).
  4. ^ Pandya, A (1993). Pagon, R. A.; Adam, M. P.; Ardinger, H. H.; Bird, T. D.; Dolan, C. R.; Fong, C. T.; Smith, R. J. H.; Stephens, K (eds.). "Nonsyndromic Hearing Loss and Deafness, Mitochondrial". PMID 20301595. {{cite journal}}: Cite journal requires |journal= (help)
  5. ^ Gentamicin Toxicity at the American Hearing Research Foundation
  6. ^ Lopez-Novoa, Jose (2011). "New insights into the mechanism of aminoglycoside nephrotoxicity: an integrative point of view". Kidney International. 79: 33–45. doi:10.1038/ki.2010.337. PMID 20861826. Retrieved September 30, 2014.
  7. ^ Sundin, D.P.; Sandoval, R.; Molitoris, B.A. (2001). "Gentamicin Inhibits Renal Protein and Phospholipid Metabolism in Rats: Implications Involving Intracellular Trafficking". J Am Soc Nephrol. 12: 114–123.
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