Skip to main content

Drug-Induced Ototoxicity!

 DRUG-INDUCED OTOTOXICITY

What is drug Induced Ototoxicity?

  • Drug-Induced ototoxicity can affect hearing (auditory or cochlear function0, balance (vestibular function) depending on the drug.
  • Drugs of almost every class have been reported to produce tinnitus (sounds in ear), as have placebos.

The following agents are associated with measurable changes in hearing or vestibular defect when administered systemically.



1. AMINOGLYCOSIDES:

  • Aminoglycosides antibiotics can cause cochlear or vestibular toxicities.
  • Cochlear toxicity: occurs as progressive hear loss, starting with highest tones and advancing to lower tones. Thus, considerable damage can occur before the patient recognizes it.
  • Symptoms of Vestibular damage: include;

  1.  Dizziness
  2. Vertigo
  3. Ataxia

  • Both forms of ototoxicity are bilateral and potentially reversible, but permanent damage is common and can progress even after discontinuation of aminoglycosides.
  • Clinically detectable ototoxicity in as many as 5% patients.
  • Most aminoglycosides-induced ototoxicity is associated with parenteral therapy but has also been associated with topical oral and irrigation use of these of these drugs, especially Neomycin.
  • Possible predisposing factors: 

  1. Decreased renal function.
  2. Long duration of therapy
  3. Large total damage
  4. Plasma level above therapeutic range
  5. Concurrent use of ototoxic drugs
  6. Dehydration
  7. Old age
  8. Genetic susceptibility to aminoglycoside-induced ototoxicity


2. HETEROCYCLIC ANTIDEPRESSANTS:

  • The presence of Tricyclic Antidepressants-associated tinnitus is associated to be 1%
  • Tinnitus can subside (occur) despite continuous therapy.


3.CHLORQUINE:

  • Nerve deafness is rare but consistent feature of chloroquine therapy.
  • Its onset is usually delayed and is thought of as irreversible. A partly reversible case and a case resulting from 1g have also been reported.


4.DIURETICS (LOOP DIURETICS):

  • Rapid onset hearing loss occurs at high dose, IV administration of Furosemide.
  • Gradual onset is with Ethacrynic acid.
  • Renal failure is usually the predisposing factor, but only renal failure patients are likely to receive large IV dose.
  • Co-administration of Aminoglycoside antibiotics often result in increased ototoxicity.
  • Permanent hearing loss has been reported with Ethacrynic acid and Furosemide.
  • Bumetanide or Torsemide produce less ototoxicity than Ethacrynic acid and Furosemide.


5.NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs):

  • Although not as common as Salicylates, NSAIDs have been associated with hearing impairment and deafness, including some cases of permanent damage.
  • Tinnitus and vestibular dysfunction are also reported.


Comments

Popular posts from this blog

Diabetes Mellitus: Clinical Presentation and Diagnosis!

 CLINICAL PRESENTATION AND DIAGNOSIS OF DM 2. SCREENING American Diabetes Association (ADA) recommends routine screening for T2 DM every 3 years in all adults starting at 45 years of age. Testing of T2 DM should be considered in any adult, regardless of their age, who have a BMI greater than or equal to 25kg/m2. The ADA does not currently recommend widespread screening for T1 DM because of the relatively low incidence in the general population, although measurement of Islet antibodies may be appropriate for high-risk individuals. 3.GESTATIONAL DIABETES: "Gestational diabetes is the glucose intolerance in women during pregnancy". All pregnant women who have risk factors for T2 DM should be screened for undiagnosed T2 DM at their first prenatal visit using standard diagnostic criteria.  Any women found to have diabetes in the early point at pregnancy is considered to have T2 DM or GDM. All other pregnant women, not currently known to have DM should be screened for GDM with a 75...

Hospital Acquired Pneumonia- Definition, Predisposing Factors, Clinical Features and Management!

 HOSPITAL ACQUIRED PNEUMONIA Definition: "HAP refers to a new episode of pneumonia occurring at least 2 days after the administration to hospital. It is the most common Hospital Acquired Infection (HAI) and leading cause of HAI-associated death". Predisposing factors: Aspiration of nasopharyngeal secretion Bacteria introduced into the lower GIT. Bacteriaemia Old age Mode of Spread:  Droplet infection Infecting agent: Bacteria: S.pneumonia , S.aureus , H.influenza Virus: Adenovirus, Corona virus, Herpes Simplex Clinical Features: Purulent sputum New radiological infiltrates Temperature > 38 degree Celsius Leukocytosis Investigations: Chest Pain:  to confirm the diagnosis and exclude complication. Pulse Oximetry : to monitor response to oxygen therapy, if SaO2 < 93% features of sever pneumonia, identify ventilatory failure or acidosis. Cell count:  ESR, Neutrophil leukocytosis Microbiological studies:  for severe CAP and those that do not respond to ...

Management of H.pylori and NSAID-associated ulcers Eradication!

MANAGEMENT FOR H.PYLORI ERADICATION It is known that H.pylori infection is associated with over 90% of duodenal ulcers and 80% of Gastric Ulcers. Antibiotics alone or acid-suppressing agents alone, do not eradicate H.pylori . Both therapies act synergistically as growth of the organism occurs at elevated pH and antibiotics efficacy is enhanced during growth. Additionally, increasing intragastric pH may enhance antibiotic absorption. High eradication rates are achieved by a short course of Triple Therapy consisting of:            1 .PPI                                         2. Clarithromycin                         3. Amoxicillin/Metronidazole          in a twice recommended simultaneous regimen. First-Line Therapy :  European Guidelines recommended 1 we...