Neuromuscular blockade, aminoglycosides causing

Neuromuscular blockade. Aminoglycosides may impair neuromuscular transmission and aggravate (or reveal) myasthenia gravis, or cause a transient myasthenic syndrome in patients whose neuromuscular transmission is normal. 

Adults. 3 g PO q6h x 4 PRN Supl 1-2 g IM or IV repeat PRN Preeclampsia/pre-mature labor 4 g load then g/h IV inf Cardiac arrest 1-2 g IV push (2-4 mL 50% soln) in 10 mL DjW AMI Load 1-2 g in 50-100 mL D5W, over 5-60 min IV then 0.5-1.0 g/h IV up to 24 h (ECC 2005) Feds. 25-50 mg/kg/dose IM or IV q4-6h for 3-4 doses repeat PRN dose w/ low urine output or renal insuff Caution [B, +] Contra Heart block, renal failure Disp Inj 10, 20, 40, 80, 125, 500 mg/mL bulk powder SE CNS depression, D, flushing, heart block Interactions T CNS depression W/ antidepressants, antipsychotics, anxiolytics, barbiturates, hypnotics, narcotics EtOH T neuromuscular blockade Wf aminoglycosides, atracurium, gallamine, pancuronium, tubocurarine, vecuronium EMS Check for absent patellar reflexes this may indicate tox may cause hypokalemia (flattened T waves) and hypocalcemia OD May cause hypotension, resp arrest, T PR, QRS, and QT interval, AV block, and cardiac arrest calcium salts can be given to reverse resp depression... 

All the aminoglycosides produce cochlear and vestibular damage (ototoxicity) which is a dose and duration of treatment related side effect. Another serious side effect is nephrotoxicity. Aminoglycosides also reduce the acetylcholine release from the motor nerve endings and cause neuromuscular blockade. 

Numerous reports have described enhancement of neuromuscular blockade by antibiotics (eg, aminoglycosides). Many of the antibiotics have been shown to cause a depression of evoked release of acetylcholine similar to that caused by administering magnesium. The mechanism of this prejunctional effect appears to be blockade of specific P-type calcium channels in the motor nerve terminal. 

Toxic effects, which depends on dose and duration of treatment, mainly manifest as ototoxicity. Aminoglycosides also may cause nephrotoxicity and are reversible if they are withdrawn. They are known to cause neuromuscular blockade hence, care is necessary when used along with neuromuscular-blocking agents. Other reactions include allergy and cross-reactivity infections, as well as... 

The aminoglycoside, amikacin. The aminoglycosides can inhibit Ca++ uptake which is required for the release of acetylcholine at the neuromuscular junction, and can cause neuromuscular blockade. This is rare at usual doses of the drug, but patients with myasthenia gravis are particularly susceptible. 

Electrolyte imbalance, and diseases that lead to electrolyte imbalance, such as adrenal cortical insufficiency, alter neuromuscular blockade. Depending on the nature of the imbalance, either enhancement or inhibition may be expected. Magnesium sulfate, used in the management of toxemia of pregnancy, enhances the skeletal-muscle-relaxing effects of pancuronium. Antibiotics such as aminoglycosides, tetracyclines, clindamycin, lincomycin, colistin, and sodium colistimethate augment the pancuronium-induced neuromuscular blockade. Anesthetics such as halothane, enflurane, and isoflurane enhance the action of pancuronium, whereas azathioprine will cause a reversal of neuromuscular blockade. 

Nervous system The adverse effects of antituberculosis drugs on the nervous system have been reviewed [1 ]. Isoniazid is most often associated with nervous system reactions, most prominently peripheral neuropathy, psychosis, and seizures. Optic neuropathy can occur with ethambutol and ototoxicity and neuromuscular blockade with aminoglycosides. Cycloserine can cause psychosis and seizures, and the psychosis in particular limits its use. Fluoroquinolones are rare causes of seizures and delirium. Significant neurotoxicity has not been documented with newer forms of therapy under development. 

C. Aminoglycosides can cause neuromuscular junction blockade by the mechanism of displacing Ca+" from the neuromuscular junction and thus leading to the Ca" " -dependent prejunctional release of acetylcholine. This is of chnical significance only in patients with myasthenia gravis, hypocalcemia, and hypermagnesemia. 

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