Neuromuscular blockade aminoglycosides

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. 

Interactions Inhaled anesthetics, especially isoflurane, strongly potentiate and prolong neuromuscular blockade. Aminoglycoside antibiotics and antiarrhythmic drugs potentiate and prolong the relaxant action of neuromuscular blockers to a lesser degree. 

Neurotoxicity (damage to the nervous system by a toxic substance) may also be seen with the administration of the aminoglycosides. Signs and symptoms of neurotoxicity include numbness, skin tingling, circum-oral (around the mouth) paresthesia, peripheral paresthesia, tremors, muscle twitching, convulsions, muscle weakness, and neuromuscular blockade (acute muscular paralysis and apnea). 

When an aminoglycoside is being administered, it is important to monitor the patient s respiratory rate because neuromuscular blockade has been reported with the administration of these dragp. The nurse reports any changes in the respiratory rate or rhythm to the primary health care provider because immediate treatment may be necessary. 

Neuromuscular blockade or respiratory paralysis may occur after administration of the aminoglycosides Therefore, it is extremely important that any symptoms of respiratory difficulty be reported immediately. If neuromuscular blockade occurs, it may be reversed by the administration of calcium salts but mechanical ventilation may be required. 

Neuromuscular blockade Neurotoxicity can occur. Aminoglycosides may aggravate muscle weakness because of a potential curare-like effect on the neuromuscular junction. 

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... 

Certain antibiotics (e.g., aminoglycosides, macroUdes, polymyxins, lincomycin) enhance neuromuscular blockade by either decreasing ACh release or blocking the... 

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. 

In very high doses, aminoglycosides can produce a curare-like effect with neuromuscular blockade that results in respiratory paralysis. This paralysis is usually reversible by calcium gluconate (given promptly) or neostigmine. Hypersensitivity occurs infrequently. 

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. 

Aminoglycoside-induced neuromuscular blockade can be clinically relevant in patients with respiratory acidosis, in myasthenia gravis, and in other neuromuscular diseases. Severe illness, the simultaneous use of anesthetics, for example in the immediate postoperative phase, and apphcation of the antibiotic to serosal surfaces are predisposing factors (10). 

Clindamycin, either alone or in combination with neuromuscular blocking drugs or aminoglycosides, has been associated with neuromuscular blockade. 

Neuromuscular blockade is a rare side-effect of the aminoglycosides, related to blockade of acetylcholine at the nicotinic cholinergic receptor. This is most often seen as respiratory depression and apnea when anesthetic agents are administered... 

Indications Neuromuscular blockade, endotracheal intubation Category Non-depolarizing neuromuscular blocker Half-life initial 2 minutes terminal 20 minutes Clinically important, potentially hazardous interactions with amikacin, aminoglycosides, anesthetics, antibiotics, gentamicin, halothane, kanamycin, neomycin, piperacillin, streptomycin, tobramycin... 

AMINOGLYCOSIDES Nephrotoxic, ototoxic, may prolong the neuromuscular blockade effect of muscle relaxants. Check level post-HD... 

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