Phenytoin neuromuscular blockade

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  • Topics: induction of
  • Phenytoin
  • The monobasic amino acid antibiotics lincomycin and clindamycin
  • In this study, we compared the pharmacokinetics and pharmacodynamics of cisatracurium after a prolonged infusion in patients with or without CAT

    There is a range of pharmacokinetics and pharmacodynamics in liver failure due to varying effects on volume of distribution, metabolism, biliary

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    With vecuronium, the dose-response curves for the two

    Monitor closely for more rapid than expected recovery from neuromuscular blockade; increase dosage of the neuromuscular blocking agent if necessary

    D

    Introduction Neuromuscular blockade in anesthetic management refers to the phenomenon in which non-depolarizing neuromuscular blocking drugs (NMBDs)

    , the time requir

    In addition, donepezil is known to produce prolonged neuromuscular blockade with depolarizing NMBAs such as

    Carbamazepine, phenytoin, phenobarbital and primidone induce many cytochrome P450 (CYP) and glucuronyl transferase (GT Similarly, the total duration of neuromuscular blockade, measured to recovery to 90% of control ECEMG, was significantly shorter in the phenytoin group (122 +/- 25 min compared with 269 +/- 64 min Neuromuscular blocking agents (NMBAs) can be an effective modality to address challenges that arise daily in the intensive care unit (ICU)

    Patients receiving chronic anticonvulsant therapy have been reported to show resistance to certain nondepolarizing

    Fosphenytoin-Phenytoin may enhance the neuromuscular-blocking effect of Neuromuscular

    Larger and more frequent doses of steroidal neuromuscular blocking agents are required to paralyze patients taking anticonvulsants (carbamazepine and phenytoin)

    Accentuates neuromuscular-blockade by nondepolarizing drugs; to a lesser degree also accentuates blockade by succinylcholine (Anectine) Interaction may be more pronounced with magnesium and vecuronium (Norcuron) than with other agents Patients chronically treated with phenytoin (Dilantin) are resistant to neuromuscular-blockade produced by Neuromuscular blockade, as an adjuvant therapy in the ventilatory and medical management of common critical illnesses, has an important but increasingly controversial role in the delivery of 21st century care in the modern ICU

    Ecothiopate, tacrine, organophosphates, propanidid, metoclopramide and bambuterol depress cholinesterase activity and prolong the duration of the neuromuscular block

    NMBAs may be useful in the intensive care unit (ICU) for several indications

    Many cases of resistance to neuromuscular blocking agents (NMBAs) have been anecdotally reported

    Depolarising neuromuscular blocking drugs

    While neuromuscular blocking agents block the motor manifestations, they do not treat the underlying seizure activity; Fosphenytoin and phenytoin – Fosphenytoin is started with a loading dose of 20 mg phenytoin equivalents (PE)/kg infused at 100 to 150 mg PE/min; phenytoin is started with a loading dose of 20 mg/kg and infused at 25 to 50 Steroid-based neuromuscular blocking drugs seem to be the most affected by the interaction, and for these drugs a recent study estimated a fivefold increase in vecuronium requirement in patients taking phenytoin

    Reversal of neuromuscular blocking agents — When neuromuscular blockade is necessary, we suggest reversal of neuromuscular blockade with sugammadex rather than neostigmine for patients with MG

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